An increase in MITOCHONDRIAL VOLUME due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
Mitochondria in hepatocytes. As in all mitochondria, there are an outer membrane and an inner membrane, together creating two separate mitochondrial compartments: the internal matrix space and a much narrower intermembrane space. In the liver mitochondrion, an estimated 67% of the total mitochondrial proteins is located in the matrix. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p343-4)
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
Property of membranes and other structures to permit passage of light, heat, gases, liquids, metabolites, and mineral ions.
The quantity of volume or surface area of MITOCHONDRIA.
A glycoside of a kaurene type diterpene that is found in some plants including Atractylis gummifera (ATRACTYLIS); COFFEE; XANTHIUM, and CALLILEPIS. Toxicity is due to inhibition of ADENINE NUCLEOTIDE TRANSLOCASE.
Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.
A family of peptidyl-prolyl cis-trans isomerases that bind to CYCLOSPORINS and regulate the IMMUNE SYSTEM. EC 5.2.1.-
The voltage difference, normally maintained at approximately -180mV, across the INNER MITOCHONDRIAL MEMBRANE, by a net movement of positive charge across the membrane. It is a major component of the PROTON MOTIVE FORCE in MITOCHONDRIA used to drive the synthesis of ATP.
Thin structures that encapsulate subcellular structures or ORGANELLES in EUKARYOTIC CELLS. They include a variety of membranes associated with the CELL NUCLEUS; the MITOCHONDRIA; the GOLGI APPARATUS; the ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.
The mitochondria of the myocardium.
A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A group of cytochromes with covalent thioether linkages between either or both of the vinyl side chains of protoheme and the protein. (Enzyme Nomenclature, 1992, p539)
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Electron microscopy in which the ELECTRONS or their reaction products that pass down through the specimen are imaged below the plane of the specimen.
Chemical agents that uncouple oxidation from phosphorylation in the metabolic cycle so that ATP synthesis does not occur. Included here are those IONOPHORES that disrupt electron transfer by short-circuiting the proton gradient across mitochondrial membranes.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
A closely related group of toxic substances elaborated by various strains of Streptomyces. They are 26-membered macrolides with lactone moieties and double bonds and inhibit various ATPases, causing uncoupling of phosphorylation from mitochondrial respiration. Used as tools in cytochemistry. Some specific oligomycins are RUTAMYCIN, peliomycin, and botrycidin (formerly venturicidin X).
The two lipoprotein layers in the MITOCHONDRION. The outer membrane encloses the entire mitochondrion and contains channels with TRANSPORT PROTEINS to move molecules and ions in and out of the organelle. The inner membrane folds into cristae and contains many ENZYMES important to cell METABOLISM and energy production (MITOCHONDRIAL ATP SYNTHASE).
Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds.
Inorganic salts of phosphoric acid.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell.
The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Derivatives of SUCCINIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a 1,4-carboxy terminated aliphatic structure.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.
A multisubunit enzyme complex containing CYTOCHROME A GROUP; CYTOCHROME A3; two copper atoms; and 13 different protein subunits. It is the terminal oxidase complex of the RESPIRATORY CHAIN and collects electrons that are transferred from the reduced CYTOCHROME C GROUP and donates them to molecular OXYGEN, which is then reduced to water. The redox reaction is simultaneously coupled to the transport of PROTONS across the inner mitochondrial membrane.
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
Elements of limited time intervals, contributing to particular results or situations.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.

Role of mitochondrial dysfunction in the Ca2+-induced decline of transmitter release at K+-depolarized motor neuron terminals. (1/451)

The present study tested whether a Ca2+-induced disruption of mitochondrial function was responsible for the decline in miniature endplate current (MEPC) frequency that occurs with nerve-muscle preparations maintained in a 35 mM potassium propionate (35 mM KP) solution containing elevated calcium. When the 35 mM KP contained control Ca2+ (1 mM), the MEPC frequency increased and remained elevated for many hours, and the mitochondria within twitch motor neuron terminals were similar in appearance to those in unstimulated terminals. All nerve terminals accumulated FM1-43 when the dye was present for the final 6 min of a 300-min exposure to 35 mM KP with control Ca2+. In contrast, when Ca2+ was increased to 3.6 mM in the 35 mM KP solution, the MEPC frequency initially reached frequencies >350 s-1 but then gradually fell approaching frequencies <50 s-1. A progressive swelling and eventual distortion of mitochondria within the twitch motor neuron terminals occurred during prolonged exposure to 35 mM KP with elevated Ca2+. After approximately 300 min in 35 mM KP with elevated Ca2+, only 58% of the twitch terminals accumulated FM1-43. The decline in MEPC frequency in 35 mM KP with elevated Ca2+ was less when 15 mM glucose was present or when preparations were pretreated with 10 microM oligomycin and then bathed in the 35 mM KP with glucose. When glucose was present, with or without oligomycin pretreatment, a greater percentage of twitch terminals accumulated FM1-43. However, the mitochondria in these preparations were still greatly swollen and distorted. We propose that prolonged depolarization of twitch motor neuron terminals by 35 mM KP with elevated Ca2+ produced a Ca2+-induced decrease in mitochondrial ATP production. Under these conditions, the cytosolic ATP/ADP ratio was decreased thereby compromising both transmitter release and refilling of recycled synaptic vesicles. The addition of glucose stimulated glycolysis which contributed to the maintenance of required ATP levels.  (+info)

Uptake and effects of copper in rat liver mitochondria. (2/451)

The rate and extent of Cu2+ uptake by rat liver mitochondria was measured under various conditions. 1. The uptake is both greater and faster without an energy supply. 2. The uptake, when occuring in ionic media, has a biphasic character, that is it always slows down after an initial burst, and then re-accelerates. 3. Uptake of Cu2+ in the presence of energy initiates K+ uptake from K+-containing media with accompanying swelling and respiratory stimulation. Depending on the amounts of Cu2+ added and the K+ concentration, an inhibition of respiration later ensues. 4. Chelation of the Cu2+ by substrates (notably glutamate) decreases the effects. 5. Prior exposure to Cu2+ decreases or prevents energy-dependent Ca2+ uptake.  (+info)

The effect of peroxisome proliferators on mitochondrial bioenergetics. (3/451)

Peroxisome proliferators are a group of structurally diverse chemicals that cause the proliferation of peroxisomes in rodents. The purpose of this investigation was to test the hypothesis that the shared effect of these compounds on peroxisome proliferation is mediated through a common inhibitory effect on mitochondrial bioenergetics. Freshly isolated rat liver mitochondria were energized with succinate. The effect of the chemicals on mitochondrial bioenergetics was analyzed by monitoring calcium-induced changes in membrane potential and swelling, as well as changes in mitochondrial respiration. Mitochondrial membrane potential was measured with a TPP(+)-sensitive electrode, and swelling was recorded spectrophotometrically. Mitochondrial oxygen uptake was monitored with a Clark-type oxygen electrode. Gemfibrozil and WY-14,643 induced the mitochondrial permeability transition as characterized by calcium-induced swelling and depolarization of membrane potential, both of which were inhibited by cyclosporine A. Fenofibrate, clofibrate, ciprofibrate and diethylhexyl phthalate, on the other hand, caused a direct dose-dependent depolarization of mitochondrial membrane potential. However, the mechanism of membrane depolarization varied among the test chemicals. Bezafibrate and trichloroethylene elicited no effect on succinate-supported mitochondrial bioenergetics. The results of this investigation demonstrate that although most, but not all, peroxisome proliferators interfere with mitochondrial bioenergetics, the specific biomolecular mechanism differs among the individual compounds.  (+info)

Effect of histidine on myocardial mitochondria and platelet aggregation during thrombotic cerebral ischemia in rats. (4/451)

AIM: To study the effect of histidine on cerebral thrombosis and possible mechanism. METHODS: Cerebral-cardiac stroke was produced by photochemically induced thrombotic cerebral ischemia in rats. RESULTS: Platelet aggregation in whole blood increased markedly, peak heights at 4 and 24 h were (5.1 +/- 0.5) omega and (4.3 +/- 0.5) omega, respectively. Heart mitochondria volume (V), volume density (Vv), surface density (Nm), and surface density of outer membrane (Sv1) increased (8.2 +/- 5.5, 0.59 +/- 0.16, 0.11 +/- 0.03, and 0.22 +/- 0.05, respectively, P < 0.01), but numerical density (Nv), specific surface of inner membrane (delta 2) and of the cristae (delta 3) decreased (0.07 +/- 0.02, 2.8 +/- 0.8, and 2.4 +/- 0.7, respectively, P < 0.01) after cerebral thrombosis. The myocardial histopathologic characteristics were different from those of ischemic necrosis and myocardial damage caused by ischemic reperfusion. In rat treated with histidine after photochemical reaction, platelet aggregation decreased markedly [(2.93 +/- 1.08) omega, P < 0.01], reversible change often went with parameters related to the inner mitochondrial membrane but not the outer mitochondrial membrane. CONCLUSION: Histidine depressed platelet aggregation and reduced myocardial mitochondrial damage resulted from cerebral ischemia.  (+info)

Effects of heat shock on the functional morphology of cell organelles observed by video-enhanced microscopy. (5/451)

In living astrocytes and MDCK cells we observed morphological phenomena during and after heat shock (HS) utilizing our new perfusable microchamber system, which monitors pH, pO(2), pCO(2), and temperature. By means of electronic light microscopy and confocal laser scanning microscopy, mitochondria were demonstrated to swell and to reduce their motility. The specific fluorescent probe MitoTracker Green revealed that the mitochondrial morphology changed from a rodlike into an annular shape with a central vacuole-findings which were corroborated by transmission electron microscopy. After HS (shift from 37 degrees C to 45 degrees C for 15 min) the mitochondrial membrane potential (DeltaPsi(m)) was depressed in most but not all mitochondria as monitored with the fluorescent probe JC-1. The dual emission images of JC-1 illustrated a heterogeneous red staining of distinct areas of single mitochondria. The shape changes as well as the drop of the membrane potential of the mitochondria indicated severe cellular stress and a direct intervention on the mitochondrial permeability transition.  (+info)

Ionophoretic properties and mitochondrial effects of cereulide: the emetic toxin of B. cereus. (6/451)

The emetic toxin of Bacillus cereus, found to cause immobilization of spermatozoa and swelling of their mitochondria, was purified and its structure found to be identical to the earlier known toxin cereulide. It increased the conductance in black-lipid membranes in KCl solutions in an ionophore-like manner. It formed adducts with K+, Na+, and NH4+ but the conductance was highly selective for K+ in relation to Na+ and H+ (three orders of magnitude). The increase in the kinetics of conductance indicated a stoichiometric ratio between the cereulide and K+. Its ionophoretic properties are thus similar to those of valinomycin. In addition, its effects on rat liver mitochondria were similar: it stimulated swelling and respiration in respiring mitochondria in the presence but not in the absence of K+, it reduced the transmembrane potential under these conditions. In nonrespiring mitochondria, swelling was seen in KNO3- but not in NaNO3-containing media, less in acetate. In NaNO3 media addition of the cereulide caused a transient diffusion potential which was reduced by adding K+. It is concluded that the toxic effects of cereulide are due to it being a K+ ionophore.  (+info)

Mitochondria and cell death. Mechanistic aspects and methodological issues. (7/451)

Mitochondria are involved in cell death for reasons that go beyond ATP supply. A recent advance has been the discovery that mitochondria contain and release proteins that are involved in the apoptotic cascade, like cytochrome c and apoptosis inducing factor. The involvement of mitochondria in cell death, and its being cause or consequence, remain issues that are extremely complex to address in situ. The response of mitochondria may critically depend on the type of stimulus, on its intensity, and on the specific mitochondrial function that has been primarily perturbed. On the other hand, the outcome also depends on the integration of mitochondrial responses that cannot be dissected easily. Here, we try to identify the mechanistic aspects of mitochondrial involvement in cell death as can be derived from our current understanding of mitochondrial physiology, with special emphasis on the permeability transition and its consequences (like onset of swelling, cytochrome c release and respiratory inhibition); and to critically evaluate methods that are widely used to monitor mitochondrial function in situ.  (+info)

Structural changes of mitochondria related to apoptosis: swelling and megamitochondria formation. (8/451)

Recently we have found that the formation of megamitochondria in culture cells of various sources, induced by chemicals capable of generating free radicals, is followed by apoptotic changes of the cell. Detailed analysis on functional and morphological aspects of megamitochondria has enabled us to speculate that the formation of megamitochondria may be a prerequisite for free radical-mediated apoptosis: free radicals modify the mitochondrial membranes resulting in the fusion of adjacent mitochondria (megamitochondria formation). If the intracellular level of free radicals is continuously kept high, the permeability transition pores of the megamitochondria membranes are opened and megamitochondria become swollen. Oxygen consumption and the ability to synthesise ATP by swollen megamitochondria decrease distinctly. At the same time, cytochrome c is released from swollen megamitochondria into the cytoplasm. If lowered rates of the generation of reactive oxygen species from swollen megamitochondria, possibly due to decrease in their oxygen consumption, are effective enough to lower the intracellular level of free radicals, megamitochondria may return to normal. If not, decrease in the membrane potential of megamitochondria membranes causes the release of apoptosis-inducing factor into the cytoplasm. Cytochrome c and apoptosis-inducing factor thus released into the cytoplasm may cause cytoplasmic and nuclear apoptotic changes. Experimental data to support this hypothesis are presented.  (+info)

Mitochondrial swelling is a pathological change in the structure of mitochondria, which are the energy-producing organelles found in cells. This condition is characterized by an increase in the volume of the mitochondrial matrix, which is the space inside the mitochondrion that contains enzymes and other molecules involved in energy production.

Mitochondrial swelling can occur as a result of various cellular stressors, such as oxidative damage, calcium overload, or decreased levels of adenosine triphosphate (ATP), which is the primary energy currency of the cell. This swelling can lead to disruption of the mitochondrial membrane and release of cytochrome c, a protein involved in apoptosis or programmed cell death.

Mitochondrial swelling has been implicated in several diseases, including neurodegenerative disorders, ischemia-reperfusion injury, and drug toxicity. It can be observed under an electron microscope as part of an ultrastructural analysis of tissue samples or detected through biochemical assays that measure changes in mitochondrial membrane potential or matrix volume.

Mitochondria are specialized structures located inside cells that convert the energy from food into ATP (adenosine triphosphate), which is the primary form of energy used by cells. They are often referred to as the "powerhouses" of the cell because they generate most of the cell's supply of chemical energy. Mitochondria are also involved in various other cellular processes, such as signaling, differentiation, and apoptosis (programmed cell death).

Mitochondria have their own DNA, known as mitochondrial DNA (mtDNA), which is inherited maternally. This means that mtDNA is passed down from the mother to her offspring through the egg cells. Mitochondrial dysfunction has been linked to a variety of diseases and conditions, including neurodegenerative disorders, diabetes, and aging.

I'd be happy to help! However, I believe there might be a slight misunderstanding in your question. Mitochondria are organelles found in the cells of all complex living organisms, including humans, while the liver is a large, solid organ located in the upper right portion of the abdomen. They don't have a medical definition together. I can certainly provide you with separate definitions for each:

1. Mitochondria: These are double-membrane-bound cellular organelles that generate most of the chemical energy needed to power the cell's biochemical reactions. Commonly known as the "powerhouse of the cell," mitochondria convert organic substrates, such as glucose, fatty acids, and amino acids, into adenosine triphosphate (ATP) through a process called oxidative phosphorylation. Mitochondria are dynamic structures that can change their shape, size, and number through fission (division) and fusion (merging) processes. They play essential roles in various cellular functions, including calcium signaling, apoptosis (programmed cell death), and the regulation of cellular metabolism.

2. Liver: The liver is a large, lobulated organ that lies mainly in the upper right portion of the abdominal cavity, just below the diaphragm. It plays a crucial role in various physiological functions, such as detoxification, protein synthesis, metabolism, and nutrient storage. The liver is responsible for removing toxins from the bloodstream, producing bile to aid in digestion, regulating glucose levels, synthesizing plasma proteins, and storing glycogen, vitamins, and minerals. It also contributes to the metabolism of carbohydrates, lipids, and amino acids, helping maintain energy homeostasis in the body.

I hope this clarifies any confusion! If you have any further questions or need more information, please don't hesitate to ask.

Mitochondrial membrane transport proteins are a type of integral membrane proteins located in the inner and outer mitochondrial membranes. They play a crucial role in the regulation of molecule exchange between the cytosol and the mitochondrial matrix, allowing only specific ions and molecules to pass through while maintaining the structural and functional integrity of the mitochondria.

The inner mitochondrial membrane transport proteins, also known as the mitochondrial carrier proteins or the solute carriers, are a family of about 50 different types of proteins that facilitate the passage of various metabolites, such as nucleotides, amino acids, fatty acids, and inorganic ions (like calcium, sodium, and potassium). These transport proteins usually function as exchangers or uniporters, moving one type of solute in one direction in exchange for another type of solute or a proton.

The outer mitochondrial membrane is more permeable than the inner membrane due to the presence of voltage-dependent anion channels (VDACs) and other porins that allow small molecules, ions, and metabolites to pass through. VDACs are the most abundant proteins in the outer mitochondrial membrane and play a significant role in controlling the flow of metabolites between the cytosol and the intermembrane space.

In summary, mitochondrial membrane transport proteins are essential for maintaining the proper functioning of mitochondria by regulating the movement of molecules across the inner and outer membranes. They facilitate the exchange of nutrients, metabolites, and ions required for oxidative phosphorylation, energy production, and other cellular processes.

In the context of medicine and physiology, permeability refers to the ability of a tissue or membrane to allow the passage of fluids, solutes, or gases. It is often used to describe the property of the capillary walls, which control the exchange of substances between the blood and the surrounding tissues.

The permeability of a membrane can be influenced by various factors, including its molecular structure, charge, and the size of the molecules attempting to pass through it. A more permeable membrane allows for easier passage of substances, while a less permeable membrane restricts the movement of substances.

In some cases, changes in permeability can have significant consequences for health. For example, increased permeability of the blood-brain barrier (a specialized type of capillary that regulates the passage of substances into the brain) has been implicated in a number of neurological conditions, including multiple sclerosis, Alzheimer's disease, and traumatic brain injury.

I'm sorry for any confusion, but "mitochondrial size" is not a commonly used medical term or concept with a standardized definition in the field of medicine. Mitochondria are organelles found in the cells of organisms and are known to have a variety of sizes depending on the cell type and physiological conditions. However, it's not typically discussed as a standalone measurement or diagnostic factor. If you have any specific questions related to mitochondria or their function, I would be happy to try to help answer those!

Atractyloside is a toxic diterpene compound that can be found in various plants, including Atractylis gummifera (commonly known as gum cistus or rabbit-ear cistus) and other members of the Asteraceae family. This toxin is known to inhibit the mitochondrial ADP/ATP translocase, which plays a crucial role in cellular energy production.

Inhibition of this translocase leads to a disruption in the balance of adenine nucleotides inside the mitochondria, resulting in a decrease in ATP synthesis and an increase in the formation of reactive oxygen species (ROS). This can ultimately cause cell damage and even cell death.

Atractyloside poisoning can lead to various symptoms, such as gastrointestinal distress, liver and kidney damage, neurological issues, and, in severe cases, multi-organ failure. It is essential to seek immediate medical attention if atractyloside poisoning is suspected.

Cytochromes c are a group of small heme proteins found in the mitochondria of cells, involved in the electron transport chain and play a crucial role in cellular respiration. They accept and donate electrons during the process of oxidative phosphorylation, which generates ATP, the main energy currency of the cell. Cytochromes c contain a heme group, an organic compound that includes iron, which facilitates the transfer of electrons. The "c" in cytochromes c refers to the type of heme group they contain (cyt c has heme c). They are highly conserved across species and have been widely used as a molecular marker for evolutionary studies.

Cyclophilins are a family of proteins that have peptidyl-prolyl isomerase activity, which means they help with the folding and functioning of other proteins in cells. They were first identified as binding proteins for the immunosuppressive drug cyclosporine A, hence their name.

Cyclophilins are found in various organisms, including humans, and play important roles in many cellular processes such as signal transduction, protein trafficking, and gene expression. In addition to their role in normal cell function, cyclophilins have also been implicated in several diseases, including viral infections, cancer, and neurodegenerative disorders.

In medicine, the most well-known use of cyclophilins is as a target for immunosuppressive drugs used in organ transplantation. Cyclosporine A and its derivatives work by binding to cyclophilins, which inhibits their activity and subsequently suppresses the immune response.

Mitochondrial membrane potential is the electric potential difference (voltage) across the inner mitochondrial membrane. It is negative inside the mitochondria and positive outside. This electrical gradient is established by the active transport of hydrogen ions (protons) out of the mitochondrial matrix and into the intermembrane space by complexes in the electron transport chain during oxidative phosphorylation. The energy stored in this electrochemical gradient is used to generate ATP, which is the main source of energy for cellular metabolism.

Intracellular membranes refer to the membrane structures that exist within a eukaryotic cell (excluding bacteria and archaea, which are prokaryotic and do not have intracellular membranes). These membranes compartmentalize the cell, creating distinct organelles or functional regions with specific roles in various cellular processes.

Major types of intracellular membranes include:

1. Nuclear membrane (nuclear envelope): A double-membraned structure that surrounds and protects the genetic material within the nucleus. It consists of an outer and inner membrane, perforated by nuclear pores that regulate the transport of molecules between the nucleus and cytoplasm.
2. Endoplasmic reticulum (ER): An extensive network of interconnected tubules and sacs that serve as a major site for protein folding, modification, and lipid synthesis. The ER has two types: rough ER (with ribosomes on its surface) and smooth ER (without ribosomes).
3. Golgi apparatus/Golgi complex: A series of stacked membrane-bound compartments that process, sort, and modify proteins and lipids before they are transported to their final destinations within the cell or secreted out of the cell.
4. Lysosomes: Membrane-bound organelles containing hydrolytic enzymes for breaking down various biomolecules (proteins, carbohydrates, lipids, and nucleic acids) in the process called autophagy or from outside the cell via endocytosis.
5. Peroxisomes: Single-membrane organelles involved in various metabolic processes, such as fatty acid oxidation and detoxification of harmful substances like hydrogen peroxide.
6. Vacuoles: Membrane-bound compartments that store and transport various molecules, including nutrients, waste products, and enzymes. Plant cells have a large central vacuole for maintaining turgor pressure and storing metabolites.
7. Mitochondria: Double-membraned organelles responsible for generating energy (ATP) through oxidative phosphorylation and other metabolic processes, such as the citric acid cycle and fatty acid synthesis.
8. Chloroplasts: Double-membraned organelles found in plant cells that convert light energy into chemical energy during photosynthesis, producing oxygen and organic compounds (glucose) from carbon dioxide and water.
9. Endoplasmic reticulum (ER): A network of interconnected membrane-bound tubules involved in protein folding, modification, and transport; it is divided into two types: rough ER (with ribosomes on the surface) and smooth ER (without ribosomes).
10. Nucleus: Double-membraned organelle containing genetic material (DNA) and associated proteins involved in replication, transcription, RNA processing, and DNA repair. The nuclear membrane separates the nucleoplasm from the cytoplasm and contains nuclear pores for transporting molecules between the two compartments.

I'm happy to help! However, it seems like there are two terms combined into one request: "Mitochondria" and "Heart." I will provide separate definitions for each.

Mitochondrion (singular) or Mitochondria (plural): These are specialized structures found in the cytoplasm of most eukaryotic cells (cells with a true nucleus), including human cells. They are often referred to as the "powerhouse" of the cell because they generate energy in the form of ATP (adenosine triphosphate) through a process called oxidative phosphorylation. Mitochondria contain their own DNA, which is distinct from the nuclear DNA, and are believed to have originated from ancient bacteria that established a symbiotic relationship with primitive eukaryotic cells.

Heart: In human anatomy, the heart is a muscular organ responsible for pumping blood throughout the body. It is located in the thoracic cavity, slightly left of the center, and is enclosed by the pericardium, a double-walled sac that provides protection and lubrication for the heart's movement. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it to the rest of the body. The heart's pumping action is regulated by electrical signals that originate in a group of specialized cardiac muscle cells called the sinoatrial node (SA node).

Cyclosporine is a medication that belongs to a class of drugs called immunosuppressants. It is primarily used to prevent the rejection of transplanted organs, such as kidneys, livers, and hearts. Cyclosporine works by suppressing the activity of the immune system, which helps to reduce the risk of the body attacking the transplanted organ.

In addition to its use in organ transplantation, cyclosporine may also be used to treat certain autoimmune diseases, such as rheumatoid arthritis and psoriasis. It does this by suppressing the overactive immune response that contributes to these conditions.

Cyclosporine is available in capsule, oral solution, and injectable forms. Common side effects of the medication include kidney problems, high blood pressure, tremors, headache, and nausea. Long-term use of cyclosporine can also increase the risk of certain types of cancer and infections.

It is important to note that cyclosporine should only be used under the close supervision of a healthcare provider, as it requires regular monitoring of blood levels and kidney function.

Electron microscopy (EM) is a type of microscopy that uses a beam of electrons to create an image of the sample being examined, resulting in much higher magnification and resolution than light microscopy. There are several types of electron microscopy, including transmission electron microscopy (TEM), scanning electron microscopy (SEM), and reflection electron microscopy (REM).

In TEM, a beam of electrons is transmitted through a thin slice of the sample, and the electrons that pass through the sample are focused to form an image. This technique can provide detailed information about the internal structure of cells, viruses, and other biological specimens, as well as the composition and structure of materials at the atomic level.

In SEM, a beam of electrons is scanned across the surface of the sample, and the electrons that are scattered back from the surface are detected to create an image. This technique can provide information about the topography and composition of surfaces, as well as the structure of materials at the microscopic level.

REM is a variation of SEM in which the beam of electrons is reflected off the surface of the sample, rather than scattered back from it. This technique can provide information about the surface chemistry and composition of materials.

Electron microscopy has a wide range of applications in biology, medicine, and materials science, including the study of cellular structure and function, disease diagnosis, and the development of new materials and technologies.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

Cytochrome c is a small protein that is involved in the electron transport chain, a key part of cellular respiration in which cells generate energy in the form of ATP. Cytochrome c contains a heme group, which binds to and transports electrons. The cytochrome c group refers to a class of related cytochromes that have similar structures and functions. These proteins are found in the mitochondria of eukaryotic cells (such as those of plants and animals) and in the inner membranes of bacteria. They play a crucial role in the production of energy within the cell, and are also involved in certain types of programmed cell death (apoptosis).

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Transmission electron microscopy (TEM) is a type of microscopy in which an electron beam is transmitted through a ultra-thin specimen, interacting with it as it passes through. An image is formed from the interaction of the electrons with the specimen; the image is then magnified and visualized on a fluorescent screen or recorded on an electronic detector (or photographic film in older models).

TEM can provide high-resolution, high-magnification images that can reveal the internal structure of specimens including cells, viruses, and even molecules. It is widely used in biological and materials science research to investigate the ultrastructure of cells, tissues and materials. In medicine, TEM is used for diagnostic purposes in fields such as virology and bacteriology.

It's important to note that preparing a sample for TEM is a complex process, requiring specialized techniques to create thin (50-100 nm) specimens. These include cutting ultrathin sections of embedded samples using an ultramicrotome, staining with heavy metal salts, and positive staining or negative staining methods.

Uncoupling agents are chemicals that interfere with the normal process of oxidative phosphorylation in cells. In this process, the energy from food is converted into ATP (adenosine triphosphate), which is the main source of energy for cellular functions. Uncouplers disrupt this process by preventing the transfer of high-energy electrons to oxygen, which normally drives the production of ATP.

Instead, the energy from these electrons is released as heat, leading to an increase in body temperature. This effect is similar to what happens during shivering or exercise, when the body generates heat to maintain its core temperature. Uncoupling agents are therefore also known as "mitochondrial protonophores" because they allow protons to leak across the inner mitochondrial membrane, bypassing the ATP synthase enzyme that would normally use the energy from this proton gradient to produce ATP.

Uncoupling agents have been studied for their potential therapeutic uses, such as in weight loss and the treatment of metabolic disorders. However, they can also be toxic at high doses, and their long-term effects on health are not well understood.

Reactive Oxygen Species (ROS) are highly reactive molecules containing oxygen, including peroxides, superoxide, hydroxyl radical, and singlet oxygen. They are naturally produced as byproducts of normal cellular metabolism in the mitochondria, and can also be generated by external sources such as ionizing radiation, tobacco smoke, and air pollutants. At low or moderate concentrations, ROS play important roles in cell signaling and homeostasis, but at high concentrations, they can cause significant damage to cell structures, including lipids, proteins, and DNA, leading to oxidative stress and potential cell death.

Oligomycins are a group of antibiotics produced by various species of Streptomyces bacteria. They are characterized by their ability to inhibit the function of ATP synthase, an enzyme that plays a crucial role in energy production within cells. By binding to the F1 component of ATP synthase, oligomycins prevent the synthesis of ATP, which is a key source of energy for cellular processes.

These antibiotics have been used in research to study the mechanisms of ATP synthase and mitochondrial function. However, their therapeutic use as antibiotics is limited due to their toxicity to mammalian cells. Oligomycin A is one of the most well-known and studied members of this group of antibiotics.

Mitochondrial membranes refer to the double-layered structure that surrounds the mitochondrion, an organelle found in the cells of most eukaryotes. The outer mitochondrial membrane is a smooth, porous membrane that allows small molecules and ions to pass through freely, while the inner mitochondrial membrane is highly folded and selectively permeable, controlling the movement of larger molecules and maintaining the electrochemical gradient necessary for ATP synthesis. The space between the two membranes is called the intermembrane space, and the space within the inner membrane is called the matrix. Together, these membranes play a crucial role in energy production, metabolism, and cellular homeostasis.

Oxidative phosphorylation is the metabolic process by which cells use enzymes to generate energy in the form of adenosine triphosphate (ATP) from the oxidation of nutrients, such as glucose or fatty acids. This process occurs in the inner mitochondrial membrane of eukaryotic cells and is facilitated by the electron transport chain, which consists of a series of protein complexes that transfer electrons from donor molecules to acceptor molecules. As the electrons are passed along the chain, they release energy that is used to pump protons across the membrane, creating a gradient. The ATP synthase enzyme then uses the flow of protons back across the membrane to generate ATP, which serves as the main energy currency for cellular processes.

Phosphates, in a medical context, refer to the salts or esters of phosphoric acid. Phosphates play crucial roles in various biological processes within the human body. They are essential components of bones and teeth, where they combine with calcium to form hydroxyapatite crystals. Phosphates also participate in energy transfer reactions as phosphate groups attached to adenosine diphosphate (ADP) and adenosine triphosphate (ATP). Additionally, they contribute to buffer systems that help maintain normal pH levels in the body.

Abnormal levels of phosphates in the blood can indicate certain medical conditions. High phosphate levels (hyperphosphatemia) may be associated with kidney dysfunction, hyperparathyroidism, or excessive intake of phosphate-containing products. Low phosphate levels (hypophosphatemia) might result from malnutrition, vitamin D deficiency, or certain diseases affecting the small intestine or kidneys. Both hypophosphatemia and hyperphosphatemia can have significant impacts on various organ systems and may require medical intervention.

Oxygen consumption, also known as oxygen uptake, is the amount of oxygen that is consumed or utilized by the body during a specific period of time, usually measured in liters per minute (L/min). It is a common measurement used in exercise physiology and critical care medicine to assess an individual's aerobic metabolism and overall health status.

In clinical settings, oxygen consumption is often measured during cardiopulmonary exercise testing (CPET) to evaluate cardiovascular function, pulmonary function, and exercise capacity in patients with various medical conditions such as heart failure, chronic obstructive pulmonary disease (COPD), and other respiratory or cardiac disorders.

During exercise, oxygen is consumed by the muscles to generate energy through a process called oxidative phosphorylation. The amount of oxygen consumed during exercise can provide important information about an individual's fitness level, exercise capacity, and overall health status. Additionally, measuring oxygen consumption can help healthcare providers assess the effectiveness of treatments and rehabilitation programs in patients with various medical conditions.

Cell death is the process by which cells cease to function and eventually die. There are several ways that cells can die, but the two most well-known and well-studied forms of cell death are apoptosis and necrosis.

Apoptosis is a programmed form of cell death that occurs as a normal and necessary process in the development and maintenance of healthy tissues. During apoptosis, the cell's DNA is broken down into small fragments, the cell shrinks, and the membrane around the cell becomes fragmented, allowing the cell to be easily removed by phagocytic cells without causing an inflammatory response.

Necrosis, on the other hand, is a form of cell death that occurs as a result of acute tissue injury or overwhelming stress. During necrosis, the cell's membrane becomes damaged and the contents of the cell are released into the surrounding tissue, causing an inflammatory response.

There are also other forms of cell death, such as autophagy, which is a process by which cells break down their own organelles and proteins to recycle nutrients and maintain energy homeostasis, and pyroptosis, which is a form of programmed cell death that occurs in response to infection and involves the activation of inflammatory caspases.

Cell death is an important process in many physiological and pathological processes, including development, tissue homeostasis, and disease. Dysregulation of cell death can contribute to the development of various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases.

Cell respiration is the process by which cells convert biochemical energy from nutrients into adenosine triphosphate (ATP), and then release waste products. The three main stages of cell respiration are glycolysis, the citric acid cycle (also known as the Krebs cycle), and the electron transport chain.

During glycolysis, which takes place in the cytoplasm, glucose is broken down into two molecules of pyruvate, producing a small amount of ATP and reducing power in the form of NADH.

The citric acid cycle occurs in the mitochondria and involves the breakdown of acetyl-CoA (formed from pyruvate) to produce more ATP, NADH, and FADH2.

Finally, the electron transport chain, also located in the mitochondria, uses the energy from NADH and FADH2 to pump protons across the inner mitochondrial membrane, creating a proton gradient. The flow of protons back across the membrane drives the synthesis of ATP, which is used as a source of energy by the cell.

Cell respiration is a crucial process that allows cells to generate the energy they need to perform various functions and maintain homeostasis.

Necrosis is the premature death of cells or tissues due to damage or injury, such as from infection, trauma, infarction (lack of blood supply), or toxic substances. It's a pathological process that results in the uncontrolled and passive degradation of cellular components, ultimately leading to the release of intracellular contents into the extracellular space. This can cause local inflammation and may lead to further tissue damage if not treated promptly.

There are different types of necrosis, including coagulative, liquefactive, caseous, fat, fibrinoid, and gangrenous necrosis, each with distinct histological features depending on the underlying cause and the affected tissues or organs.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

Succinates, in a medical context, most commonly refer to the salts or esters of succinic acid. Succinic acid is a dicarboxylic acid that is involved in the Krebs cycle, which is a key metabolic pathway in cells that generates energy through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins.

Succinates can also be used as a buffer in medical solutions and as a pharmaceutical intermediate in the synthesis of various drugs. In some cases, succinate may be used as a nutritional supplement or as a component of parenteral nutrition formulations to provide energy and help maintain acid-base balance in patients who are unable to eat normally.

It's worth noting that there is also a condition called "succinic semialdehyde dehydrogenase deficiency" which is a genetic disorder that affects the metabolism of the amino acid gamma-aminobutyric acid (GABA). This condition can lead to an accumulation of succinic semialdehyde and other metabolic byproducts, which can cause neurological symptoms such as developmental delay, hypotonia, and seizures.

Adenosine Triphosphate (ATP) is a high-energy molecule that stores and transports energy within cells. It is the main source of energy for most cellular processes, including muscle contraction, nerve impulse transmission, and protein synthesis. ATP is composed of a base (adenine), a sugar (ribose), and three phosphate groups. The bonds between these phosphate groups contain a significant amount of energy, which can be released when the bond between the second and third phosphate group is broken, resulting in the formation of adenosine diphosphate (ADP) and inorganic phosphate. This process is known as hydrolysis and can be catalyzed by various enzymes to drive a wide range of cellular functions. ATP can also be regenerated from ADP through various metabolic pathways, such as oxidative phosphorylation or substrate-level phosphorylation, allowing for the continuous supply of energy to cells.

Membrane potential is the electrical potential difference across a cell membrane, typically for excitable cells such as nerve and muscle cells. It is the difference in electric charge between the inside and outside of a cell, created by the selective permeability of the cell membrane to different ions. The resting membrane potential of a typical animal cell is around -70 mV, with the interior being negative relative to the exterior. This potential is generated and maintained by the active transport of ions across the membrane, primarily through the action of the sodium-potassium pump. Membrane potentials play a crucial role in many physiological processes, including the transmission of nerve impulses and the contraction of muscle cells.

Cell membrane permeability refers to the ability of various substances, such as molecules and ions, to pass through the cell membrane. The cell membrane, also known as the plasma membrane, is a thin, flexible barrier that surrounds all cells, controlling what enters and leaves the cell. Its primary function is to protect the cell's internal environment and maintain homeostasis.

The permeability of the cell membrane depends on its structure, which consists of a phospholipid bilayer interspersed with proteins. The hydrophilic (water-loving) heads of the phospholipids face outward, while the hydrophobic (water-fearing) tails face inward, creating a barrier that is generally impermeable to large, polar, or charged molecules.

However, specific proteins within the membrane, called channels and transporters, allow certain substances to cross the membrane. Channels are protein structures that span the membrane and provide a pore for ions or small uncharged molecules to pass through. Transporters, on the other hand, are proteins that bind to specific molecules and facilitate their movement across the membrane, often using energy in the form of ATP.

The permeability of the cell membrane can be influenced by various factors, such as temperature, pH, and the presence of certain chemicals or drugs. Changes in permeability can have significant consequences for the cell's function and survival, as they can disrupt ion balances, nutrient uptake, waste removal, and signal transduction.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Oxidation-Reduction (redox) reactions are a type of chemical reaction involving a transfer of electrons between two species. The substance that loses electrons in the reaction is oxidized, and the substance that gains electrons is reduced. Oxidation and reduction always occur together in a redox reaction, hence the term "oxidation-reduction."

In biological systems, redox reactions play a crucial role in many cellular processes, including energy production, metabolism, and signaling. The transfer of electrons in these reactions is often facilitated by specialized molecules called electron carriers, such as nicotinamide adenine dinucleotide (NAD+/NADH) and flavin adenine dinucleotide (FAD/FADH2).

The oxidation state of an element in a compound is a measure of the number of electrons that have been gained or lost relative to its neutral state. In redox reactions, the oxidation state of one or more elements changes as they gain or lose electrons. The substance that is oxidized has a higher oxidation state, while the substance that is reduced has a lower oxidation state.

Overall, oxidation-reduction reactions are fundamental to the functioning of living organisms and are involved in many important biological processes.

Proto-oncogene proteins c-bcl-2 are a group of proteins that play a role in regulating cell death (apoptosis). The c-bcl-2 gene produces one of these proteins, which helps to prevent cells from undergoing apoptosis. This protein is located on the membrane of mitochondria and endoplasmic reticulum and it can inhibit the release of cytochrome c, a key player in the activation of caspases, which are enzymes that trigger apoptosis.

In normal cells, the regulation of c-bcl-2 protein helps to maintain a balance between cell proliferation and cell death, ensuring proper tissue homeostasis. However, when the c-bcl-2 gene is mutated or its expression is dysregulated, it can contribute to cancer development by allowing cancer cells to survive and proliferate. High levels of c-bcl-2 protein have been found in many types of cancer, including leukemia, lymphoma, and carcinomas, and are often associated with a poor prognosis.

Ion channels are specialized transmembrane proteins that form hydrophilic pores or gaps in the lipid bilayer of cell membranes. They regulate the movement of ions (such as sodium, potassium, calcium, and chloride) across the cell membrane by allowing these charged particles to pass through selectively in response to various stimuli, including voltage changes, ligand binding, mechanical stress, or temperature changes. This ion movement is essential for many physiological processes, including electrical signaling, neurotransmission, muscle contraction, and maintenance of resting membrane potential. Ion channels can be categorized based on their activation mechanisms, ion selectivity, and structural features. Dysfunction of ion channels can lead to various diseases, making them important targets for drug development.

Electron Transport Complex IV is also known as Cytochrome c oxidase. It is the last complex in the electron transport chain, located in the inner mitochondrial membrane of eukaryotic cells and the plasma membrane of prokaryotic cells. This complex contains 13 subunits, two heme groups (a and a3), and three copper centers (A, B, and C).

In the electron transport chain, Complex IV receives electrons from cytochrome c and transfers them to molecular oxygen, reducing it to water. This process is accompanied by the pumping of protons across the membrane, contributing to the generation of a proton gradient that drives ATP synthesis via ATP synthase (Complex V). The overall reaction catalyzed by Complex IV can be summarized as follows:

4e- + 4H+ + O2 → 2H2O

Defects in Cytochrome c oxidase can lead to various diseases, including mitochondrial encephalomyopathies and neurodegenerative disorders.

Caspases are a family of protease enzymes that play essential roles in programmed cell death, also known as apoptosis. These enzymes are produced as inactive precursors and are activated when cells receive signals to undergo apoptosis. Once activated, caspases cleave specific protein substrates, leading to the characteristic morphological changes and DNA fragmentation associated with apoptotic cell death. Caspases also play roles in other cellular processes, including inflammation and differentiation. There are two types of caspases: initiator caspases (caspase-2, -8, -9, and -10) and effector caspases (caspase-3, -6, and -7). Initiator caspases are activated in response to various apoptotic signals and then activate the effector caspases, which carry out the proteolytic cleavage of cellular proteins. Dysregulation of caspase activity has been implicated in a variety of diseases, including neurodegenerative disorders, ischemic injury, and cancer.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Caspase-3 is a type of protease enzyme that plays a central role in the execution-phase of cell apoptosis, or programmed cell death. It's also known as CPP32 (CPP for ced-3 protease precursor) or apopain. Caspase-3 is produced as an inactive protein that is activated when cleaved by other caspases during the early stages of apoptosis. Once activated, it cleaves a variety of cellular proteins, including structural proteins, enzymes, and signal transduction proteins, leading to the characteristic morphological and biochemical changes associated with apoptotic cell death. Caspase-3 is often referred to as the "death protease" because of its crucial role in executing the cell death program.

BCL-2-associated X protein, often abbreviated as BAX, is a type of protein belonging to the BCL-2 family. The BCL-2 family of proteins plays a crucial role in regulating programmed cell death, also known as apoptosis. Specifically, BAX is a pro-apoptotic protein, which means that it promotes cell death.

BAX is encoded by the BAX gene, and it functions by forming pores in the outer membrane of the mitochondria, leading to the release of cytochrome c and other pro-apoptotic factors into the cytosol. This triggers a cascade of events that ultimately leads to cell death.

Dysregulation of BAX and other BCL-2 family proteins has been implicated in various diseases, including cancer and neurodegenerative disorders. For example, reduced levels of BAX have been observed in some types of cancer, which may contribute to tumor growth and resistance to chemotherapy. On the other hand, excessive activation of BAX has been linked to neuronal death in conditions such as Alzheimer's disease and Parkinson's disease.

Antioxidants are substances that can prevent or slow damage to cells caused by free radicals, which are unstable molecules that the body produces as a reaction to environmental and other pressures. Antioxidants are able to neutralize free radicals by donating an electron to them, thus stabilizing them and preventing them from causing further damage to the cells.

Antioxidants can be found in a variety of foods, including fruits, vegetables, nuts, and grains. Some common antioxidants include vitamins C and E, beta-carotene, and selenium. Antioxidants are also available as dietary supplements.

In addition to their role in protecting cells from damage, antioxidants have been studied for their potential to prevent or treat a number of health conditions, including cancer, heart disease, and age-related macular degeneration. However, more research is needed to fully understand the potential benefits and risks of using antioxidant supplements.

Cardiac myocytes are the muscle cells that make up the heart muscle, also known as the myocardium. These specialized cells are responsible for contracting and relaxing in a coordinated manner to pump blood throughout the body. They differ from skeletal muscle cells in several ways, including their ability to generate their own electrical impulses, which allows the heart to function as an independent rhythmical pump. Cardiac myocytes contain sarcomeres, the contractile units of the muscle, and are connected to each other by intercalated discs that help coordinate contraction and ensure the synchronous beating of the heart.

Glutathione is a tripeptide composed of three amino acids: cysteine, glutamic acid, and glycine. It is a vital antioxidant that plays an essential role in maintaining cellular health and function. Glutathione helps protect cells from oxidative stress by neutralizing free radicals, which are unstable molecules that can damage cells and contribute to aging and diseases such as cancer, heart disease, and dementia. It also supports the immune system, detoxifies harmful substances, and regulates various cellular processes, including DNA synthesis and repair.

Glutathione is found in every cell of the body, with particularly high concentrations in the liver, lungs, and eyes. The body can produce its own glutathione, but levels may decline with age, illness, or exposure to toxins. As such, maintaining optimal glutathione levels through diet, supplementation, or other means is essential for overall health and well-being.

Oxidative stress is defined as an imbalance between the production of reactive oxygen species (free radicals) and the body's ability to detoxify them or repair the damage they cause. This imbalance can lead to cellular damage, oxidation of proteins, lipids, and DNA, disruption of cellular functions, and activation of inflammatory responses. Prolonged or excessive oxidative stress has been linked to various health conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and aging-related diseases.

The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.

The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.

Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.

Biological transport refers to the movement of molecules, ions, or solutes across biological membranes or through cells in living organisms. This process is essential for maintaining homeostasis, regulating cellular functions, and enabling communication between cells. There are two main types of biological transport: passive transport and active transport.

Passive transport does not require the input of energy and includes:

1. Diffusion: The random movement of molecules from an area of high concentration to an area of low concentration until equilibrium is reached.
2. Osmosis: The diffusion of solvent molecules (usually water) across a semi-permeable membrane from an area of lower solute concentration to an area of higher solute concentration.
3. Facilitated diffusion: The assisted passage of polar or charged substances through protein channels or carriers in the cell membrane, which increases the rate of diffusion without consuming energy.

Active transport requires the input of energy (in the form of ATP) and includes:

1. Primary active transport: The direct use of ATP to move molecules against their concentration gradient, often driven by specific transport proteins called pumps.
2. Secondary active transport: The coupling of the movement of one substance down its electrochemical gradient with the uphill transport of another substance, mediated by a shared transport protein. This process is also known as co-transport or counter-transport.

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Edema is the medical term for swelling caused by excess fluid accumulation in the body tissues. It can affect any part of the body, but it's most commonly noticed in the hands, feet, ankles, and legs. Edema can be a symptom of various underlying medical conditions, such as heart failure, kidney disease, liver disease, or venous insufficiency.

The swelling occurs when the capillaries leak fluid into the surrounding tissues, causing them to become swollen and puffy. The excess fluid can also collect in the cavities of the body, leading to conditions such as pleural effusion (fluid around the lungs) or ascites (fluid in the abdominal cavity).

The severity of edema can vary from mild to severe, and it may be accompanied by other symptoms such as skin discoloration, stiffness, and pain. Treatment for edema depends on the underlying cause and may include medications, lifestyle changes, or medical procedures.

These can lead to mitochondrial swelling and depolarization. Excessive activity of the crinophagy form of autophagy in the ... Loss of function in these genes can lead to damaged mitochondrial accumulation and protein aggregates that can lead to cellular ... Esteves AR, Arduíno DM, Silva DF, Oliveira CR, Cardoso SM (January 2011). "Mitochondrial Dysfunction: The Road to Alpha- ...
It binds to the mitochondrial matrix by insertion into the inner membrane. DTPP itself can cause mitochondrial swelling in ... Leo, S; Szabadkai, G; Rizzuto, R (December 2008). "The mitochondrial antioxidants MitoE(2) and MitoQ(10) increase mitochondrial ... "The targeted anti-oxidant MitoQ causes mitochondrial swelling in kidney tissue. It and depolarization in kidney tissue". ... It forms the basis for many mitochondrial-targeted drugs, including MitoQ, MitoE, and SkQ. ...
"Light Scattering from Intact Cells Reports Oxidative-Stress-Induced Mitochondrial Swelling". Biophysical Journal. 88 (4): 2929- ...
In the initial parts of the dendrites, mitochondrial swelling and dilation can be seen. This swelling can also be seen in the ... The first signs of degeneration seen after the removal of the bulb was mitochondrial swelling and then an increase in electron ... There is swelling in mitochondria and other membrane bound organelles. There is also a marked increase in cytoplasmic ... Mitochondria, endoplasmic reticulum, Golgi apparatus and multivesicular bodies all appear to swell, though this can be best ...
The process is characterized by mitochondrial swelling, cytoplasm vacuolization, and swelling of the nucleus and cytoplasm. ... In necrosis, a cell undergoes swelling, followed by uncontrolled rupture of the cell membrane with cell contents being expelled ...
... opening induces mitochondrial swelling and outer membrane of the mitochondria (OMM) rupture. Moreover, PTP opening induce ... and mitochondrial calcium uniporter (MCU) accumulates calcium into the mitochondrial matrix for electrochemical gradient. ... Mitochondrial outer membrane permeabilization (MOMP), is a reason of the higher matrix Ca2 + levels, which is acts as a trigger ... 2012). "PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress". Cell Death ...
However, in electron microscopy relaxed myofibrils, as well as glycogen loss and mitochondrial swelling can be observered. It ... If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral ...
... induced mitochondrial swelling". Asian Pacific Journal of Tropical Biomedicine. 3 (10): 757-66. doi:10.1016/S2221-1691(13)60152 ...
Deletions in this protein causes swelling, a loss of membrane potential, and mitochondrial fragmentation. Recently, it has been ... These can lead to mitochondrial swelling and depolarization. It is important to keep the dysfunctional mitochondria regulated, ... and partially through the inner mitochondrial membrane via the TIM complex, so it then spans the inner mitochondrial membrane. ... Mitochondrial damage-associated molecular patterns (DAMPs) such as parts of damaged organelles or mtDNA are secreted by cells ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... Endonuclease G, mitochondrial is an enzyme that in humans is encoded by the ENDOG gene. This protein primarily participates in ... Zhao ST, Chen M, Li SJ, Zhang MH, Li BX, Das M, Bean JC, Kong JM, Zhu XH, Gao TM (8 September 2009). "Mitochondrial BNIP3 ... Ohsato T, Ishihara N, Muta T, Umeda S, Ikeda S, Mihara K, Hamasaki N, Kang D (Dec 2002). "Mammalian mitochondrial endonuclease ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... "Structural features of the precursor to mitochondrial aspartate aminotransferase responsible for binding to hsp70". The Journal ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... Kenmochi N, Suzuki T, Uechi T, Magoori M, Kuniba M, Higa S, Watanabe K, Tanaka T (2001). "The human mitochondrial ribosomal ... 28S ribosomal protein S29, mitochondrial, also known as death-associated protein 3 (DAP3), is a protein that in humans is ... As part of the mitoribosome, DAP3 participates in the translation of the 13 ETC complex proteins encoded in the mitochondrial ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... PTPIP51 is a member of the RMDN protein family and localizes to the outer mitochondrial membrane, cytoplasm, and nucleus. This ... In addition, PTPIP51 has a mitochondrial targeting sequence at its N-terminal which is responsible for inducing apoptosis, ... PTPIP51 has been observed to induce apoptosis by disrupting the mitochondrial membrane potential, resulting in the release of ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... it additionally stimulates mitochondrial release of AIFM1, which then translocates to the nucleus to effect apoptosis, which ... induction of mitochondrial permeability transition, and activation of caspase-9 and 3. In neuronal cells, ... "Interaction of pro-apoptotic protein HGTD-P with heat shock protein 90 is required for induction of mitochondrial apoptotic ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... VDACs also contain a mitochondrial targeting sequence for the protein's translocation to the outer mitochondrial membrane. In ... These channels may also function as a mitochondrial binding site for hexokinase and glycerol kinase. The VDAC is an important ... Ha H, Hajek P, Bedwell DM, Burrows PD (Jun 1993). "A mitochondrial porin cDNA predicts the existence of multiple human porins ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... VDACs also contain a mitochondrial targeting sequence for the protein's translocation to the outer mitochondrial membrane. ... Sampson MJ, Ross L, Decker WK, Craigen WJ (Nov 1998). "A novel isoform of the mitochondrial outer membrane protein VDAC3 via ... These channels may also function as a mitochondrial binding site for hexokinase and glycerol kinase. The VDAC is an important ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... FASTKD1 shares structural characteristics of the FASTKD family, including an N-terminal mitochondrial targeting domain and ... Articles with short description, Short description matches Wikidata, Genes on human chromosome 2, Mitochondrial proteins). ... "Fast kinase domain-containing protein 3 is a mitochondrial protein essential for cellular respiration". Biochemical and ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... This protein also possesses an N-terminal mitochondrial leader sequence which targets it to the mitochondrial matrix, where it ... This gene is a mitochondrial member of the iron/manganese superoxide dismutase family. It encodes a mitochondrial matrix ... It encodes a mitochondrial protein that forms a homotetramer and binds one manganese ion per subunit. This protein binds to the ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... FASTKD2 has been linked to mitochondrial encephalomyopathy associated with cytochrome c oxidase deficiency (mitochondrial ... As a member of the FASTKD family, FASTKD2 localizes to the inner mitochondrial membrane to modulate their energy balance, ... FASTKD2 shares structural characteristics of the FASTKD family, including a ~50-amino acid N-terminal mitochondrial targeting ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... increase mitochondrial volume, and improve metabolic homeostasis in a rat model of T2DM. BGP-15 has now proceeded to Phase 2b ...
The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane ... Ye Y, Huang A, Huang C, Liu J, Wang B, Lin K, Chen Q, Zeng Y, Chen H, Tao X, Wei G, Wu Y (2013). "Comparative mitochondrial ...
This pore causes the mitochondria to swell and the outer mitochondrial membrane to rupture (Diamond & McCabe, 2007). With this ... This change likely causes the mitochondrial permeability transition (MPT), where the mitochondrial transmembrane potential ... how the death signal is relayed in the mitochondrial pathway of apoptosis". Structure. 19 (8): 1074-1083. doi:10.1016/j.str. ... in cardiomyocytes through its ability to inhibit Apaf1/caspase-9 apoptosome formation without preventing mitochondrial ...
... can lead to mitochondrial swelling and cell death through apoptosis or necrosis depending on the particular biological setting ... Mitochondrial permeability transition pore: an enigmatic gatekeeper (2012) NHS&T, Vol 1(3):47-51 Mitochondrial Permeability ... located in the mitochondrial outer membrane and cyclophilin-D in the mitochondrial matrix. Mice lacking the gene for ... The mitochondrial permeability transition pore (mPTP or MPTP; also referred to as PTP, mTP or MTP) is a protein that is formed ...
Upon the onset of a cellular energy crisis, mitochondrial function tends to decline. This is due to alternating inner membrane ... mitoKATP channels open and close to regulate both internal Ca2+ concentration and the degree of membrane swelling. This helps ... Inoue I, Nagase H, Kishi K, Higuti T (July 1991). "ATP-sensitive K+ channel in the mitochondrial inner membrane". Nature. 352 ( ... Xu M, Wang Y, Ayub A, Ashraf M (September 2001). "Mitochondrial K(ATP) channel activation reduces anoxic injury by restoring ...
The hydrogen flux disrupts the mitochondrial membrane potential and results in mitochondrial swelling, outer membrane rupture, ... These changes impair mitochondrial energy production and drive cardiac myocyte apoptosis. Intralipid (5mL/kg) provided five ... Myocardial damage with the resumption of blood flow after an ischemic event is termed "reperfusion injury". The mitochondrial ... Martel C, Huynh L, Garnier A, Ventura-Clapier R, Brenner C (2012). "Inhibition of the Mitochondrial Permeability Transition for ...
... including characteristic cytoplasmic vacuole formation and late mitochondrial swelling and clumping. The number and size of ... This swollen appearance can be attributed to intracellular ion imbalance and eventual osmotic lysis. Once ruptured, particles ... Mitochondrial staining reveals that rounded paraptotic cells with elevated levels of prohibitin appear to be undergoing ... Changes to structural, signal transduction, and mitochondrial proteins have all been observed during paraptosis. In cells ...
"Mitochondrial Swelling" by people in Harvard Catalyst Profiles by year, and whether "Mitochondrial Swelling" was a major or ... "Mitochondrial Swelling" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... Below are the most recent publications written about "Mitochondrial Swelling" by people in Profiles. ... Below are MeSH descriptors whose meaning is more general than "Mitochondrial Swelling". ...
This particular phytonutrient blend aims to support cellular function, as well as mitochondrial operation and growth. DeltaGOLD ... The Swell Score, Inc 1072 Casitas Pass Rd. Unit 134 Carpinteria, CA 93013 ...
The mitochondrial swelling that we observed in the present study could have been caused by oxidative stress. Blue light ... Electron Microscopy Revealed Mitochondrial Swelling after LTE to Blue Light. In the STE and control groups, although empty ... In our study, however, the only sign of ultrastructural damage to RGCs was mitochondrial swelling in the IPL, which was clearly ... but causes mitochondrial swelling in retinal ganglion cells (RGCs) and in the inner plexiform layer (IPL). ...
These can lead to mitochondrial swelling and depolarization. Excessive activity of the crinophagy form of autophagy in the ... Loss of function in these genes can lead to damaged mitochondrial accumulation and protein aggregates that can lead to cellular ... Esteves AR, Arduíno DM, Silva DF, Oliveira CR, Cardoso SM (January 2011). "Mitochondrial Dysfunction: The Road to Alpha- ...
... lower muscle mitochondrial oxidative capacity, more mitochondrial damage, and higher glycolytic enzyme expression. These ... This study demonstrates detrimental mitochondrial and muscular outcomes in the adult male rat exposed to postnatal hyperoxia. ... This study demonstrates detrimental mitochondrial and muscular outcomes in the adult male rat exposed to postnatal hyperoxia. ... more mitochondrial damage, and higher glycolytic enzyme expression. These differences were not present in female rats with the ...
This enzymatic injury results in swelling and vacuolization of mitochondrial and cell death. Within the mitochondria, thallium ...
Mitochondrial profiles showed enlarged swollen mitochondria in Pink1-/- AECIIs. Boxed regions are shown enlarged at right. ... Increased mitochondrial size can be associated with alterations in mitochondrial dynamics (32); moreover, mitochondrial fusion ... PINK1 is a key regulator of mitochondrial quality control, including mitochondrial respiration, mitochondrial dynamics, and ... Impaired mitochondrial function and fission/fusion dynamics in AECIIs with age. (A) Mitochondrial respiration parameters in ...
Moreover, viral proteins can bind to mitochondrial complexes, disrupting mitochondrial function and causing the immune cells to ... It is important to note that the roles of mitochondrial damage and inflammatory responses caused by SARS-CoV-2 in the ... Targeting mitochondrial function may provide promising new clinical approaches for long-COVID patients; however, further ... One of the underlying mechanisms of long COVID may be mitochondrial dysfunction. Severe acute respiratory syndrome coronavirus ...
The observation of a watery swelling of axons and of spheroids has been established using histochemical methods.10 However, ... followed by neurofilamentous accumulation and finally mitochondrial flocculent densities (MFDs). The last change is usually ... There was no correlation between the extent of axonal swelling or degeneration along the corticospinal tracts in superior areas ... A sequential pathogenesis was found, with clear axonal swelling, ... signs of axonal swelling and depletion of large myelinated ...
... of a 463-bp fragment of the mitochondrial 12S rDNA (8) amplified from the adult worm and the microfilariae revealed 97.9%-99.2 ... Recurrent Swelling and Microfilaremia Caused by Dirofilaria repens Infection after Travel to India On This Page ... Recurrent Swelling and Microfilaremia Caused by Dirofilaria repens Infection after Travel to India. Volume 27, Number 6-June ... Recurrent Swelling and Microfilaremia Caused by Dirofilaria repens Infection after Travel to India. Emerging Infectious ...
Protection of hepatocyte mitochondrial ultrastructure and function by strict blood glucose control with insulin in critically ... 6B,C). Similarly, the obvious changes such as swelling, distortion and vesicles formation were evident in kupffer cells due to ... This loss of normal cristae structure and dense mitochondria is indicative of derogative mitochondrial function103,104,105. ... Szeto, H. H. Cell-permeable, mitochondrial-targeted, peptide antioxidants. AAPS J. 8, E277-E283 (2006). ...
The kidneys had mitochondrial swelling with disorganization and disruption of the mitochondrial cristae. The vacuoles result ... The mitochondria displayed swelling, disorganization, disruption of the mitochondrial cristae, and electron-dense matrix. Some ... At necropsy, the liver was swollen and no other macroscopic lesions were observed. Histologically, centrolobular and midzonal ... Ultrastructurally, the myocardium had cardiomyocytes swelling with separation of myofibrils bundles and rupture and ...
Effects on the Ammonia-Induced Mitochondrial Permeability Transition andCell Swelling in Cultured Astrocytes (Peer Reviewed ... Cinnamon Polyphenols Attenuate Neuronal Death and Glial Swelling in Ischemic Injury (Proceedings) (10-Dec-07) ...
Electron microscopy of rat liver tissue intoxicated with d-galactosamine revealed the swelling and loss of mitochondrial ... Ear swelling caused by croton oil was also inhibited when sulfated polysaccharides from F. vesiculosus and L. variegata were ... Fucoidan treatment of HL-60 cells induced activation of caspases 8, 9, and 3, the cleavage of Bid, and altered mitochondrial ... 2009) studied the liver mitochondrial and microsomal fraction from rats to evaluate the antioxidative effect of oral gavaging ...
Herein, we address the complex crosstalk that involves mitochondrial biogenesis, mitochondrial destabilization accompanied by ... cells undergo mitochondrial destabilization due to calcium release from the endoplasmic reticulum, and die. ... A combination of ultrasound and curcumin increases the number of swollen mitochondria and impairs mitochondrial membrane ... In this context, mitochondrial biogenesis-taken as the increase of the mitochondrial network-is a complex response to various ...
Involvement of mitochondrial swelling in cytochrome c release from mitochondria treated with calcium and alloxan ...
Further electron microscopic studies revealed that quercetin attenuates aluminum-induced mitochondrial swelling, loss of ... Quercetin (a natural flavonoid) protects it from oxidative damage and has been shown to decrease mitochondrial damage in ... increased mitochondrial superoxide dismutase (MnSOD) activity). In addition, quercetin also prevents aluminum-induced ...
As a result, there is an increase in mitochondrial size (mitochondria swelling), breakage of mitochondria into smaller pieces, ... and Mitochondrial Dysfunction. Am J Hum Genet. 2017 Nov 2;101(5):833-843. doi: 10.1016/j.ajhg.2017.09.016. Citation on PubMed ... which likely decreases its ability to transport molecules across the mitochondrial inner membrane. ...
Quartz disrupted cellular lysosomes, increased mitochondrial pyknosis, caused swollen nuclei, nuclear vacuolation, and ...
Distilled Water and Foot Massager for cure edema and swelling. ... Lipoic acid is a mitochondrial nutrient that stimulates ... Ive had varicose veins and pain and swelling in my lower legs on and off for years. The swelling started when I was taking ... I promise it will take the swelling away. Please try it for a week and see results. My knee was swollen and the doctor ... I also get swelling in my left leg and anxiety that seems diet related, Im thinking from MSG, but I havent figured that out ...
The authors suggest that the neuroimaging mimics spinal cord infarction (SCI). However, the initial MRI shows a swollen, ... While we agree with the authors that consideration of underlying mitochondrial disorders in the right clinical scenario is ... 1 for presenting an interesting case of a longitudinally extensive spinal cord lesion in a patient with a mitochondrial ... who harbors a familial mitochondrial sequence variant, presented with inflammatory myelopathy. Association of LHON and multiple ...
The response of cardiomyocytes and the mitochondrial system of rats subjected to a four-month hypokinesia was studied. ... Some organelles were swollen. Mitochondria with unusual dark cristae and mitochondria with cristae in a "twisted" configuration ... The response of cardiomyocytes and the mitochondrial system of rats subjected to a four-month hypokinesia was studied. ... In electron microscopy, along with normal cardiomyocytes, cells with the swollen sarcoplasm and degrading myofibers were ...
Ultrastructure visible hepatocyte mitochondrial swelling and endosomal vesicle degeneration alleviate, hepatic tissue ... lung-fire is contained and pharyngeal swelling sore throat, and spleen-fire is contained and dispute tooth swells, and phlegm- ... de-black.Swelling of harnessing the river is full, tells vomiting, cold type of pain in abdomen, vomits and diarrhoea ... chest and abdomen swelling and pain, twinge, calentura coma, epilepsy is gone mad, jaundice dark coloured urine.Promoting QI ...
... mitochondrial swelling, mitochondrial permeability (mMPTP) opening and mitochondrial DNA (mtDNA) damage [4]. This experiment ... The occurrence of cell apoptosis is a complex process involving many factors, such as ROS production, mitochondrial ... ROS can cause membrane lipid peroxidation, protein cross-linking and degradation, DNA cleavage, and mitochondrial dysfunction ... Excessive ROS will increase mitochondrial membrane permeability, ...
The mitochondria in the BP group and P group showed almost no swelling or vacuole degeneration, with intact mitochondrial crest ... The mitochondria in the BP group and P group showed almost no swelling or vacuole degeneration, with intact mitochondrial crest ... The mitochondria in the BP and P groups showed nearly no swelling or vacuole degeneration, with intact mitochondrial crest ... partial mitochondrial necrosis and lysis (shown in white arrow), and disordered mitochondrial crest structure, which mostly ...
In this study, we observed the effects of propofol on multiple aspects of mitochondrial dysfunction by studying the mitochond … ... but few studies have focused on the direct effect of propofol on mitochondrial dysfunction. ... The calcium-induced mitochondrial swelling was quantified by measuring the decrease in light transmission at 540 nm with a ... Propofol prevented calcium-induced mitochondrial swelling in a concentration-dependent manner. It did not affect the ...

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