An active neurotoxic metabolite of 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE. The compound reduces dopamine levels, inhibits the biosynthesis of catecholamines, depletes cardiac norepinephrine and inactivates tyrosine hydroxylase. These and other toxic effects lead to cessation of oxidative phosphorylation, ATP depletion, and cell death. The compound, which is related to PARAQUAT, has also been used as an herbicide.
A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.
A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
A family of proteins involved in the transport of organic cations. They play an important role in the elimination of a variety of endogenous substances, xenobiotics, and their metabolites from the body.
An organic cation transporter found in kidney. It is localized to the basal lateral membrane and is likely to be involved in the renal secretion of organic cations.
Pyridinium compounds are organic salts formed when pyridine, a basic heterocyclic organic compound, reacts with acids, resulting in a positively charged nitrogen atom surrounded by aromatic rings.
Integral membrane proteins of the LIPID BILAYER of SECRETORY VESICLES that catalyze transport and storage of biogenic amine NEUROTRANSMITTERS such as ACETYLCHOLINE; SEROTONIN; MELATONIN; HISTAMINE; and CATECHOLAMINES. The transporters exchange vesicular protons for cytoplasmic neurotransmitters.
A botanical insecticide that is an inhibitor of mitochondrial electron transport.
Pesticides used to destroy unwanted vegetation, especially various types of weeds, grasses (POACEAE), and woody plants. Some plants develop HERBICIDE RESISTANCE.
A group of membrane transport proteins that transport biogenic amine derivatives of catechol across the PLASMA MEMBRANE. Catecholamine plasma membrane transporter proteins regulate neural transmission as well as catecholamine metabolism and recycling.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.
A class of sodium-independent nucleoside transporters that mediate the facilitative transport of NUCLEOSIDES.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
Neurons whose primary neurotransmitter is DOPAMINE.
A family of vesicular amine transporter proteins that catalyze the transport and storage of CATECHOLAMINES and indolamines into SECRETORY VESICLES.
A drug formerly used as an antipsychotic and treatment of various movement disorders. Tetrabenazine blocks neurotransmitter uptake into adrenergic storage vesicles and has been used as a high affinity label for the vesicle transport system.
The middle of the three primitive cerebral vesicles of the embryonic brain. Without further subdivision, midbrain develops into a short, constricted portion connecting the PONS and the DIENCEPHALON. Midbrain contains two major parts, the dorsal TECTUM MESENCEPHALI and the ventral TEGMENTUM MESENCEPHALI, housing components of auditory, visual, and other sensorimoter systems.
An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4.
Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of dopaminergic neurons. They remove DOPAMINE from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS and are the target of DOPAMINE UPTAKE INHIBITORS.
A deaminated metabolite of LEVODOPA.
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)
Membrane proteins whose primary function is to facilitate the transport of molecules across a biological membrane. Included in this broad category are proteins involved in active transport (BIOLOGICAL TRANSPORT, ACTIVE), facilitated transport and ION CHANNELS.
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
Positively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis.
The black substance in the ventral midbrain or the nucleus of cells containing the black substance. These cells produce DOPAMINE, an important neurotransmitter in regulation of the sensorimotor system and mood. The dark colored MELANIN is a by-product of dopamine synthesis.
An enzyme that catalyzes the conversion of L-tyrosine, tetrahydrobiopterin, and oxygen to 3,4-dihydroxy-L-phenylalanine, dihydrobiopterin, and water. EC 1.14.16.2.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation.
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.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
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)
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
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.

Poly(ADP-ribose) polymerase activation mediates 1-methyl-4-phenyl-1, 2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism. (1/255)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin that causes parkinsonism in humans and nonhuman animals, and its use has led to greater understanding of the pathogenesis of Parkinson's disease. However, its molecular targets have not been defined. We show that mice lacking the gene for poly(ADP-ribose) polymerase (PARP), which catalyzes the attachment of ADP ribose units from NAD to nuclear proteins after DNA damage, are dramatically spared from MPTP neurotoxicity. MPTP potently activates PARP exclusively in vulnerable dopamine containing neurons of the substantia nigra. MPTP elicits a novel pattern of poly(ADP-ribosyl)ation of nuclear proteins that completely depends on neuronally derived nitric oxide. Thus, NO, DNA damage, and PARP activation play a critical role in MPTP-induced parkinsonism and suggest that inhibitors of PARP may have protective benefit in the treatment of Parkinson's disease.  (+info)

Comparison of the pharmacological properties of cloned rat, human, and bovine norepinephrine transporters. (2/255)

The aims of this study were to characterize the recently cloned rat norepinephrine transporter (NET) in more detail and in particular to study possible species differences in its pharmacological properties compared with the human and bovine NETs. The study was carried out by measuring the uptake of [(3)H]norepinephrine in COS-7 cells expressing the NET after transient transfection with rat, human, or bovine NET cDNA. There were small but significant differences between the rat NET and the human or bovine NETs with respect to the affinities of sodium ions (greater for rat than for bovine) of the substrates norepinephrine, epinephrine, and 1-methyl-4-phenylpyridinium (greater for human than for rat), and of the inhibitor cocaine (greater for human and bovine than for rat), whereas the affinities of dopamine and of most inhibitors, including tricyclic antidepressants, showed no species differences. The fact that the affinities for some substrates, cocaine and sodium ions exhibited small but significant interspecies differences among the rat, human, and bovine NETs suggests that ligand recognition, the translocation process, and sodium ion dependence are influenced differentially by just a few amino acid exchanges in the primary sequences of the transporters. On the other hand, the lack of any major differences in the pharmacological properties of the rat, human, and bovine NETs in this study suggests that data obtained in previous studies on rat tissues and bovine cells can be extrapolated, in all except the most quantitative analyses, to the properties of the human NET.  (+info)

LLC-PK(1) cells stably expressing the human norepinephrine transporter: A functional model of carrier-mediated norepinephrine release in protracted myocardial ischemia. (3/255)

In myocardial ischemia, adrenergic terminals undergo ATP depletion, hypoxia, and intracellular pH reduction, causing the accumulation of axoplasmic norepinephrine (NE) and intracellular Na(+) [via the Na(+)-H(+) exchanger (NHE)]. This forces the reversal of the Na(+)- and Cl(-)-dependent NE transporter (NET), triggering massive carrier-mediated NE release and, thus, arrhythmias. We have now developed a cellular model of carrier-mediated NE release using an LLC-PK(1) cell line stably transfected with human NET cDNA (LLC-NET). LLC-NET cells transported [(3)H]NE and [(3)H]N-methyl-4-phenylpyridinium ([(3)H]MPP(+)) in an inward direction. This uptake was abolished by the NET inhibitors desipramine (100 nM) and mazindol (300 nM) and by extracellular Na(+) removal. Na(+)-gradient reversal induced an efflux of (3)H-substrate from preloaded LLC-NET cells. Desipramine and mazindol blocked this efflux. Because of its greater intracellular stability and higher sensitivity to Na(+)-gradient reversal, [(3)H]MPP(+) proved preferable to [(3)H]NE as an NET substrate; therefore, only [(3)H]MPP(+) was used for subsequent studies. The K(+)/H(+) ionophore nigericin (10 microM) evoked a large efflux of [(3)H]MPP(+). This efflux was potentiated by the Na(+),K(+)-ATPase inhibitor ouabain (100 microM), was sensitive to desipramine, and was blocked by the NHE inhibitor 5-(N-ethyl-N-isopropyl)-amiloride (EIPA; 10 microM). In contrast, EIPA failed to inhibit the [(3)H]MPP(+) efflux elicited by the Na(+) ionophore gramicidin (10 microM). Furthermore, [(3)H]MPP(+) efflux induced by the NHE-stimulant proprionate (25 mM) was negatively modulated by imidazoline receptor activation. Our findings suggest that LLC-NET cells are a sensitive model for studying transductional processes of carrier-mediated NE release associated with myocardial ischemia.  (+info)

Ion dependence of carrier-mediated release in dopamine or norepinephrine transporter-transfected cells questions the hypothesis of facilitated exchange diffusion. (4/255)

The mechanism of release mediated by the human dopamine and norepinephrine transporter (DAT and NET, respectively) was studied by a superfusion technique in human embryonic kidney 293 cells stably transfected with the respective transporter cDNA and loaded with the metabolically inert substrate [(3)H]1-methyl-4-phenylpyridinium. Release was induced by amphetamine, dopamine, and norepinephrine or by lowering the sodium or chloride concentration in the superfusion buffer (iso-osmotic replacement by lithium and isethionate, respectively). Efflux of [(3)H]1-methyl-4-phenylpyridinium was analyzed at 30-s time resolution. In both transporters, release induced by the substrates amphetamine, dopamine, and norepinephrine followed the same time course as release induced by the removal of chloride and was faster than that caused by the removal of sodium. In the presence of low sodium (DAT: 10 mM; NET: 5 mM) none of the substrates was able to induce release from either type of cell, but adding back sodium to control conditions promptly restored the releasing action. In the presence of low chloride (DAT: 3 mM; NET: 2 mM), however, amphetamine as well as the catecholamines stimulated release from both types of cell. In contrast with the ion dependence of release observed in superfusion experiments, uptake initial rates of substrates at concentrations used in release experiments were the same or even higher at low sodium than at low chloride. The results indicate a decisive role of extracellular sodium for carrier-mediated release unrelated to the sodium-dependent uptake of the releasing substrate, and suggest a release mechanism different from simple exchange diffusion considering only the amines as substrates.  (+info)

1-Methyl-4-phenyl-2,3-dihydropyridinium is transformed by ubiquinone to the selective nigrostriatal toxin 1-methyl-4-phenylpyridinium. (5/255)

We have studied the interaction of coenzyme Q with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its metabolites, 1-methyl-4-phenyl-2,3-dihydropyridinium (MPDP(+)) and 1-methyl-4-phenylpyridinium (MPP(+)), the real neurotoxin to cause Parkinson's disease. Incubation of MPTP or MPDP(+) with rat brain synaptosomes induced complete reduction of endogenous ubiquinone-9 and ubiquinone-10 to corresponding ubiquinols. The reduction occurred in a time- and MPTP/MPDP(+) concentration-dependent manner. The reduction of ubiquinone induced by MPDP(+) went much faster than that by MPTP. MPTP did not reduce liposome-trapped ubiquinone-10, but MPDP(+) did. The real toxin MPP(+) did not reduce ubiquinone in either of the systems. The reduction by MPTP but not MPDP(+) was completely prevented by pargyline, a type B monoamine oxidase (MAO-B) inhibitor, in the synaptosomes. The results indicate that involvement of MAO-B is critical for the reduction of ubiquinone by MPTP but that MPDP(+) is a reductant of ubiquinone per se. It is suggested that ubiquinone could be an electron acceptor from MPDP(+) and promote the conversion from MPDP(+) to MPP(+) in vivo, thus accelerating the neurotoxicity of MPTP.  (+info)

The D-loop structure of human mtDNA is destabilized directly by 1-methyl-4-phenylpyridinium ion (MPP+), a parkinsonism-causing toxin. (6/255)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine has been reported to cause parkinsonism via its neurotoxic form, 1-methyl-4-phenylpyridinium ion (MPP+), which inhibits complex I of the mitochondrial respiratory chain. Its parkinsonism-causing mechanisms attract a great deal of interest as a model of the disease. Recently, we reported that MPP+ strongly decreases the amount of mtDNA independent of the inhibition of complex I. Maintenance of a proper amount of mtDNA is essential for the normal function of mitochondria as exemplified in many mitochondrial diseases. The most characteristic feature in vertebral mtDNA replication is that H-strand synthesis proceeds displacing the parental H-strand as a long single strand. It forms the D-loop, a triplex replication intermediate composed of the parental L-strand, nascent H-strand and displaced H-strand. Here we show that MPP+ does not inhibit DNA synthesis by DNA polymerase gamma, but rather releases the nascent H-strands from mtDNA both in organello and in vitro. This indicates that MPP+ directly destabilizes the D-loop structure, thereby inhibiting replication. This study raises a new mechanism, i.e. destabilization of replication intermediates, for depletion of mtDNA.  (+info)

Kinetic and selectivity differences between rodent, rabbit, and human organic cation transporters (OCT1). (7/255)

Organic cation transporters play an important role in the absorption, distribution, and elimination of clinical agents, toxic substances, and endogenous compounds. In kidney preparations, significant differences in functional characteristics of organic cation transport between various species have been reported. However, the underlying molecular mechanisms responsible for these interspecies differences are not known. The goal of this study was to determine the kinetics and substrate selectivities of organic cation transporter (OCT1) homologs from mouse, rat, rabbit, and human that may contribute to interspecies differences in the renal and hepatic handling of organic cations. With a series of n-tetraalkylammonium (nTAA) compounds, a correlation between increasing alkyl chain length and affinity for the four OCT1 homologs was observed. However, the apparent affinity constants (K(i)) differed among the species homologs. For the mouse homolog mOCT1, apparent K(i) values ranged from 7 microM for tetrabutylammonium to 2000 microM for tetramethylammonium. In contrast, the human homolog hOCT1 exhibited weaker interactions with the nTAA compounds. Trans-stimulation studies and current measurements in voltage-clamped oocytes demonstrated that larger nTAA compounds were transported at greater rates in oocytes expressing hOCT1, whereas smaller nTAAs were transported at greater rates in oocytes expressing mOCT1 or rOCT1. The rabbit homolog rbOCT1 exhibited intermediate properties in its interactions with nTAAs compared with its rodent and human counterparts. This report demonstrates that the human OCT1 homolog has functional properties distinct from those of the rodent and rabbit OCT1 homologs. The study underscores potential difficulties in extrapolating data from preclinical studies in animal models to humans.  (+info)

Characterization of MPP+ secretion across human intestinal Caco-2 cell monolayers: role of P-glycoprotein and a novel Na(+)-dependent organic cation transport mechanism. (8/255)

1. In the kidney, a number of transport proteins involved in the secretion of permanently charged organic cations have recently been cloned. To evaluate the possible similarities between intestine and kidney in the handling of organic cations we investigated the transport of 1-methyl-4-phenylpyridinium (MPP+) across monolayers of intestinal Caco-2 cells. MPP+ is a prototypic substrate of the cloned organic cation transporters hOCT1 and hOCT2. 2. In Caco-2 cell monolayers, the basolateral to apical flux of MPP+ was significantly greater than the apical to basolateral flux, consistent with net secretion of MPP+. 3. Net secretion of MPP+ was abolished by addition of either 10 microM cyclosporin A or 100 microM verapamil to the apical membrane. In contrast, secretion of MPP+ was unaffected by addition of either TEA (2 mM) or decynium-22 (2 microM) to either apical or basolateral membranes. These results suggest that MPP+ secretion is mediated primarily by P-glycoprotein located at the apical membrane. We found no evidence of a role for hOCT1 or hOCT2 in the secretion of MPP+. 4. In addition to net secretion of MPP+, we found evidence of a Na(+)-dependent MPP+ uptake mechanism at the apical membrane of Caco-2 cells. 5. Na(+)-dependent MPP+ uptake was sensitive to inhibition by the organic cations; decynium-22 (2 microM), TEA (2 mM) and cimetidine (5 mM) but not by carnitine, guanidine or proline. 6. These results suggest that net secretion of MPP+ across the apical membrane of Caco-2 cells is a function of the relative contributions of MPP+ secretion mediated by P-glycoprotein and MPP+ absorption mediated by a novel Na(+)-dependent transport mechanism.  (+info)

1-Methyl-4-phenylpyridinium (MPP+) is a neurotoxic compound that is widely used in scientific research to study Parkinson's disease and other neurological disorders. MPP+ is an ionic form of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which is a lipophilic compound that can cross the blood-brain barrier and be converted to MPP+ by monoamine oxidase B (MAO-B) in glial cells.

MPP+ is taken up by dopaminergic neurons through the dopamine transporter (DAT), where it inhibits complex I of the electron transport chain, leading to mitochondrial dysfunction and energy depletion. This results in the death of dopaminergic neurons, which are the primary cells affected in Parkinson's disease.

MPP+ has been used as a model compound to study the mechanisms of neurodegeneration in Parkinson's disease and other neurological disorders, and it has also been used in the development of potential therapeutic strategies for these conditions.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a chemical compound that can cause permanent parkinsonian symptoms. It is not a medication or a treatment, but rather a toxin that can damage the dopamine-producing neurons in the brain, leading to symptoms similar to those seen in Parkinson's disease.

MPTP itself is not harmful, but it is metabolized in the body into a toxic compound called MPP+, which accumulates in and damages dopaminergic neurons. MPTP was discovered in the 1980s when a group of drug users in California developed parkinsonian symptoms after injecting a heroin-like substance contaminated with MPTP.

Since then, MPTP has been used as a research tool to study Parkinson's disease and develop new treatments. However, it is not used clinically and should be handled with caution due to its toxicity.

Methyl-phenyl-tetrahydropyridine (MPTP) poisoning is a rare neurological disorder that occurs due to the accidental exposure or intentional intake of MPTP, a chemical compound that can cause permanent parkinsonian symptoms. MPTP is metabolized into MPP+, which selectively destroys dopaminergic neurons in the substantia nigra pars compacta region of the brain, leading to Parkinson's disease-like features such as rigidity, bradykinesia, resting tremors, and postural instability. MPTP poisoning can be a model for understanding Parkinson's disease pathophysiology and developing potential treatments.

Organic cation transport proteins (OCTs) are a group of membrane transporters that facilitate the movement of organic cations across biological membranes. These transporters play an essential role in the absorption, distribution, and elimination of various endogenous and exogenous substances, including drugs and toxins.

There are four main types of OCTs, namely OCT1, OCT2, OCT3, and OCTN1 (also known as novel organic cation transporter 1 or OCT6). These proteins belong to the solute carrier (SLC) family, specifically SLC22A.

OCTs have a broad substrate specificity and can transport various organic cations, such as neurotransmitters (e.g., serotonin, dopamine, histamine), endogenous compounds (e.g., creatinine, choline), and drugs (e.g., metformin, quinidine, morphine). The transport process is typically sodium-independent and can occur in both directions, depending on the concentration gradient of the substrate.

OCTs are widely expressed in various tissues, including the liver, kidney, intestine, brain, heart, and placenta. Their expression patterns and functions vary among different OCT types, contributing to their diverse roles in physiology and pharmacology. Dysfunction of OCTs has been implicated in several diseases, such as drug toxicity, neurodegenerative disorders, and cancer.

In summary, organic cation transport proteins are membrane transporters that facilitate the movement of organic cations across biological membranes, playing crucial roles in the absorption, distribution, and elimination of various substances, including drugs and toxins.

Organic Cation Transporter 1 (OCT1) is a protein that belongs to the solute carrier family 22 (SLC22A). It is primarily expressed in the liver and plays an essential role in the uptake and elimination of various organic cations, including many drugs, from the systemic circulation into hepatocytes. OCT1 also transports some endogenous substances such as neurotransmitters and hormones. Mutations or variants in the OCT1 gene can affect drug response and disposition, making it an important factor to consider in personalized medicine.

Pyridinium compounds are organic salts that contain a positively charged pyridinium ion. Pyridinium is a type of cation that forms when pyridine, a basic heterocyclic organic compound, undergoes protonation. The nitrogen atom in the pyridine ring accepts a proton (H+) and becomes positively charged, forming the pyridinium ion.

Pyridinium compounds have the general structure of C5H5NH+X-, where X- is an anion or negatively charged ion. These compounds are often used in research and industry, including as catalysts, intermediates in chemical synthesis, and in pharmaceuticals. Some pyridinium compounds have been studied for their potential therapeutic uses, such as in the treatment of bacterial infections or cancer. However, it is important to note that some pyridinium compounds can also be toxic or reactive, so they must be handled with care.

Vesicular biogenic amine transport proteins (VMATs) are a type of transmembrane protein that play a crucial role in the packaging and transport of biogenic amines, such as serotonin, dopamine, norepinephrine, and histamine, into synaptic vesicles within neurons. These proteins are located on the membranes of neurosecretory vesicles and function to regulate the concentration of these neurotransmitters in the cytoplasm and maintain their storage in vesicles until they are released into the synapse during neurotransmission. VMATs are members of the solute carrier family 18 (SLC18) and consist of two isoforms, VMAT1 and VMAT2, which differ in their distribution and substrate specificity. VMAT1 is primarily found in non-neuronal cells, such as endocrine and neuroendocrine cells, while VMAT2 is predominantly expressed in neurons. Dysregulation of VMATs has been implicated in several neurological and psychiatric disorders, including Parkinson's disease, depression, and attention deficit hyperactivity disorder (ADHD).

Rotenone is not strictly a medical term, but it is a pesticide that is used in some medical situations. According to the National Pesticide Information Center, rotenone is a pesticide derived from the roots and stems of several plants, including Derris Eliptica, Lonchocarpus utilis, and Tephrosia vogelii. It is used as a pesticide to control insects, mites, and fish in both agricultural and residential settings.

In medical contexts, rotenone has been studied for its potential effects on human health, particularly in relation to Parkinson's disease. Some research suggests that exposure to rotenone may increase the risk of developing Parkinson's disease, although more studies are needed to confirm this link. Rotenone works by inhibiting the mitochondria in cells, which can lead to cell death and neurodegeneration.

It is important to note that rotenone is highly toxic and should be handled with care. It can cause skin and eye irritation, respiratory problems, and gastrointestinal symptoms if ingested or inhaled. Therefore, it is recommended to use personal protective equipment when handling rotenone and to follow all label instructions carefully.

Herbicides are a type of pesticide used to control or kill unwanted plants, also known as weeds. They work by interfering with the growth processes of the plant, such as inhibiting photosynthesis, disrupting cell division, or preventing the plant from producing certain essential proteins.

Herbicides can be classified based on their mode of action, chemical composition, and the timing of their application. Some herbicides are selective, meaning they target specific types of weeds while leaving crops unharmed, while others are non-selective and will kill any plant they come into contact with.

It's important to use herbicides responsibly and according to the manufacturer's instructions, as they can have negative impacts on the environment and human health if not used properly.

Catecholamine plasma membrane transport proteins, also known as neurotransmitter transporters or simply transporters, are a type of membrane protein responsible for the reuptake of catecholamines (such as dopamine, norepinephrine, and epinephrine) from the synaptic cleft back into the presynaptic neuron. These proteins play a crucial role in regulating neurotransmitter concentrations in the synapse and terminating neurotransmission. They are targets for various psychoactive drugs, including antidepressants, psychostimulants, and cocaine.

Neurotoxins are substances that are poisonous or destructive to nerve cells (neurons) and the nervous system. They can cause damage by destroying neurons, disrupting communication between neurons, or interfering with the normal functioning of the nervous system. Neurotoxins can be produced naturally by certain organisms, such as bacteria, plants, and animals, or they can be synthetic compounds created in a laboratory. Examples of neurotoxins include botulinum toxin (found in botulism), tetrodotoxin (found in pufferfish), and heavy metals like lead and mercury. Neurotoxic effects can range from mild symptoms such as headaches, muscle weakness, and tremors, to more severe symptoms such as paralysis, seizures, and cognitive impairment. Long-term exposure to neurotoxins can lead to chronic neurological conditions and other health problems.

Dopamine agents are medications that act on dopamine receptors in the brain. Dopamine is a neurotransmitter, a chemical messenger that transmits signals in the brain and other areas of the body. It plays important roles in many functions, including movement, motivation, emotion, and cognition.

Dopamine agents can be classified into several categories based on their mechanism of action:

1. Dopamine agonists: These medications bind to dopamine receptors and mimic the effects of dopamine. They are used to treat conditions such as Parkinson's disease, restless legs syndrome, and certain types of dopamine-responsive dystonia. Examples include pramipexole, ropinirole, and rotigotine.
2. Dopamine precursors: These medications provide the building blocks for the body to produce dopamine. Levodopa is a commonly used dopamine precursor that is converted to dopamine in the brain. It is often used in combination with carbidopa, which helps to prevent levodopa from being broken down before it reaches the brain.
3. Dopamine antagonists: These medications block the action of dopamine at its receptors. They are used to treat conditions such as schizophrenia and certain types of nausea and vomiting. Examples include haloperidol, risperidone, and metoclopramide.
4. Dopamine reuptake inhibitors: These medications increase the amount of dopamine available in the synapse (the space between two neurons) by preventing its reuptake into the presynaptic neuron. They are used to treat conditions such as attention deficit hyperactivity disorder (ADHD) and depression. Examples include bupropion and nomifensine.
5. Dopamine release inhibitors: These medications prevent the release of dopamine from presynaptic neurons. They are used to treat conditions such as Tourette's syndrome and certain types of chronic pain. Examples include tetrabenazine and deutetrabenazine.

It is important to note that dopamine agents can have significant side effects, including addiction, movement disorders, and psychiatric symptoms. Therefore, they should be used under the close supervision of a healthcare provider.

Equilibrative nucleoside transport proteins (ENTs) are a type of membrane transporter that regulate the bidirectional movement of nucleosides across the cell membrane. They facilitate the diffusion of nucleosides down their concentration gradient, hence the term "equilibrative." These transport proteins play a crucial role in maintaining intracellular nucleoside concentrations and ensuring proper nucleotide synthesis for various cellular processes, including DNA replication, repair, and gene expression. There are two major families of ENTs: the human equilibrative nucleoside transporters (hENTs) and the concentrative nucleoside transporters (CNTs). The hENT family includes four members (hENT1-4), while the CNT family consists of three members (CNT1-3). These transport proteins have been identified as potential targets for cancer therapy, as inhibiting their function can selectively sensitize tumor cells to nucleoside analog-based chemotherapies.

Dopamine is a type of neurotransmitter, which is a chemical messenger that transmits signals in the brain and nervous system. It plays several important roles in the body, including:

* Regulation of movement and coordination
* Modulation of mood and motivation
* Control of the reward and pleasure centers of the brain
* Regulation of muscle tone
* Involvement in memory and attention

Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area. It is released by neurons (nerve cells) and binds to specific receptors on other neurons, where it can either excite or inhibit their activity.

Abnormalities in dopamine signaling have been implicated in several neurological and psychiatric conditions, including Parkinson's disease, schizophrenia, and addiction.

Secondary Parkinson's disease, also known as acquired or symptomatic Parkinsonism, is a clinical syndrome characterized by the signs and symptoms of classic Parkinson's disease (tremor at rest, rigidity, bradykinesia, and postural instability) but caused by a known secondary cause. These causes can include various conditions such as brain injuries, infections, drugs or toxins, metabolic disorders, and vascular damage. The underlying pathology of secondary Parkinson's disease is different from that of classic Parkinson's disease, which is primarily due to the degeneration of dopamine-producing neurons in a specific area of the brain called the substantia nigra pars compacta.

Dopaminergic neurons are a type of specialized brain cells that produce, synthesize, and release the neurotransmitter dopamine. These neurons play crucial roles in various brain functions, including motivation, reward processing, motor control, and cognition. They are primarily located in several regions of the midbrain, such as the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA).

Dopaminergic neurons have a unique physiology characterized by their ability to generate slow, irregular electrical signals called pacemaker activity. This distinctive firing pattern allows dopamine to be released in a controlled manner, which is essential for proper brain function.

The degeneration and loss of dopaminergic neurons in the SNc are associated with Parkinson's disease, a neurodegenerative disorder characterized by motor impairments such as tremors, rigidity, and bradykinesia (slowness of movement). The reduction in dopamine levels caused by this degeneration leads to an imbalance in the brain's neural circuitry, resulting in the characteristic symptoms of Parkinson's disease.

Vesicular Monoamine Transporter Proteins (VMATs) are a type of transmembrane protein that play a crucial role in the packaging and transport of monoamines, such as serotonin, dopamine, and norepinephrine, into synaptic vesicles within neurons. There are two main isoforms of VMATs, VMAT1 and VMAT2, which differ in their distribution and function.

VMAT1 (also known as SLC18A1) is primarily found in neuroendocrine cells and is responsible for transporting monoamines into large dense-core vesicles. VMAT2 (also known as SLC18A2), on the other hand, is mainly expressed in presynaptic neurons and is involved in the transport of monoamines into small synaptic vesicles.

Both VMAT1 and VMAT2 are integral membrane proteins that utilize a proton gradient to drive the uptake of monoamines against their concentration gradient, allowing for their storage and subsequent release during neurotransmission. Dysregulation of VMAT function has been implicated in several neurological and psychiatric disorders, including Parkinson's disease and depression.

Tetrabenazine is a prescription medication used to treat conditions associated with abnormal involuntary movements, such as chorea in Huntington's disease. It works by depleting the neurotransmitter dopamine in the brain, which helps to reduce the severity and frequency of these movements.

Here is the medical definition:

Tetrabenazine is a selective monoamine-depleting agent, with preferential uptake by dopamine neurons. It is used in the treatment of chorea associated with Huntington's disease. Tetrabenazine inhibits vesicular monoamine transporter 2 (VMAT2), leading to depletion of presynaptic dopamine and subsequent reduction in post-synaptic dopamine receptor activation. This mechanism of action is thought to underlie its therapeutic effect in reducing chorea severity and frequency.

(Definitions provided by Stedman's Medical Dictionary and American Society of Health-System Pharmacists)

The mesencephalon, also known as the midbrain, is the middle portion of the brainstem that connects the hindbrain (rhombencephalon) and the forebrain (prosencephalon). It plays a crucial role in several important functions including motor control, vision, hearing, and the regulation of consciousness and sleep-wake cycles. The mesencephalon contains several important structures such as the cerebral aqueduct, tectum, tegmentum, cerebral peduncles, and several cranial nerve nuclei (III and IV).

Monoamine oxidase (MAO) is an enzyme found on the outer membrane of mitochondria in cells throughout the body, but primarily in the gastrointestinal tract, liver, and central nervous system. It plays a crucial role in the metabolism of neurotransmitters and dietary amines by catalyzing the oxidative deamination of monoamines. This enzyme exists in two forms: MAO-A and MAO-B, each with distinct substrate preferences and tissue distributions.

MAO-A preferentially metabolizes serotonin, norepinephrine, and dopamine, while MAO-B is mainly responsible for breaking down phenethylamines and benzylamines, as well as dopamine in some cases. Inhibition of these enzymes can lead to increased neurotransmitter levels in the synaptic cleft, which has implications for various psychiatric and neurological conditions, such as depression and Parkinson's disease. However, MAO inhibitors must be used with caution due to their potential to cause serious adverse effects, including hypertensive crises, when combined with certain foods or medications containing dietary amines or sympathomimetic agents.

Dopamine plasma membrane transport proteins, also known as dopamine transporters (DAT), are a type of protein found in the cell membrane that play a crucial role in the regulation of dopamine neurotransmission. They are responsible for the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron, thereby terminating the signal transduction of dopamine and regulating the amount of dopamine available for further release.

Dopamine transporters belong to the family of sodium-dependent neurotransmitter transporters and are encoded by the SLC6A3 gene in humans. Abnormalities in dopamine transporter function have been implicated in several neurological and psychiatric disorders, including Parkinson's disease, attention deficit hyperactivity disorder (ADHD), and substance use disorders.

In summary, dopamine plasma membrane transport proteins are essential for the regulation of dopamine neurotransmission by mediating the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron.

3,4-Dihydroxyphenylacetic Acid (3,4-DOPAC) is a major metabolite of dopamine, which is a neurotransmitter in the brain. Dopamine is metabolized by the enzyme monoamine oxidase to form dihydroxyphenylacetaldehyde, which is then further metabolized to 3,4-DOPAC by the enzyme aldehyde dehydrogenase.

3,4-DOPAC is found in the urine and can be used as a marker for dopamine turnover in the brain. Changes in the levels of 3,4-DOPAC have been associated with various neurological disorders such as Parkinson's disease and schizophrenia. Additionally, 3,4-DOPAC has been shown to have antioxidant properties and may play a role in protecting against oxidative stress in the brain.

Parkinson's disease is a progressive neurodegenerative disorder that affects movement. It is characterized by the death of dopamine-producing cells in the brain, specifically in an area called the substantia nigra. The loss of these cells leads to a decrease in dopamine levels, which results in the motor symptoms associated with Parkinson's disease. These symptoms can include tremors at rest, stiffness or rigidity of the limbs and trunk, bradykinesia (slowness of movement), and postural instability (impaired balance and coordination). In addition to these motor symptoms, non-motor symptoms such as cognitive impairment, depression, anxiety, and sleep disturbances are also common in people with Parkinson's disease. The exact cause of Parkinson's disease is unknown, but it is thought to be a combination of genetic and environmental factors. There is currently no cure for Parkinson's disease, but medications and therapies can help manage the symptoms and improve quality of life.

Membrane transport proteins are specialized biological molecules, specifically integral membrane proteins, that facilitate the movement of various substances across the lipid bilayer of cell membranes. They are responsible for the selective and regulated transport of ions, sugars, amino acids, nucleotides, and other molecules into and out of cells, as well as within different cellular compartments. These proteins can be categorized into two main types: channels and carriers (or pumps). Channels provide a passive transport mechanism, allowing ions or small molecules to move down their electrochemical gradient, while carriers actively transport substances against their concentration gradient, requiring energy usually in the form of ATP. Membrane transport proteins play a crucial role in maintaining cell homeostasis, signaling processes, and many other physiological functions.

Parkinsonian disorders are a group of neurological conditions characterized by motor symptoms such as bradykinesia (slowness of movement), rigidity, resting tremor, and postural instability. These symptoms are caused by the degeneration of dopamine-producing neurons in the brain, particularly in the substantia nigra pars compacta.

The most common Parkinsonian disorder is Parkinson's disease (PD), which is a progressive neurodegenerative disorder. However, there are also several other secondary Parkinsonian disorders, including:

1. Drug-induced parkinsonism: This is caused by the use of certain medications, such as antipsychotics and metoclopramide.
2. Vascular parkinsonism: This is caused by small vessel disease in the brain, which can lead to similar symptoms as PD.
3. Dementia with Lewy bodies (DLB): This is a type of dementia that shares some features with PD, such as the presence of alpha-synuclein protein clumps called Lewy bodies.
4. Progressive supranuclear palsy (PSP): This is a rare brain disorder that affects movement, gait, and eye movements.
5. Multiple system atrophy (MSA): This is a progressive neurodegenerative disorder that affects multiple systems in the body, including the autonomic nervous system, motor system, and cerebellum.
6. Corticobasal degeneration (CBD): This is a rare neurological disorder that affects both movement and cognition.

It's important to note that while these disorders share some symptoms with PD, they have different underlying causes and may require different treatments.

A cation is a type of ion, which is a charged particle, that has a positive charge. In chemistry and biology, cations are formed when a neutral atom loses one or more electrons during chemical reactions. The removal of electrons results in the atom having more protons than electrons, giving it a net positive charge.

Cations are important in many biological processes, including nerve impulse transmission, muscle contraction, and enzyme function. For example, sodium (Na+), potassium (K+), calcium (Ca2+), and magnesium (Mg2+) are all essential cations that play critical roles in various physiological functions.

In medical contexts, cations can also be relevant in the diagnosis and treatment of various conditions. For instance, abnormal levels of certain cations, such as potassium or calcium, can indicate specific diseases or disorders. Additionally, medications used to treat various conditions may work by altering cation concentrations or activity within the body.

The Substantia Nigra is a region in the midbrain that plays a crucial role in movement control and reward processing. It is composed of two parts: the pars compacta and the pars reticulata. The pars compacta contains dopamine-producing neurons, whose loss or degeneration is associated with Parkinson's disease, leading to motor symptoms such as tremors, rigidity, and bradykinesia.

In summary, Substantia Nigra is a brain structure that contains dopamine-producing cells and is involved in movement control and reward processing. Its dysfunction or degeneration can lead to neurological disorders like Parkinson's disease.

Tyrosine 3-Monooxygenase (also known as Tyrosinase or Tyrosine hydroxylase) is an enzyme that plays a crucial role in the synthesis of catecholamines, which are neurotransmitters and hormones in the body. This enzyme catalyzes the conversion of the amino acid L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by adding a hydroxyl group to the 3rd carbon atom of the tyrosine molecule.

The reaction is as follows:

L-Tyrosine + O2 + pterin (co-factor) -> L-DOPA + pterin (oxidized) + H2O

This enzyme requires molecular oxygen and a co-factor such as tetrahydrobiopterin to carry out the reaction. Tyrosine 3-Monooxygenase is found in various tissues, including the brain and adrenal glands, where it helps regulate the production of catecholamines like dopamine, norepinephrine, and epinephrine. Dysregulation of this enzyme has been implicated in several neurological disorders, such as Parkinson's disease.

Neuroprotective agents are substances that protect neurons or nerve cells from damage, degeneration, or death caused by various factors such as trauma, inflammation, oxidative stress, or excitotoxicity. These agents work through different mechanisms, including reducing the production of free radicals, inhibiting the release of glutamate (a neurotransmitter that can cause cell damage in high concentrations), promoting the growth and survival of neurons, and preventing apoptosis (programmed cell death). Neuroprotective agents have been studied for their potential to treat various neurological disorders, including stroke, traumatic brain injury, Parkinson's disease, Alzheimer's disease, and multiple sclerosis. However, more research is needed to fully understand their mechanisms of action and to develop effective therapies.

Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.

PC12 cells are a type of rat pheochromocytoma cell line, which are commonly used in scientific research. Pheochromocytomas are tumors that develop from the chromaffin cells of the adrenal gland, and PC12 cells are a subtype of these cells.

PC12 cells have several characteristics that make them useful for research purposes. They can be grown in culture and can be differentiated into a neuron-like phenotype when treated with nerve growth factor (NGF). This makes them a popular choice for studies involving neuroscience, neurotoxicity, and neurodegenerative disorders.

PC12 cells are also known to express various neurotransmitter receptors, ion channels, and other proteins that are relevant to neuronal function, making them useful for studying the mechanisms of drug action and toxicity. Additionally, PC12 cells can be used to study the regulation of cell growth and differentiation, as well as the molecular basis of cancer.

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.

The corpus striatum is a part of the brain that plays a crucial role in movement, learning, and cognition. It consists of two structures called the caudate nucleus and the putamen, which are surrounded by the external and internal segments of the globus pallidus. Together, these structures form the basal ganglia, a group of interconnected neurons that help regulate voluntary movement.

The corpus striatum receives input from various parts of the brain, including the cerebral cortex, thalamus, and other brainstem nuclei. It processes this information and sends output to the globus pallidus and substantia nigra, which then project to the thalamus and back to the cerebral cortex. This feedback loop helps coordinate and fine-tune movements, allowing for smooth and coordinated actions.

Damage to the corpus striatum can result in movement disorders such as Parkinson's disease, Huntington's disease, and dystonia. These conditions are characterized by abnormal involuntary movements, muscle stiffness, and difficulty initiating or controlling voluntary movements.

Nerve degeneration, also known as neurodegeneration, is the progressive loss of structure and function of neurons, which can lead to cognitive decline, motor impairment, and various other symptoms. This process occurs due to a variety of factors, including genetics, environmental influences, and aging. It is a key feature in several neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. The degeneration can affect any part of the nervous system, leading to different symptoms depending on the location and extent of the damage.

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.

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.

NG-Nitroarginine Methyl Ester (L-NAME) is not a medication, but rather a research chemical used in scientific studies. It is an inhibitor of nitric oxide synthase, an enzyme that synthesizes nitric oxide, a molecule involved in the relaxation of blood vessels.

Therefore, L-NAME is often used in experiments to investigate the role of nitric oxide in various physiological and pathophysiological processes. It is important to note that the use of L-NAME in humans is not approved for therapeutic purposes due to its potential side effects, which can include hypertension, decreased renal function, and decreased cerebral blood flow.

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.

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Generation of reactive oxygen species in 1-methyl-4-phenylpyridinium (MPP+) treated dopaminergic neurons occurs as an NADPH ... "Generation of reactive oxygen species in 1-methyl-4-phenylpyridinium (MPP+) treated dopaminergic neurons occurs as an NADPH ... Keywords: 6-hydroxydopamine, angiotensin II type 1 receptor, adenosine 5-triphosphate, cell determinant, cyclohexamide, ... 1-methyl-4-phenylpyridinium, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, nicotinamide adenine dinucleotide phosphate, non- ...
Y1 - 1988/1/1. N2 - It is widely believed that the nigrostriatal toxicity of MPTP is due to its oxidation by brain monoamine ... 1, 01.01.1988, p. 17-23.. Research output: Contribution to journal › Review article › peer-review ... Singer, T. P., Ramsay, R. R., McKeown, K., Trevor, A., & Castagnoli, N. E. (1988). Mechanism of the neurotoxicity of 1-methyl-4 ... phenylpyridinium (MPP)+, the toxic bioactivation product of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Toxicology, 49 ...
1-Methyl-4-phenylpyridinium ion (MPP(+)), an active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, induces cell ... Proteasome-dependent degradation of cyclin D1 in 1-methyl-4-phenylpyridinium ion (MPP+)-induced cell cycle arrest.. Bai, Jie; ... In this study, we found that MPP(+) suppressed the proliferation with accumulation in G(1) phase without inducing cell death in ... 1-Metil-4-fenilpiridínio/metabolismo Ciclina D1/metabolismo Cisteína Endopeptidases/metabolismo Complexos Multienzimáticos/ ...
While nesiritide was projected to generate $1 billion in sales in 2006, these studies triggered controversy that eventually led ... Supplement/1.full.pdf Sackner-Bernstein, JD; Skopicki, HA; Aaronson, KD (Mar 2005). "Risk of worsening renal function with ... "Changes in neuronal dopamine homeostasis following 1-methyl-4-phenylpyridinium (MPP+) exposure". Journal of Biological ...
In this study we investigated the effects of modulating intracellular urate concentration on 1-methyl-4-phenyl-pyridinium (MPP+ ... 4B, F-I), corresponding to a complete blockade of MPP+ toxicity. Urate on its own did not affect TH-IR cell number (Fig. 4C). ... 1A-D) were treated for 24 hours with increasing concentrations of MPP+. Toxicant treatment reduced the number of dopaminergic ... Figure 4. Urates protective effect on dopaminergic neurons in mixed cultures.. A) MPP+ concentration-dependent effect on ...
Interleukin-1 beta (IL-1β) also known as catabolin, is a cytokine protein that in humans is encoded by the IL-1β gene and is ... 1] have examined the effect of ibuprofen on dopaminergic neuron injury in the mouse model of PD. This study showed that the ... Antioxid Redox Signal 1: 5-27.. *Mao P, Manczak M, Shirendeb UP, Reddy PH (2013) MitoQ, a mitochondria-targeted antioxidant, ... IL-1β was high after injection of LPS. These data suggest that mild inflammation caused by LPS increased the vulnerability of ...
Aquaporin-4 (AQP4) is critically involved in brain water and volume homeostasis and has been implicated in a wide range of ... 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). Here, we investigated the effect of Aqp4 deletion on microglial activation in ... mice subjected to unilateral intrastriatal injection of 1-methyl-4-phenylpyridinium (MPP+, the toxic metabolite of MPTP). Our ...
4]. Xue-mei Liu, Qi-fu Huang, Yun-ling Zhang, Jin-li Lou, Hong-sheng Liu, Hong Zheng. Effects of Tribulus terrestris L. ... Figure 4. Effects of PNSs on bax protein expression in BMSCs A: Control group; B: H2O2 group; C: PNSs (0.1 g/L) group. a: Bax ... 4]. Asada T, Kushida T, Umeda M, Oe K, Matsuya H, Wada T, Sasai K, Ikehara S, Iida H . Prevention of corticosteroid-induced ... doi: 10.1002/ptr.v23:1 [10]. Wang CZ, McEntee E, Wicks S, Wu JA, Yuan CS. , Phytochemical and analytical studies of Panax ...
Knockout of miR-29b2/c inhibited the expression of inflammatory factors in 1-methyl-4-phenylpyridinium (MPP+)-treated primary ... Here we show that the serum levels of miR-29s in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice exhibited ... Xiaochen Bai1,2, *, , Xiaoshuang Zhang1, *, , Rong Fang1, *, , Jinghui Wang1, *, , Yuanyuan Ma1, , Zhaolin Liu1, , Hongtian ... Qing Li1, , Jingyu Ge1, , Mei Yu1, , Jian Fei3,4, , Ruilin Sun4, , Fang Huang1, , * 1 Department of Translational Neuroscience ...
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SK-N-SH cells were exposed to 1-methyl-4-phenylpyridinium (MPP+) to mimic PD model in vitro. The levels of HOTAIR, miR-874-5p ...
2023;(4):59-67 Analysis of GBA muta-tions in patients with Parkinsons disease in the Krasnoyarsk region. S.S. Korsakov Journal ... 2023;(4):103-108 Orthostatic hypo-tension in patients with Parkinsons disease. S.S. Korsakov Journal of Neurology and ... American journal of translational research. 2016;8(1):12-27. * Donadio V, Incensi A, Rizzo G, et al. The effect of curcumin on ... Archives of Applied Science Research. 2009;1(2):86-108. * Pervaiz T, Jiu S, Faghihi F, et al. Naturally occurring anthocyanin, ...
In situ hybridization, coupled with immunoreactivity for the marker ionized calcium binding adaptor molecule 1 (IBA1), revealed ... 4-HNE). Following light damage, retinas pretreated with 670-nm light had reduced immunoreactivity for the oxidative damage ... maker 4-HNE in the ONL and outer segments, compared to controls. In conjunction, there was significant reduction in retinal ... Figure 4. In situ hybridization for C3 mRNA in the retina following 670-nm light and bright continuous white light (BCL) ...
This is the first non-toxic means of preventing MPTP and MPP+ (cation 1-methyl-4-Mitochondrial DNA has protection systems, ... This is the first non-toxic means of preventing MPTP and MPP+ (cation 1-methyl-4-phenylpyridinium) induced biochemical damage. ... 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), the diabetogenic toxin streptozotocin and endogenous compounds such as dopamine ... 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), the diabetogenic toxin streptozotocin and endogenous compounds such as dopamine ...
... affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not ... 3, 4] Exposure to the weed killer paraquat or to the fungicides maneb or mancozeb is particularly toxic, increasing the risk ... 3, 4] Increased PD risk was also associated with proxy conditions of exposure to organic pollutants, such as farming, well- ... MPTP crosses the blood-brain barrier and is oxidized to 1-methyl-4-phenylpyridinium (MPP+) by monoamine oxidase (MAO)-B. [6] ...
Contactin-1/F3 regulates neuronal migration and morphogenesis throughmodulating RhoA activity by Chen YA, Lu IL, et al. ... Inhibitory effects of curcumin and cyclocurcumin in 1-methyl-4-phenylpyridinium (MPP+) induced neurotoxicity in differentiated ...
The toxicity caused by cell exposure to 1-methyl-4-phenylpyridinium ion (MPP+) is a useful model in the study of Parkinsons ...
The toxicity caused by cell exposure to 1-methyl-4-phenylpyridinium ion (MPP+) is a useful model in the study of Parkinsons ... The toxicity caused by cell exposure to 1-methyl-4-phenylpyridinium ion (MPP+) is a useful model in the study of Parkinsons ...
Physique 1 (a) The OD value of PD model cells was gradually increased after treatment with CM-CUR, CM-MSC, and CUR at 24?h and ... Figure 1(c)). Then we detected the apoptosis related factors bcl-2 and caspase-3 using RT-PCR. The bcl-2 mRNA manifestation was ... Figure 1(b)). Compared with the control group, the model group was very seriously injured (< 0.01). Among the three groups, the ... on PC12 cells induced by 1-methyl-4-phenylpyridinium ion (MPP+), a cell model of Parkinsons disease (PD). from the human ...
This review focuses on the clinical application of iPSCs in FILD and describes 1) an overview of iPSCs and FILD, 2) FILD ... By modelling Parkinsons disease-related drug toxicity using 1-Methyl-4-phenylpyridinium (MPP+), we showed a preferential ... treatment with iPSCs, 3) FILD treatment with iPSC-derived cells, 4) problems with the use of iPSCs and 5) possibilities for ...
Methods: We evaluated whether elevating serum UA levels in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced ... Methods: We evaluated whether elevating serum UA levels in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced ... Methods: We evaluated whether elevating serum UA levels in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced ... Methods: We evaluated whether elevating serum UA levels in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced ...
2-Oxoisovalerate Dehydrogenase (Lipoamide) use 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) 2-PAM Compounds use ... 1,2-Benzoquinones use Benzoquinones 1,2-Cyclic-Inositol-Phosphate Phosphodiesterase use Glycerophosphoinositol ... 1-Acylglycerol-3-Phosphate O-Acyltransferase 1-Acylglycerophosphocholine Acyltransferase use 1-Acylglycerophosphocholine O- ... 3-Phosphoshikimate 1-Carboxyvinyltransferase 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl) ...
2-Oxoisovalerate Dehydrogenase (Lipoamide) use 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) 2-PAM Compounds use ... 4 Hydroxyphenylpyruvate Dioxygenase Deficiency Disease use Tyrosinemias 4-Nitrophenol-2-Hydroxylase use Cytochrome P-450 CYP2E1 ... 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer ... 2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10-dimethoxy- ...
2-Oxoisovalerate Dehydrogenase (Lipoamide) use 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) 2-PAM Compounds use ... 1,2-Benzoquinones use Benzoquinones 1,2-Cyclic-Inositol-Phosphate Phosphodiesterase use Glycerophosphoinositol ... 1-Acylglycerol-3-Phosphate O-Acyltransferase 1-Acylglycerophosphocholine Acyltransferase use 1-Acylglycerophosphocholine O- ... 3-Phosphoshikimate 1-Carboxyvinyltransferase 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl) ...
Justyna Stefanowicz-Hajduk1, Magdalena Gucwa1, Adam Hajduk2, J Renata Ochocka1. 1Department of Biology and Pharmaceutical ... Naringenin protects against 1-methyl-4-phenylpyridinium- induced neuroinflammation and resulting reactive oxygen species ... 4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell death, the generation of reactive oxygen species ( ...
"2-methyl-5-isopropyl-p-benzoquinone" EXACT [] synonym: "2-methyl-5-propan-2-ylcyclohexa-2,5-diene-1,4-dione" EXACT [] synonym ... water with NG-Nitroarginine Methyl Ester def: "Drinking water with a specified concentration of NG-Nitroarginine Methyl Ester ( ... a methyl group (a one-carbon alkyl substituent with chemical formula -CH3), a nitroso group (R-N=O) and a urea group (two -NH2 ... 2-methyl-1-oxo-1-(propan-2-yloxy)propan-2-yl]oxy group at position 1 on the phenyl ring. Used as a lipid -lowering drug." [ ...
2-methyl-1-(methylphenylamino)-4,6-di(p-tolyl)pyridinium tetrafluoroborate 263-965-9 63149-30-4 Expert judgement ... 2-methyl-4,6-di(p-tolyl)pyrylium tetrafluoroborate 265-917-2 65776-60-5 Expert judgement ... 2-Propenoic acid, 2-methyl-, polymer with ethyl 2-propenoate and 2-propenoic acid, borated, sodium salt - 67784-76-3 Expert ... Quaternary ammonium compounds, diethyl methyl (gamma-omega-perfluoro-C8-14-β-alkenyl), tetraphenyl borates - 145477-02-7 Expert ...
... induces ion methyl methylisoquinolines monoamine mpp mptp oxidase oxidation oxidized parkinsonism pc12 phenyl phenylpyridinium ... induces ion methyl methylisoquinolines monoamine mpp mptp oxidase oxidation oxidized parkinsonism pc12 phenyl phenylpyridinium ... ERVFRD-1 ESRRG ETFB ETHE1 ETNPPL ETS1 ETV3 ETV4 ETV5 EVI2A EXOC3 EXOC6 EXOSC1 EXOSC3 EXOSC7 F12 FAAH2 FAM114A2 FAM122A FAM126B ...
  • Generation of reactive oxygen species in 1-methyl-4-phenylpyridinium (MPP+) treated dopaminergic neurons occurs as an NADPH oxidase-dependent two-wave cascade. (tufts.edu)
  • In this study we investigated the effects of modulating intracellular urate concentration on 1-methyl-4-phenyl-pyridinium (MPP + )-induced degeneration of dopaminergic neurons in cultures of mouse ventral mesencephalon prepared to contain low (neuron-enriched cultures) or high (neuron-glial cultures) percentage of astrocytes. (plos.org)
  • Neuroinflammation is a hallmark of Parkinson's disease (PD), and we have previously shown that astrocytes in substantia nigra (SN) are enriched in AQP4 relative to cortical astrocytes, and that their complement of AQP4 is further increased following treatment with the parkinsonogenic toxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). (stami.no)
  • Here, we investigated the effect of Aqp4 deletion on microglial activation in mice subjected to unilateral intrastriatal injection of 1-methyl-4-phenylpyridinium (MPP+, the toxic metabolite of MPTP). (stami.no)
  • Here we show that the serum levels of miR-29s in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice exhibited dynamic changes. (aging-us.com)
  • Mitochondrial DNA has protection systems, which are less evolved than those of nuclear DNA, which protect it against environmental toxins such as the Parkinson inducing agent, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), the diabetogenic toxin streptozotocin and endogenous compounds such as dopamine. (vernemendel.com)
  • Methods: We evaluated whether elevating serum UA levels in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonian mouse model would restore neurogenesis in the subventricular zone (SVZ). (elsevierpure.com)
  • The purpose of this study is to evaluate the therapeutic effects of human umbilical cord-derived mesenchymal stem cells (hUC-MSC) activated by curcumin (CUR) on PC12 cells induced by 1-methyl-4-phenylpyridinium ion (MPP+), a cell model of Parkinson's disease (PD). (careersfromscience.org)
  • 1985. Spin-trapping of methyl radical in the oxidative metabolism of 1,2-dimethylhydrazine. (cdc.gov)
  • Photoreceptor death was also assessed using outer nuclear layer (ONL) thickness measurements, and oxidative stress using immunohistochemistry for 4-hydroxynonenal (4-HNE). (springer.com)
  • Following light damage, retinas pretreated with 670-nm light had reduced immunoreactivity for the oxidative damage maker 4-HNE in the ONL and outer segments, compared to controls. (springer.com)
  • The toxicity caused by cell exposure to 1-methyl-4-phenylpyridinium ion (MPP+) is a useful model in the study of Parkinson's disease (PD). (anid.cl)
  • This preliminary report describes the use of a series of compounds having the heterocyclic scaffold linked to various amino acids to probe the S' subsites of human leukocyte elastase (HLE), proteinase 3 (PR 3), and cathepsin G (Cat G). For comparative purposes, a series of compounds derived from a related scaffold, isothiazolidin-3-one 1,1 dioxide (II), was also generated. (wichita.edu)
  • Proteasome-dependent degradation of cyclin D1 in 1-methyl-4-phenylpyridinium ion (MPP+)-induced cell cycle arrest. (bvsalud.org)
  • 1-Methyl-4-phenylpyridinium ion (MPP(+)), an active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine , induces cell death and inhibition of cell proliferation in various cells . (bvsalud.org)
  • In this study, we found that MPP(+) suppressed the proliferation with accumulation in G(1) phase without inducing cell death in p53-deficient MG63 osteosarcoma cells . (bvsalud.org)
  • 1988. Species-specific response to the rodent carcinogens 1,2-dimethylhydrazine and 1,2-dibromo-3-chloropropane in rodent bone-marrow micronucleus assays. (cdc.gov)
  • Physique 1 (a) The OD value of PD model cells was gradually increased after treatment with CM-CUR, CM-MSC, and CUR at 24?h and 48?h ($ 957485-64-2 IC50 (careersfromscience.org)
  • Funding came from the United States National Institutes of Health http://www.nih.gov/(R21NS058324 and K24NS060991), US Department of Defense http://www.defense.gov/(W81XWH-11-1-0150), and the American Parkinson Disease Association http://www.apdaparkinson.org/userND/index.asp . (plos.org)
  • Knockout of miR-29b2/c inhibited the expression of inflammatory factors in 1-methyl-4-phenylpyridinium (MPP + )-treated primary cultures of mixed glia, primary astrocytes, or LPS-treated primary microglia. (aging-us.com)
  • The inhibitors were readily obtained by attaching various heterocyclic thiols, as well as a basic primary specificity residue P(1), to the 1,2,5-thiadiazolidin-3-one 1,1-dioxide scaffold. (wichita.edu)
  • PD is the second most common neurodegenerative disease [ 1 ], only superseded by Alzheimer's disease. (omicsonline.org)
  • Parkinson disease (PD) is one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not halted, by treatment. (medscape.com)
  • Parkinson disease is recognized as one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years. (medscape.com)
  • 1991. Control of 1,2-dimethylhydrazine-induced crypt hyperplasia by naturalkiller cells and its relevance to carcinogenics. (cdc.gov)
  • Journal of Neuroinflammation 8, no. 1 (12, 2011): 1-13. (tufts.edu)
  • Aquaporin-4 (AQP4) is critically involved in brain water and volume homeostasis and has been implicated in a wide range of pathological conditions. (stami.no)
  • Dopamine (DA) and its metabolites 3,4-dihydroxyphenylaceticacid (DOPAC) and homovanillic acid (HVA) were determined by high performance liquid chromatography (HPLC) analysis. (mdsabstracts.org)
  • Ketamine, a non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist, is used as a pediatric anesthetic for surgical procedures. (nih.gov)
  • 1990. Toxicological profile for 1,2-phenylhydrazine. (cdc.gov)
  • Neural cells collected from the rat forebrain were incubated for 24h with 1, 10 or 20 microM ketamine alone or with ketamine plus 1, 5, 10 or 20 microM 7-nitroindazole. (nih.gov)
  • Recent rapid advances in PD genetics have revealed a prominent role for mitochondrial dysfunction in the pathogenesis of the disease, and the products of several PD-associated genes, including SNCA , Parkin , PINK1 , DJ-1 , LRRK2 and HTR2A , show a degree of localization to the mitochondria under certain conditions. (medscape.com)
  • and additional findings supported inhibition of mitochondrial complex 1 as the underlying mechanism for these effects. (nih.gov)
  • BAK, another antimicrobial QUATS that is structurally similar to CPC, and the pesticide rotenone, a known complex 1 inhibitor, also showed mitochondrial inhibitory and antiestrogenic effects. (nih.gov)
  • JC-1 was used to detect mitochondrial transmembrane potential changes in SH-SY5Y cells under a flow cytometry. (mdsabstracts.org)
  • 4. LncRNA SNHG5 promotes cervical cancer progression by regulating the miR-132/SOX4 pathway. (nih.gov)
  • However, the role and underlying mechanism of SOS1 intronic transcript 1 (SOS1-IT1) in the progression of PD is still unclear. (nih.gov)
  • Strain susceptibility and resistance to 1,2-dimethylhydrazine-induced enteric tumors in germfree rats (40146). (cdc.gov)
  • Re-evaluation of 1,2-dimethylhydrazine in the mouse bone marrow micronucleus assay: Observation of a positive response. (cdc.gov)
  • However, this mechanism eventually fails, and the cell bodies of the motoneurons become visibly abnormal and completely degenerate [ 4 ]. (biomedcentral.com)
  • In vitro studies of striatal vesicles containing the vesicular monoamine transporter (VMAT2): rat versus mouse differences in sequestration of 1-methyl-4-phenylpyridinium. (nih.gov)
  • 1-methyl-4-phenyl pyridine (MPP + ) induced SK-N-SH cells were used to construct PD cell models in vitro. (nih.gov)
  • 1991. Control of 1,2-dimethylhydrazine-induced crypt hyperplasia by naturalkiller cells and its relevance to carcinogenics. (cdc.gov)
  • Parkinson disease (PD) is one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not halted, by treatment. (medscape.com)
  • Parkinson disease is recognized as one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years. (medscape.com)
  • Amyotrophic lateral sclerosis, with a global prevalence of 4-8 cases per 100,000 individuals, is the fourth leading cause of death by neurodegenerative diseases and follows Parkinson's, Alzheimer's, and Huntington's disease. (biomedcentral.com)