Electron Transport Complex III
A multisubunit enzyme complex that contains CYTOCHROME B GROUP; CYTOCHROME C1; and iron-sulfur centers. It catalyzes the oxidation of ubiquinol to UBIQUINONE, and transfers the electrons to CYTOCHROME C. In MITOCHONDRIA the redox reaction is coupled to the transport of PROTONS across the inner mitochondrial membrane.
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)
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).
Hemeproteins whose characteristic mode of action involves transfer of reducing equivalents which are associated with a reversible change in oxidation state of the prosthetic group. Formally, this redox change involves a single-electron, reversible equilibrium between the Fe(II) and Fe(III) states of the central iron atom (From Enzyme Nomenclature, 1992, p539). The various cytochrome subclasses are organized by the type of HEME and by the wavelength range of their reduced alpha-absorption bands.
NAD(P)H:(quinone acceptor) oxidoreductases. A family that includes three enzymes which are distinguished by their sensitivity to various inhibitors. EC 18.104.22.168 (NAD(P)H DEHYDROGENASE (QUINONE);) is a flavoprotein which reduces various quinones in the presence of NADH or NADPH and is inhibited by dicoumarol. EC 22.214.171.124 (NADH dehydrogenase (quinone)) requires NADH, is inhibited by AMP and 2,4-dinitrophenol but not by dicoumarol or folic acid derivatives. EC 126.96.36.199 (NADPH dehydrogenase (quinone)) requires NADPH and is inhibited by dicoumarol and folic acid derivatives but not by 2,4-dinitrophenol.
Cytochrome b Group
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).
A water-soluble, colorless crystal with an acid taste that is used as a chemical intermediate, in medicine, the manufacture of lacquers, and to make perfume esters. It is also used in foods as a sequestrant, buffer, and a neutralizing agent. (Hawley's Condensed Chemical Dictionary, 12th ed, p1099; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1851)
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)
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
Carbonyl Cyanide m-Chlorophenyl Hydrazone
The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)
A flavoprotein and iron sulfur-containing oxidoreductase that catalyzes the oxidation of NADH to NAD. In eukaryotes the enzyme can be found as a component of mitochondrial electron transport complex I. Under experimental conditions the enzyme can use CYTOCHROME C GROUP as the reducing cofactor. The enzyme was formerly listed as EC 188.8.131.52.
Reactive Oxygen Species
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 coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)
Cytochrome c Group
NADH, NADPH Oxidoreductases
A group of oxidoreductases that act on NADH or NADPH. In general, enzymes using NADH or NADPH to reduce a substrate are classified according to the reverse reaction, in which NAD+ or NADP+ is formally regarded as an acceptor. This subclass includes only those enzymes in which some other redox carrier is the acceptor. (Enzyme Nomenclature, 1992, p100) EC 1.6.
Characterization of a leukotriene C4 export mechanism in human platelets: possible involvement of multidrug resistance-associated protein 1. (1/715)Platelets express leukotriene (LT) C4 synthase and can thus participate in the formation of bioactive LTC4. To further elucidate the relevance of this capability, we have now determined the capacity of human platelets to export LTC4. Endogenously formed LTC4 was efficiently released from human platelets after incubation with LTA4 at 37 degrees C, whereas only 15% of produced LTC4 was exported when the cells were incubated at 0 degrees C. The activation energy of the process was calculated to 49.9 +/- 7.7 kJ/mol, indicating carrier-mediated LTC4 export. This was also supported by the finding that the transport was saturable, reaching a maximal export rate of 470 +/- 147 pmol LTC4/min x 10(9) platelets. Furthermore, markedly suppressed LTC4 transport was induced by a combination of the metabolic inhibitors antimycin A and 2-deoxyglucose, suggesting energy-dependent export. The presence in platelets of multidrug resistance-associated protein 1 (MRP1), a protein described to be an energy-dependent LTC4 transporter in various cell types, was demonstrated at the mRNA and protein level. Additional support for a role of MRP1 in platelet LTC4 export was obtained by the findings that the process was inhibited by probenecid and the 5-lipoxygenase-activating protein (FLAP) inhibitor, MK-886. The present findings further support the physiological relevance of platelet LTC4 production. (+info)
Ubiquinol:cytochrome c oxidoreductase. Effects of inhibitors on reverse electron transfer from the iron-sulfur protein to cytochrome b. (2/715)The effects of inhibitors on the reduction of the bis-heme cytochrome b of ubiquinol: cytochrome c oxidoreductase (complex III, bc1 complex) has been studied in bovine heart submitochondrial particles (SMP) when cytochrome b was reduced by NADH and succinate via the ubiquinone (Q) pool or by ascorbate plus N,N,N', N'-tetramethyl-p-phenylenediamine via cytochrome c1 and the iron-sulfur protein of complex III (ISP). The inhibitors used were antimycin (an N-side inhibitor), beta-methoxyacrylate derivatives, stigmatellin (P-side inhibitors), and ethoxyformic anhydride, which modifies essential histidyl residues in ISP. In agreement with our previous findings, the following results were obtained: (i) When ISP/cytochrome c1 were prereduced or SMP were treated with a P-side inhibitor, the high potential heme bH was fully and rapidly reduced by NADH or succinate, whereas the low potential heme bL was only partially reduced. (ii) Reverse electron transfer from ISP/c1 to cytochrome b was inhibited more by antimycin than by the P-side inhibitors. This reverse electron transfer was unaffected when, instead of normal SMP, Q-extracted SMP containing 200-fold less Q (0. 06 mol Q/mol cytochrome b or c1) were used. (iii) The cytochrome b reduced by reverse electron transfer through the leak of a P-side inhibitor was rapidly oxidized upon subsequent addition of antimycin. This antimycin-induced reoxidation did not happen when Q-extracted SMP were used. The implications of these results on the path of electrons in complex III, on oxidant-induced extra cytochrome b reduction, and on the inhibition of forward electron transfer to cytochrome b by a P-side plus an N-side inhibitor have been discussed. (+info)
Light-induced oxidation-reduction reactions of cytochromes in the green sulfur photosynthetic bacterium Prosthecochloris aesturarii. (3/715)The light-induced oxidation-reduction reactions of cytochromes in intact cells, starved cells, and chlorobium vesicle fractions of the green sulfur photosynthetic bacterium Prosthecochloris aesturarii were studied under anaerobic conditions. On the basis of both kinetic and spectral properties, at least three cytochrome species were found to be involved in the light-induced oxidation-reduction reactions of intact cells. These cytochromes were designated according to the positions of alpha-band maxima as C555 (rapid and slow components) and C552 (intermediate). By comparing the light-minus-dark difference spectra with the reduced-minus-oxidized difference spectra of purified cytochromes of this organism, rapid component C555 and intermediate component C552 are suggested to correspond to the purified cytochromes c-555(550) and c-551.5, respectively. Although the identity of the slow-phase component is uncertain, one possibility is that the slow phase is due to the bound form of c-555(550). In substrate-depleted (starved) cells, only one cytochrome species, C555 remained in the reduced state in the dark and oxidized upon actinic illumination. This corresponds to the rapid C555 component in intact cells. In the case of chlorobium vesicle fractions, one cytochrome species having an alpha-band maximum at 554 nm was oxidized by actinic light. The effects of several inhibitors on the absorbance changes of intact cells were studied. Antimycin A decreased the rate of the dark reduction of rapid C555 component. The complex effects of CCCP (carbonyl cyanide m-chlorophenylhydrazone) on the oxidation-reduction reactions of cytochromes were interpreted as the results of inhibition of the electron donation to oxidized C552 and C555 (slow), and a shift of the dark steady-state redox levels of cytochromes. Based on these findings, it is suggested that the rapid C555 component is located in a cyclic electron transfer pathway. The other two cytochromes, C552 and C555 (slow), may be located in non-cyclic electron transfer pathways and receive electrons from exogenous substrates such as sodium sulfide. A tentative scheme for the electron transfer system in Prosthecochloris aestuarii is presented and its nature is discussed. (+info)
Roles of Na(+)-Ca2+ exchange and of mitochondria in the regulation of presynaptic Ca2+ and spontaneous glutamate release. (4/715)The release of neurotransmitter from presynaptic terminals depends on an increase in the intracellular Ca2+ concentration ([Ca2+]i). In addition to the opening of presynaptic Ca2+ channels during excitation, other Ca2+ transport systems may be involved in changes in [Ca2+]i. We have studied the regulation of [Ca2+]i in nerve terminals of hippocampal cells in culture by the Na(+)-Ca2+ exchanger and by mitochondria. In addition, we have measured changes in the frequency of spontaneous excitatory postsynaptic currents (sEPSC) before and after the inhibition of the exchanger and of mitochondrial metabolism. We found rather heterogeneous [Ca2+]i responses of individual presynaptic terminals after inhibition of Na(+)-Ca2+ exchange. The increase in [Ca2+]i became more uniform and much larger after additional treatment of the cells with mitochondrial inhibitors. Correspondingly, sEPSC frequencies changed very little when only Na(+)-Ca2+ exchange was inhibited, but increased dramatically after additional inhibition of mitochondria. Our results provide evidence for prominent roles of Na(+)-Ca2+ exchange and mitochondria in presynaptic Ca2+ regulation and spontaneous glutamate release. (+info)
Interorganelle signaling is a determinant of longevity in Saccharomyces cerevisiae. (5/715)Replicative capacity, which is the number of times an individual cell divides, is the measure of longevity in the yeast Saccharomyces cerevisiae. In this study, a process that involves signaling from the mitochondrion to the nucleus, called retrograde regulation, is shown to determine yeast longevity, and its induction resulted in postponed senescence. Activation of retrograde regulation, by genetic and environmental means, correlated with increased replicative capacity in four different S. cerevisiae strains. Deletion of a gene required for the retrograde response, RTG2, eliminated the increased replicative capacity. RAS2, a gene previously shown to influence longevity in yeast, interacts with retrograde regulation in setting yeast longevity. The molecular mechanism of aging elucidated here parallels the results of genetic studies of aging in nematodes and fruit flies, as well as the caloric restriction paradigm in mammals, and it underscores the importance of metabolic regulation in aging, suggesting a general applicability. (+info)
Oxygen sensing in yeast: evidence for the involvement of the respiratory chain in regulating the transcription of a subset of hypoxic genes. (6/715)Oxygen availability affects the transcription of a number of genes in nearly all organisms. Although the molecular mechanisms for sensing oxygen are not precisely known, heme is thought to play a pivotal role. Here, we address the possibility that oxygen sensing in yeast, as in mammals, involves a redox-sensitive hemoprotein. We have found that carbon monoxide (CO) completely blocks the anoxia-induced expression of two hypoxic genes, OLE1 and CYC7, partially blocks the induction of a third gene, COX5b, and has no effect on the expression of other hypoxic or aerobic genes. In addition, transition metals (Co and Ni) induce the expression of OLE1 and CYC7 in a concentration-dependent manner under aerobic conditions. These findings suggest that the redox state of an oxygen-binding hemoprotein is involved in controlling the expression of at least two hypoxic yeast genes. By using mutants deficient in each of the two major yeast CO-binding hemoproteins (cytochrome c oxidase and flavohemoglobin), respiratory inhibitors, and cob1 and rho0 mutants, we have found that the respiratory chain is involved in the anoxic induction of these two genes and that cytochrome c oxidase is likely the hemoprotein "sensor." Our findings also indicate that there are at least two classes of hypoxic genes in yeast (CO sensitive and CO insensitive) and imply that multiple pathways/mechanisms are involved in modulating the expression of hypoxic yeast genes. (+info)
Role of tyrosine phosphorylation in the reassembly of occludin and other tight junction proteins. (7/715)After the simulation of anoxia by ATP depletion of MDCK cell monolayers with metabolic inhibitors, the tight junction (TJ) is known to become structurally perturbed, leading to loss of the permeability barrier. Peripheral TJ proteins such as zonula occludens 1 (ZO-1), ZO-2, and cingulin become extremely insoluble and associate into large macromolecular complexes (T. Tsukamoto and S. K. Nigam. J. Biol. Chem. 272: 16133-16139, 1997). For up to 3 h, this process is reversible by ATP repletion. We now show that the reassembly process depends on tyrosine phosphorylation. Recovery of transepithelial electrical resistance in ATP-replete monolayers was markedly inhibited by the tyrosine kinase inhibitor, genistein. Indirect immunofluorescence revealed a decrease in staining of occludin, a membrane component of the TJ, in the region of the TJ after ATP depletion, which reversed after ATP repletion; this reversal process was inhibited by genistein. Examination of the Triton X-100 solubilities of occludin and several nonmembrane TJ proteins revealed a shift of occludin and nonmembrane TJ proteins into an insoluble pool following ATP depletion. These changes reversed after ATP repletion, and the movement of insoluble occludin, ZO-1, and ZO-2 back into the soluble pool was again via a genistein-sensitive mechanism. Rate-zonal centrifugation analyses of detergent-soluble TJ proteins showed a reversible increase in higher density fractions following ATP depletion-repletion, although this change was not affected by genistein. In 32P-labeled cells, dephosphorylation of all studied TJ proteins was observed during ATP depletion, followed by rephosphorylation during ATP repletion; rephosphorylation of occludin was inhibited by genistein. Furthermore, during the ATP repletion phase, tyrosine phosphorylation of Triton X-100-insoluble occludin, which is localized at the junction, as well as ZO-2, p130/ZO-3 (though not ZO-1), and other proteins was evident; this tyrosine phosphorylation was completely inhibited by genistein. This indicates that tyrosine kinase activity is necessary for TJ reassembly during ATP repletion and suggests an important role for the tyrosine phosphorylation of occludin, ZO-2, p130/ZO-3, and possibly other proteins in the processes involved in TJ (re)formation. (+info)
A mechanism for the synergistic antimalarial action of atovaquone and proguanil. (8/715)A combination of atovaquone and proguanil has been found to be quite effective in treating malaria, with little evidence of the emergence of resistance when atovaquone was used as a single agent. We have examined possible mechanisms for the synergy between these two drugs. While proguanil by itself had no effect on electron transport or mitochondrial membrane potential (DeltaPsim), it significantly enhanced the ability of atovaquone to collapse DeltaPsim when used in combination. This enhancement was observed at pharmacologically achievable doses. Proguanil acted as a biguanide rather than as its metabolite cycloguanil (a parasite dihydrofolate reductase [DHFR] inhibitor) to enhance the atovaquone effect; another DHFR inhibitor, pyrimethamine, also had no enhancing effect. Proguanil-mediated enhancement was specific for atovaquone, since the effects of other mitochondrial electron transport inhibitors, such as myxothiazole and antimycin, were not altered by inclusion of proguanil. Surprisingly, proguanil did not enhance the ability of atovaquone to inhibit mitochondrial electron transport in malaria parasites. These results suggest that proguanil in its prodrug form acts in synergy with atovaquone by lowering the effective concentration at which atovaquone collapses DeltaPsim in malaria parasites. This could explain the paradoxical success of the atovaquone-proguanil combination even in regions where proguanil alone is ineffective due to resistance. The results also suggest that the atovaquone-proguanil combination may act as a site-specific uncoupler of parasite mitochondria in a selective manner. (+info)
Quercetin Protects Rat L6 Myocytes from Antimycin A-Induced Mitochondrial Dysfunction | OMICS International
Objective: Mitochondrial dysfunction is often associated with various disorders such as diabetes, Alzheimers etc. Reactive oxygen species (ROS), aging, and reducti..
Mechanisms involved in the inhibition of glycolysis by cyanide and antimycin A in Candida albicans and its reversal by hydrogen...
In Candida albicans, cyanide and antimycin A inhibited K(+) transport, not only with ethanol-O2 as the substrate, but also with glucose. The reason for this was that they inhibited not only respiration, but also fermentation, decreasing ATP production. Measurements of oxygen levels in cell suspensions allowed identification of the electron pathways involved. NADH fluorescence levels increased in the presence of the inhibitors, indirectly indicating lower levels of NAD(+) and so pointing to glyceraldehyde-3-phosphate dehydrogenase as the limiting step responsible for the inhibition of glycolysis, which was confirmed by the levels of glycolytic intermediaries. The cyanide effect could be reversed by hydrogen peroxide, mainly due to an activity by which H2O2 can be reduced by electrons flowing from NADH through a pathway that can be inhibited by antimycin A, and appears to be a cytochrome c peroxidase. Therefore, the inhibition of glycolysis by the respiratory inhibitors seems to be due to the ...
Antimycin A1 - TOKU-E
Antimycin A1 is the most hydrophobic of the four analogues of the antimycin A complex. Although broadly active as respiration inhibitors, more recent investigation has highlighted the importance of individual members of the complex as bioprobes ...
Antimycin A | C28H40N2O9 - PubChem
Antimycin A | C28H40N2O9 | CID 14957 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
This stage is more supported by the truth that the addition of antimycin A sales opportunities to ROS technology (Fig. 8c and...
This is concordant with the actuality that Isa1p has not been described as collaborating in the assembly of 2Fe?S facilities, which is the type of ISC existing
Cyanide-resistant respiration of Pseudomonas aeruginosa bacteria | Meta
The transition of the bacterial culture into the stationary growth phase is accompanied by an appearance of cyanide-resistant respiration. Chloramphenicol inhibits the development of cyanide-resistant respiration. The cyanide-resistant oxidase is localized in the bacterial membrane. Its appearance is not due to the quantitative and qualitative changes of flavins, non-heme iron, ubiquinone and cytochromes of the b and c types, but is accompanied by an increase in the copper content of the membrane preparations. Neither cyanide-sensitive, nor cyanide-resistant chains of the bacterial electron transfer contain cytochromes of the a type. The cyanide-resistant oxidase accepts electrons at the ubiquinone--cytochrome b level of the main respiratory chain. The cyanide-resistant respiration is not accompanied by a formation of hydrogen peroxide. Cytochrome o performs the function of cyanide-sensitive oxidase. The nature of cyanide-resistant oxidase still remains obscure. ...
RCSB PDB - 1PP9: Bovine cytochrome bc1 complex with stigmatellin bound Structure Summary Page
1PP9: Binding of the Respiratory Chain Inhibitor Antimycin to the Mitochondrial bc(1) Complex: A New Crystal Structure Reveals an Altered Intramolecular Hydrogen-bonding Pattern.
Famous Doctor Faces A Flight Emergency Without The Proper Resources
Hes a famous doctor and Instagram celeb, and when faced with an in-flight emergency, Dr. Mike was forced to spring into action.
The Toxoplasma Blog: Genetic Evidence for Cytochrome b Qi Site Inhibition by 4(1H)-quinolone-3-diarylethers and Antimycin in...
Toxoplasma gondii is an apicomplexan parasite that causes fatal and debilitating brain and eye disease. Endochin-like-quinolones (ELQs) are preclinical compounds that are efficacious against apicomplexan-caused diseases including toxoplasmosis, malaria and babesiosis. Of the ELQs, ELQ-316 has demonstrated the greatest efficacy against acute and chronic experimental toxoplasmosis. Although genetic analyses in other organisms have highlighted the importance of the cytochrome bc1 complex Qi site for ELQ sensitivity, the mechanism of action of ELQs against T. gondii and the mechanism of ELQ-316 remains unknown. Here we describe the selection and genetic characterization of T. gondii clones resistant to ELQ-316. A T. gondii strain selected under ELQ-316 drug pressure was found to possess a Thr222-Pro amino acid substitution that confers 49-fold resistance to ELQ-316 and 19-fold resistance to antimycin, a well-characterized Qi site inhibitor. These findings provide further evidence for ELQ Qi site ...
Myxothiazol | Antifungal Antibiotic/Complex III Inhibitor | MedChemExpress
Myxothiazol, an antifungal antibiotic, is a mitochondrial electron transport chain complex III (bc1 complex) inhibitor. Myxothiazol inhibits the growth of many yeasts and fungi at concentrations between 0.01 and 3 μg/ml. - Mechanism of Action & Protocol.
Mitochondria regulate Ca2+ wave initiation and inositol trisphosphate signal transduction in oligodendrocyte progenitors
Mitochondria in oligodendrocyte progenitor cells (OPs) Dtake up and release cytosolic Ca2+ during agonist-evoked Ca2+ waves, but it is not clear whether or how they regulate Ca2+ signaling in OPs. We asked whether mitochondria. play an active role during agonist-evoked Ca2+ release from intracellular stores. Ca2+ puffs, wave initiation, and wave propagation were measured in fluo-4 loaded OP processes using linescan confocal microscopy. Mitochondrial depolarization, measured by tetramethyl rhodamine ethyl ester (TMRE) fluorescence, accompanied Ca2+ puffs and waves. in addition, waves initiated only where mitochondria were localized. To determine whether energized mitochondria were necessary for wave generation, we blocked mitochondrial function with the electron transport chain inhibitor antimycin A (AA) in combination with oligomycin. AA decreased wave speed and puff probability. These effects were not due to global changes in ATP. We found that AA increased cytosolic Ca2+ markedly reduced ...
Mitochondrial Electron Transport Chain Inhibitors
BioVision develops and offers a wide variety of products including assay kits, antibodies, recombinant proteins & enzymes, and other innovative research tools for studying Apoptosis, Metabolism, Cell Proliferation, Cellular Stress, Cell Damage and Repair, Diabetes, Obesity and Metabolic Syndrome, Stem Cell Biology, Gene Regulation, Signal Transduction, etc. BioVisions products are currently being sold in more than 60 countries worldwide.
Biophysical Characterization of Recombinant Human Bcl-2 and Its Interactions with an Inhibitory Ligand, Antimycin A †
High endoplasmic reticulum activity renders Multiple myeloma cells hypersensitive to mitochondrial inhibitors - Fingerprint ...
Fingerprint Dive into the research topics of High endoplasmic reticulum activity renders Multiple myeloma cells hypersensitive to mitochondrial inhibitors. Together they form a unique fingerprint. ...
Fly Study Suggests, Gene Could Bypass Disease-Connected Mitochondrial Defects - Redorbit
Now, theyve shown that the same holds true in a living animal. Importantly, ubiquitous Ciona AOX activity had no apparent ill effects for the flies. Quite the contrary, mitochondria taken from AOX-expressing flies showed significant resistance to cyanide, and the flies partially resisted both cyanide and antimycin. AOX also rescued the movement defect and excess production of reactive oxygen species by mitochondria in flies with a mutant version of a gene known as dj-1b, which is the fly equivalent to the human Parkinsons disease gene DJ1 ...
Ubiquinol, 50mg - 60 caps
Take advantage of our Ubiquinol capsules the bioactive form of Q10s that is up to 800 more efficient than the common form. This is original Kaneka ubiquinol which is directly available for the body. 800 more efficient than common Q10 From the orig
How Is Ubiquinol Produced Naturally In The Body? | Ubiquinol.org
Ubiquinol is produced naturally in the body. Learn how this important nutrient is naturally produced and how its production is affected with age.
ActiveLife Q10 Ubiquinol 100 mg 60 Softgels , made by natures-way
Product Page for ActiveLife Q10 Ubiquinol 100 mg 60 Softgels made by natures-way offering price, ingredients and full item description from betterlife
Kroger - Vitacost Synergy Ubiquinol CoQH Targeted Wellness Softgels 200mg, 60 ct
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Pathogenic mutations in the 5 untranslated region of BCS1L mRNA in mitochondrial complex III deficiency. - Semantic Scholar
Mutations in the assembly chaperone BCS1L constitute a major cause of mitochondrial complex III deficiency. We studied the presence of BCS1L mutations in a complex III-deficient patient with metabolic acidosis, liver failure, and tubulopathy. A previously reported mutation, p.R56X, was identified in one BCS1L allele, and two novel heterozygous mutations, g.1181A|G and g.1164C|G, were detected in the second allele. The g.1181A|G mutation generated an alternative splicing site in the BCS1L transcript, causing a 19-nucleotides deletion in its 5UTR region. Decreased BCS1L mRNA and protein levels, and a respiratory chain complex III assembly impairment, determine a pathogenic role for the novel BCS1L mutations.
Supplementary MaterialsS1 Raw images: (PDF) pone | impacts of renin-angiotensin system inhibitors
Supplementary MaterialsS1 Raw images: (PDF) pone. but not male MLEC. In contrast, treatment with mitochondrial respiratory Complex III inhibitor Antimycin A (AA, 50M) mediated severe necrosis specifically in male MLEC, while female cells again responded primarily by apoptosis. The same effect with female cells responding to the stress by apoptosis and male cells responding by necrosis was confirmed in starved pulmonary endothelial cells isolated from human donors. Elevated necrosis seen in male cells was associated with a significant release of damage-associated alarmin, HMGB1. No stimuli induced a significant elevation of HMGB1 secretion in females. We conclude that male cells appear to be protected against mild stress conditions, such as hypoxia, possibly due to increased mitochondrial respiration. In contrast, they are more sensitive to impaired mitochondrial function, to which they respond by necrotic death. Necrosis in male vascular cells releases a significant amount of HMGB1 that could ...
The mitochondrial generation of hydrogen peroxide. General properties and effect of hyperbaric oxygen | Biochemical Journal |...
1. Pigeon heart mitochondria produce H2O2 at a maximal rate of about 20nmol/min per mg of protein. 2. Succinate-glutamate and malate-glutamate are substrates which are able to support maximal H2O2 production rates. With malate-glutamate, H2O2 formation is sensitive to rotenone. Endogenous substrate, octanoate, stearoyl-CoA and palmitoyl-carnitine are by far less efficient substrates. 3. Antimycin A exerts a very pronounced effect in enhancing H2O2 production in pigeon heart mitochondria; 0.26nmol of antimycin A/mg of protein and the addition of an uncoupler are required for maximal H2O2 formation. 4. In the presence of endogenous substrate and of antimycin A, ATP decreases and uncoupler restores the rates of H2O2 formation. 5. Reincorporation of ubiquinone-10 and ubiquinone-3 to ubiquinone-depleted pigeon heart mitochondria gives a system in which H2O2 production is linearly related to the incorporated ubiquinone. 6. The generation of H2O2 by pigeon heart mitochondria in the presence of ...
SUIT-009 - Bioblast
SUIT-009 is a short protocol for simultaneous determination of O2 flux and the rate of H2O2 production (H2O2 flux) on isolated mitochondria, tissue homogenate (except of liver) and permeabilized cells. Succinate (S) supports the reverse electron transfer (RET)-related H2O2 production in the LEAK state. Pyruvate (P) promotesNADH-pathway (N), and usually in the presence of ADP, H2O2 flux is not increased further. Antimycin A (Ama) inhibits Complex III (CIII) and could increase the H2O2 flux. The sensitivity of the Amplex UltraRed® assay (for determining H2O2 production) changes over the experimental time and upon addition of chemicals. To correct H2O2 flux for the sensitivity changes several H2O2 calibration steps are done during the experiment. The measurement is carried out in MiR05-Kit at 37 °C. For O2-Application, apply SUIT-009 O2 mt D015 or SUIT-009 O2 ce-pce D016; for O2 and H2O2 measurements (AmR), apply SUIT-009 AmR mt D021 or SUIT-009 AmR ce-pce D019. ...
Amytal Sodium Side Effects in Detail - Drugs.com
Learn about the potential side effects of Amytal Sodium (amobarbital). Includes common and rare side effects information for consumers and healthcare professionals.
S3QEL 2 | Complex III modulator | S3QEL2 | CAS [890888-12-7] | Axon 2544 | Axon Ligand™ with |99% purity available from stock...
S3QEL 2 | Complex III modulator | S3QEL2 | CAS [890888-12-7] | Axon 2544 | Axon Ligand™ with >99% purity available from supplier Axon Medchem, prime source of life science reagents for your research
Nutrusta Ubiquinol Ultra - CoQ10 VESIsorb Kaneka 100mg, 60 Softgels
Try Nutrusta Ubiquinol Ultra, 100% water & fat soluble VESIsorb® Kaneka QH formula PROVEN to have 6X times better absorption than standard QH.
Herbs for Life (Doctors Blend Products) - Enrollment
What is the difference between Ubiquinol and regular CoQ10? Ubiquinol is the most readily absorbed form of CoQ10 and is one of the most powerful fat-soluble antioxidants in the body. Ubiquinol is also the major form of CoQ10 in the body (over 95 ...
Herbs for Life (Doctors Blend Products) - Enrollment
What is the difference between Ubiquinol and regular CoQ10? Ubiquinol is the most readily absorbed form of CoQ10 and is one of the most powerful fat-soluble antioxidants in the body. Ubiquinol is also the major form of CoQ10 in the body (over 95 ...
Inhibition of Mitochondrial Complex III Blocks Neuronal Differentiation and Maintains Embryonic Stem Cell Pluripotency
The mitochondrion is emerging as a key organelle in stem cell biology, acting as a regulator of stem cell pluripotency and differentiation. In this study we sought to understand the effect of mitochondrial complex III inhibition during neuronal differentiation of mouse embryonic stem cells. When exposed to antimycin A, a specific complex III inhibitor, embryonic stem cells failed to differentiate into dopaminergic neurons, maintaining high Oct4 levels even when subjected to a specific differentiation protocol. Mitochondrial inhibition affected distinct populations of cells present in culture, inducing cell loss in differentiated cells, but not inducing apoptosis in mouse embryonic stem cells. A reduction in overall proliferation rate was observed, corresponding to a slight arrest in S phase. Moreover, antimycin A treatment induced a consistent increase in HIF-1α protein levels. The present work demonstrates that mitochondrial metabolism is critical for neuronal differentiation and emphasizes that
UQCRQ - Cytochrome b-c1 complex subunit 8 - Homo sapiens (Human) - UQCRQ gene & protein
Component of the ubiquinol-cytochrome c oxidoreductase, a multisubunit transmembrane complex that is part of the mitochondrial electron transport chain which drives oxidative phosphorylation. The respiratory chain contains 3 multisubunit complexes succinate dehydrogenase (complex II, CII), ubiquinol-cytochrome c oxidoreductase (cytochrome b-c1 complex, complex III, CIII) and cytochrome c oxidase (complex IV, CIV), that cooperate to transfer electrons derived from NADH and succinate to molecular oxygen, creating an electrochemical gradient over the inner membrane that drives transmembrane transport and the ATP synthase. The cytochrome b-c1 complex catalyzes electron transfer from ubiquinol to cytochrome c, linking this redox reaction to translocation of protons across the mitochondrial inner membrane, with protons being carried across the membrane as hydrogens on the quinol. In the process called Q cycle, 2 protons are consumed from the matrix, 4 protons are released into the intermembrane space and 2
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Non-heme 11 kDa protein of cytochrome bc1 complex (Ubiquinol-cytochrome c reductase) superfamily
The SCOP classification for the Non-heme 11 kDa protein of cytochrome bc1 complex (Ubiquinol-cytochrome c reductase) superfamily including the families contained in it. Additional information provided includes InterPro annotation (if available), Functional annotation, and SUPERFAMILY links to genome assignments, alignments, domain combinations, taxonomic visualisation and hidden Markov model information.
Cytochrome b-c1 complex subunit 10
This gene encodes the smallest known component of the ubiquinol-cytochrome c reductase complex, which forms part of the mitochondrial respiratory chain. The encoded protein may function as a binding factor for the iron-sulfur protein in this complex. [provided by RefSeq, Oct 2009 ...
MitoKit-CII MitoPedia - Bioblast
In addition, at Neurovive we have recently experienced another issue that could affect the use of these prodrugs in a rotenone-induced lactate assay and we suggest to formulate the limitation for Snv this way: Snv is a prodrug of succinate for in vitro use with the main application to deliver succinate to living cells in respiratory (oxygen consumption) protocols. Upon intracellular prodrug hydrolysis, formaldehyde is released which, at high concentration, has an inhibitory effect on glycolysis (Tiffert et al 1984). For in vitro experiments dependent of glycolysis and lacatate production as an output measure Snv should be carefully titrated to improve mitochondrial respiration without inhibiting glycolysis, which could be evidenced by restored lactate production following downstream (of CII) inhibition of the electron transfer system (using antimycin A ...
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3cx5 - Proteopedia, life in 3D
QCR6_YEAST] Component of the ubiquinol-cytochrome c reductase complex (complex III or cytochrome b-c1 complex), which is part of the mitochondrial respiratory chain that generates an electrochemical potential coupled to ATP synthesis. The complex couples electron transfer from ubiquinol to cytochrome c. QCR6 may mediate formation of the complex between cytochromes c and c1. [CYB_YEAST] Component of the ubiquinol-cytochrome c reductase complex (complex III or cytochrome b-c1 complex), which is part of the mitochondrial respiratory chain that generates an electrochemical potential coupled to ATP synthesis. The complex couples electron transfer from ubiquinol to cytochrome c. [QCR7_YEAST] Component of the ubiquinol-cytochrome c reductase complex (complex III or cytochrome b-c1 complex), which is part of the mitochondrial respiratory chain that generates an electrochemical potential coupled to ATP synthesis. The complex couples electron transfer from ubiquinol to cytochrome c. QCR7 is involved in ...
Chemical Modification and Detoxification of the Pseudomonas aeruginosa Toxin 2-Heptyl-4-hydroxyquinoline N-Oxide by...
2-Heptyl-4-hydroxyquinoline N-oxide (HQNO), a major secondary metabolite and virulence factor produced by the opportunistic pathogen Pseudomonas...
γ-Tocotrienol Protects against Mitochondrial Dysfunction and Renal Cell Death | Journal of Pharmacology and Experimental...
Renal proximal tubules are the major target of toxicant and ischemic injury in the kidney. Because mitochondria play a crucial role in ATP generation and survival of RPTCs, mitochondrial dysfunction caused by toxicant exposure or ischemia leads to RPTC injury and death and plays a major role in the development of acute kidney injury (Abid et al., 2005; Cachofeiro et al., 2008; Koyner et al., 2008). Oxidative stress is believed to be an important mechanism of toxicant- and ischemia-induced injury to RPTCs (Abid et al., 2005; Cachofeiro et al., 2008; Koyner et al., 2008). Therefore, we hypothesized that GT3, a potent antioxidant, may limit or prevent mitochondrial dysfunction, energy deficits, and cell death caused by oxidant exposure. Our data demonstrate that GT3 is taken up by RPTCs by a process that is saturated within 24 h, which suggests that GT3 is not taken up by simple diffusion. The saturation of GT3 uptake is not caused by depletion of GT3 from the cell culture media. At this point of ...
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OriGene - Uqcrh (NM 001009480) cDNA Clone
Uqcrh - Uqcrh (untagged ORF) - Rat ubiquinol-cytochrome c reductase hinge protein (Uqcrh), (10 ug) available for purchase from OriGene - Your Gene Company.
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Abcams Complex III ELISA Kit (ab124537) suitable for Tissue Extracts, Cell Lysate in human. Reliably quantify 4 µg/ml of Complex III.
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Pure Encapsulations CoQ10 500 mg 60 vegcaps Curated Suppplements - Curated Wellness
Description The essential nutrient Coenzyme Q10 is a necessary component of cellular energy production and respiration. It is a component of the mitochondrial electron transport system, which supplies the energy required for a variety of physiological functions. CoQ10 provides support to all cells of the body, and is e
What is the difference between ubiquinone and ubiquinol? | Reference.com
Ubiquinone and ubiquinol are the oxidized and reduced variants of the nutrient Coenzyme Q10, reports Meghan Lyons MS. Ubiquinol is produced by the addition of an electron to ubiquinone and vice...
CoQ10 exists in two forms, as ubiquinone (the oxidised CoQ10, spent form) and ubiquinol (the reduced and activated, antioxidant form). In order for CoQ10 to play a role in energy production and exhibit an antioxidant effect, the body must metabolise it to its antioxidant form ubiquinol, a process inhibited with increasing age, nutrient deficiency and some health conditions. Taking CoQ10 as ubiquinone is therefore not as effective as taking CoQ10 as ubiquinol (Kaneka QH™) the body-ready form which has only been available for use in supplements since 2006. Ubiquinol has numerous advantages over ubiquinone and comparing the two forms in therapeutic outcomes far surpasses its oxidised precursor.. Bioavailability When addressing the issue of therapeutics, at first glance the dose of ubiquinol may seem particularly relevant; however, it is the blood plasma level achieved by supplementation that is the significant factor in determining the effectiveness of a treatment.  As a lipid-soluble ...
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A COMPLEX DIETARY SUPPLEMENT AUGMENTS SPATIAL LEARNING, BRAIN MASS, AND MITOCHONDRIAL ELECTRON TRANSPORT CHAIN ACTIVITY IN...
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Glutathione and the mitochondrial reduction of hydroperoxides. - Semantic Scholar
Various organic hydroperoxides are reduced when added to rat liver mitochondrial suspensions. Succinate increases the rate and duration of the reductions except for linoleic acid hydroperoxide which appears to inhibit its own reduction. 3-Hydroxybutyrate replaces succinate but other reductants used are less effective. The rate of reduction of tert-butyl hydroperoxide by succinate is not inhibited by cyanide but is partly inhibited if antimycin or rotenone are also added; ATP reverses the antimycin inhibition. Other inhibitors include the uncoupler, carbonyl cyanide p-trifluoromethoxyhydrazone, ADP + Pi, the thiol reagents N-ethylmaleimide and p-hydroxymercuribenzoate and inhibitors of the mitochondrial transport of carboxylic acids. In some cases, the GSH concentration of the mitochondria during the reductions correlates with the reduction rate (e.g. with succinate and after N-ethylmaleimide) but in others it is dissociated. The results suggest that hydroperoxide reduction requires the GSH-glutathione
Benefits Of Ubiquinol Supplementation Derive From Its Potent Antioxidant And Energy-Enhancing Properties | MeMetics
Ubiquinol is produced normally in cells from Coenzyme Q10 to facilitate the energy transfer from a multitude of fat- and carbohydrate-burning chemical processes to the production of energy in the form of ATP. Ubiquinol deficiency hits the most active organs of the body first, which are the heart, brain and kidneys. Low levels of ubiquinol and CoQ10 occur as people age, or as a side effect of cholesterol-lowering therapy through statin drugs, which diminish the production of CoQ10 in the liver. CoQ10 has a lower potency than ubiquinol active form, because it has less prominent antioxidant properties, although it retains the same energy-enhancing effects. Ubiquinol energy production takes place in special cellular power-plants called mitochondria, where the nutrients we obtain from food are burned and the energy is transferred and carried by CoQ10 and ubiquinol to form more ATP, which is the molecule that releases energy whenever and wherever it is needed. Therefore, ubiquinol active form is ...
Gene Ontology Classifications
Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a ubiquinone-binding protein of low molecular mass. This protein is a small core-associated protein and a subunit of ubiquinol-cytochrome c reductase complex III, which is part of the mitochondrial respiratory chain. [provided by RefSeq, Jul 2008 ...
OriGene - UQCC1 (NM 018244) cDNA Clone
UQCC1 - UQCC (untagged)-Human ubiquinol-cytochrome c reductase complex chaperone (UQCC), nuclear gene encoding mitochondrial protein, transcript variant 1 available for purchase from OriGene - Your Gene Company.
UQCRBP1 Gene - GeneCards | UQCRBP1 Pseudogene
Complete information for UQCRBP1 gene (Pseudogene), Ubiquinol-Cytochrome C Reductase Binding Protein Pseudogene 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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|p|The body uses two forms of CoQ10. |I|Ubiquinone|/I|, also known as the oxidized form, is better known and is used primarily for energy production in the electron transport energy cycle inside the cell. |I|Ubiquinol|/I| plays a primary role in decreasin
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As you know, Co Q 10 is a fat-soluble vitamin-like substance found naturally in all forms of animal life. It is biosynthesized in the membranes of cells in humans and is vital in the production of energy. It is found in most cells, with especially high concentration in the heart (the organ that requires high levels of energy for normal operation). If that wasnt enough, its an antioxidant as well.. Co Q10 in your body needs to convert it to Ubiquinol, but as we age, we are less efficient at converting it.. For the first time, a kosher stabilized Ubiquinol is now available with Maxi CO-Q Ubiquinol™, providing 100 mg of high-absorption CoQ10 in a single liquid kosher capsule.. Try Maxi CO Q Ubiquinol™!. ...
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Antimycins are produced by a non-ribosomal peptide synthetase (NRPS)/polyketide synthase (PKS) assembly complex which acts as ... Antimycins are produced as secondary metabolites by Streptomyces bacteria, a soil bacteria. These specialized metabolites ... The following steps describe chemically what the Ant Enzymes do in order to synthesize Antimycin. Synthesis begins with ... Seipke, Ryan F; Hutchings, Matthew I (2013). "The regulation and biosynthesis of antimycins". Beilstein Journal of Organic ...
When Antimycin A is added at 25 ppb it provides a complete kill. However at 10 ppb, Antimycin A is used as a selective killing ... Antimycin A (more exactly Antimycin A1b) is a secondary metabolite produced by Streptomyces bacteria and a member of a group of ... Antimycin A is the active ingredient in Fintrol, a chemical piscicide (fish poison) used in fisheries management. Antimycin A ... Antimycin A is an inhibitor of cellular respiration, specifically oxidative phosphorylation. Antimycin A binds to the Qi site ...
Atta, M.A (2009). "Antimycin-A Antibiotic Biosynthesis Produced by Streptomyces Sp. AZ-AR-262: Taxonomy, Fermentation, ...
... s are antimycin antibiotics isolated from marine actinomycete. Imamura, N.; Nishijima, M.; Adachi, K.; Sano, H. ( ... 1993). "Novel antimycin antibiotics, urauchimycins a and B, produced by marine actinomycete". The Journal of Antibiotics. 46 (2 ...
"Two Antimycin A Analogues from Marine-Derived Actinomycete Streptomyces lusitanus". Marine Drugs. 10 (12): 668-676. doi:10.3390 ...
Examples of piscicides include rotenone, saponins, TFM, niclosamide and Antimycin A (Fintrol). Historically, fishing techniques ...
Electron transport chain
This complex is inhibited by dimercaprol (British Antilewisite, BAL), Napthoquinone and Antimycin. In Complex IV (cytochrome c ... by a high membrane potential or respiratory inhibitors such as antimycin A), Complex III may leak electrons to molecular oxygen ...
Introduced trout in lake ecosystems
When piscides are used, antimycin is often the preferred choice as there is little impact on lake invertebrates and its ... Two of the traditionally used piscidies in lake management are rotenone and antimycin. Chemical applications are often looked ...
Asian swamp eel
As such, standard fish poisons or piscicides (e.g., rotenone and antimycin A) that are transmitted across the gill membrane may ... Serial pesticide dilutions of antimycin-A were tested and found to be innocuous. No changes in morbidity and mortality were ...
Reconstitution of antimycin-insensitive electron transfer with the iron-sulfur protein and cytochrome c1". The Journal of ...
Tappel had the (erroneous) idea that inhibitors like antimycin and alkyl hydroxyquinoline-N-oxide might work by chelating iron ... "Inhibition of electron transport by antimycin A, alkyl hydroxy naphthoquinones and metal coordination compounds". Biochem. ...
Reconstitution of antimycin-insensitive electron transfer with the iron-sulfur protein and cytochrome c1". The Journal of ...
The fungus is also susceptible to antimycins produced by Streptomyces species. Conversely, P. fastigiata exhibits antimicrobial ...
"Complete Inhibition of Electron Transfer from Ubiquinol to Cytochrome by the Combined Action of Antimycin and Myxothiazol". ...
Smith MJ, Simco BA, Warren CO (December 1975). "Comparative effects of antimycin A on isolated mitochondria of channel catfish ...
Respiratory complex I
... except when inhibited by antimycin A". Journal of Neurochemistry. 148 (6): 731-745. doi:10.1111/jnc.14654. PMC 7086484. PMID ...
Coenzyme Q - cytochrome c reductase
Electron leakage occurs mainly at the Qo site and is stimulated by antimycin A. Antimycin A locks the b hemes in the reduced ... Antimycin A binds to the Qi site and inhibits the transfer of electrons in Complex III from heme bH to oxidized Q (Qi site ...
An antibiotic, antimycin A, and British anti-Lewisite, an antidote used against chemical weapons, are the two important ...
There are other chemicals that interrupt the mitochondrial electron transport chain (e.g., rotenone, antimycin A) and produce ...
Oxygen, O2 Ozonide, O− 3 Peroxide, O2− 2 Oxide, O2− Dioxygenyl, O+ 2 Antimycin A - used in fishery management, this compound ...
This can be done by poisoning rivers with chemicals such as antimycin or rotenone which have been declared safe in the U.S. by ...
SirexAA-E. Antimycin A - Chemical compound produced by Stroptomyces used as a piscicide Geosmin - Chemical compound responsible ...
... and introduction of the toxin and inhibitor of cellular respiration antimycin A. They also created small barriers to keep new ...
List of MeSH codes (D02)
... antimycin a MeSH D02.540.505.100 - brefeldin a MeSH D02.540.505.125 - candicidin MeSH D02.540.505.187 - epothilones MeSH ...
... is used in biomedical research to study oxygen consumption rate of cells usually in combination with antimycin A (an ...
He showed that the binding of certain inhibitors of oxidative phosphorylation acting at different sites (antimycin on electron ...
EPA list of extremely hazardous substances
Antimony pentafluoride Antimycin A ANTU (Alpha-Naphthylthiourea) Arsenic pentoxide Arsenous oxide Arsenous trichloride Arsine ...
List of MeSH codes (D04)
... antimycin a MeSH D04.345.349.100 - brefeldin a MeSH D04.345.349.125 - candicidin MeSH D04.345.349.156 - cytochalasins MeSH ...
Planning & Executing Successful Rotenone & Antimycin Projects | American Fisheries Society
Coordinate regulation of antimycin and candicidin biosynthesis - Fingerprint - University of Strathclyde
IMSEAR at SEARO: Relation of tryptophan metabolism to antimycin A biosynthesis in Streptomyces antibioticus.
Structural basis for electron transport mechanism of complex I-like photosynthetic NAD(P)H dehydrogenase | Nature Communications
Mitochondrial Superoxide Detection mtSOX Deep Red - Mitochondrial Superoxide Detection DOJINDO
Detection of superoxide in HeLa cells treated with antimycin by mtSOX Deep Red and MitoSOX™ Red ... Treated with Antimycin. ＜Imaging Conditions＞(Confocal microscopy). Intracellular ROS: Ex = 488, Em = 490-520 nm. mtSOX: Ex = ... The cells were washed with HBSS and stained with mtSOX Deep Red working solution containing Antimycin, and the generated ... and separately treated with mitochondrial superoxide inducer Antimycin or hydrogen peroxide. ...
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Sperm-specific COX6B2 enhances oxidative phosphorylation, proliferation, and survival in human lung adenocarcinoma | eLife
antA, Antimycin A; Cyt c, Cytochrome c; ATP Syn, ATP synthase. (B) Complex IV activity in indicated cell lines using TMPD/ ... As a positive control, cells were treated with 50 μM antimycin A during staining. For H2O2 measurements, cells reaching ... antimycin A (A8674), mannitol (M4125), KH2PO4 (P0662), MgCl2 (M8266), ADP-K+ salt (A5285), ascorbate (A5960), N,N,N′,N′- ... and antimycin A (2 μM). Results were normalized to total protein amount as determined by Pierce BCA Protein Assay Kit. Non- ...
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Immunoregulatory Protein B7-H3 Reprograms Glucose Metabolism in Cancer Cells by ROS-Mediated Stabilization of HIF1α | Cancer...
Acute frataxin knockdown in induced pluripotent stem cell-derived cardiomyocytes activates a type I interferon response |...
Note that oxygen utilization in NDI1-transfected cells was not sensitive to rotenone inhibition but that antimycin A still ... but remained sensitive to the complex III inhibitor antimycin A, indicating that NDI1 integrated into the mitochondrial ETC and ... and 5 μm antimycin (AntA) were added. ...
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Frontiers | Resistin-Like Molecule α Dysregulates Cardiac Bioenergetics in Neonatal Rat Cardiomyocytes
... and antimycin A (0.5 μM, Complex III inhibitor) into the medium at 34, 58, and 85 min, respectively. After the assay, OCR based ... and antimycin A (0.5 μM, Complex III inhibitor) were injected into the NRCMs at the indicated times for assessment of basal ... and antimycin A (0.5 μM) as ports B, C, and D injections, respectively, at the indicated times for assessment of basal ...
Metabolites | Free Full-Text | Targeting the Pentose Phosphate Pathway for SARS-CoV-2 Therapy
The order of injections was oligomycin (1 µM), FCCP (20 mM), 2-DG (0.5 µM), and rotenone/antimycin A (0.5 µM). The data was ... On the day of assay, the stock solutions of the Seahorse XF Real-Time ATP Rate Assay Kit (oligomycin, rotenone/antimycin A) ... On the day of assay, the stock solutions of the Seahorse XF Mito Stress Test Kit (oligomycin, FCCP, rotenone/antimycin A) and 2 ... The order of injections was: oligomycin and rotenone/antimycin A. The final concentrations in the assay were 1.5 µM for ...
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Neuronal cell-based high-throughput screen for enhancers of mitochondrial function reveals luteolin as a modulator of...
Molecular Microbiology - Research output - University of East Anglia
The Qo site of the mitochondrial complex III is required for the transduction of hypoxic signaling via reactive oxygen species...
B) HIF-1α protein levels of whole cell lysates from WT cybrids incubated with 1 μM antimycin A and subjected to 21% O2 (N), 1.5 ... B) HIF-1α protein levels of whole cell lysates from WT cybrids incubated with 1 μM antimycin A and subjected to 21% O2 (N), 1.5 ... 6 A). In contrast, the complex III inhibitor antimycin A, which preserves the ROS generation at the Qo site of complex III, did ... and antimycin A were purchased from Sigma-Aldrich. ...
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Anhydroophiobolin A - TOKU-E
3-Anhydroophiobolin A is the dehydrated analogue of ophiobolin A and is a major member of the ophiobolin complex of phytotoxic metabolites produced by many species of the genus Bipolaris. Like all ophiobolins, 3-anhydroophiobolin A possesses a broad biological profile with antibacterial, antifungal, antitumor, herbicidal and nematocidal activities ...
MitochondrialRotenoneStreptomycesBiosynthesisInhibitorsApoptosisProductionOligomycinTreated with rotenoneRotenone and antimycinRespirationInhibitor antimycinInhibitors antimycinMyxothiazolRespiratoryElectron transBasalOxidativeConcentrationComplex IIIMeSHResistanceCellsSimilarlyOxygenEvidentPresenceDataShowsQuestions
- HeLa cells were washed with HBSS and co-stained with mtSOX and intracellular total ROS reagent (ROS Assay Kit -Highly Sensitive DCFH-DA-: code R252 ), and separately treated with mitochondrial superoxide inducer Antimycin or hydrogen peroxide. (dojindo.com)
- Furthermore, ACO3 contributed to plant tolerance against ultraviolet B (UV-B) or antimycin A-induced mitochondrial dysfunction. (helsinki.fi)
- As an example of the capabilities of this test for compound screening a dose response to the known mitochondrial inhibitor antimycin A was prepared. (bmglabtech.com)
- Neither fluoxetine, antimycin nor rotenone could reactivate KATP channel activity blocked by glucose unlike the mitochondrial uncoupler, FCCP. (nottingham.ac.uk)
- Biologists, technicians, and mangers that apply, manage or administer project budgets and personnel or deal with public communications on rotenone or antimycin projects. (fisheries.org)
- O: Oligomycin, F: FCCP, A&R: antimycin A/rotenone. (biomedcentral.com)
- An unprecedented 1,2-shift in the biosynthesis of the 3-aminosalicylate moiety of antimycins. (mpg.de)
- Antimycins are potent inhibitors of the Bcl-2 family of anti-apoptotic proteins, which are frequently overproduced by cancer cells and confer resistance to chemotherapeutic agents whose mode of action is activation of apoptosis. (leeds.ac.uk)
- The positions of the four iron centers within the bc1 complex and the binding sites of the two specific respiratory inhibitors antimycin A and myxothiazol were identified. (weizmann.ac.il)
- Compared with the corresponding parental cells, the SP cells of SWCNT-transformed and H460 cells acquired apoptosis resistance to various chemotherapy including antimycin A, cisplatin, doxorubicin and etoposide. (cdc.gov)
- Our goal is to identify factors that control production of antimycins in order to advance our understanding of how the expression of secondary metabolism is controlled and will aid the pursuit of silent biosynthetic pathway activation. (leeds.ac.uk)
- Respiratory inhibitors, oligomycin, FCCP (uncoupling agent), and rotenone/antimycin A were used to measure basal oxygen consumption rate, maximal/spare respiration, as well as extracellular acidification rate from peripheral blood mononuclear cells (PBMC) collected from a healthy control. (nih.gov)
- Seven guidelines were evaluated and all determinations were performed in 12 replicates for each sample: Mitochondrial Basal OCR (corresponds to baseline OCR minus rotenone/antimycin-insensitive OCR) ATP-linked OCR (corresponds to basal OCR minus oligomycin-insensitive OCR). (woodgreenoutreach.org)
- OCR was measured with sequential injection of Oligomycin, FCCP and Rotenone/Antimycin (final concentration: 1, 1, and 0.5 M, respectively). (phypode.org)
- K+ or Na+ stimulated H+ efflux was completely inhibited by DCCD, DES, oligomycin and antimycin reagents which inhibit ATP driven H+ efflux. (brocku.ca)
- These alterations were similar to those caused by inhibitors of the electron transport system (azide, rotenone, antimycin A, cyanide, and oligomycin) and anaerobic glycolysis (2-deoxyglucose) and are compatible with inhibition of an energy-dependent exit pump. (elsevier.com)
- Air consumption price (OCR) and extracellular acidification price (ECAR) had been measured simultaneously, without inhibitors from the electron transfer string (oligomycin first of all, FCCP, rotenone and antimycin A) C the baseline, and following the addition from the above-mentioned inhibitors then. (cambio-red.net)
Treated with rotenone2
- Downregulation of CytC subunits I and IV was similarly found in the groups treated with rotenone and antimycin A, while increases in the lipid peroxidation (LPO) products malondialdehyde and 4-hydroxynonenal which reflect mitochondrial damage, were observed. (elsevier.com)
- Subsequently, cells had been sequentially treated with rotenone/antimycin A (Krebs routine inhibitors, all from Sigma) to quantify ATP creation, proton drip, maximal respiration, and extra respiratory capacity after Glucosamine sulfate every treatment using the outfitted software program, normalized to protein amounts assessed via the BCA assay. (newpathstopurpose.org)
Rotenone and antimycin2
- Methods: We set up an in vitro kidney perfusion model to study the direct effect of inhibitors of the mitochondrial respiratory chain, rotenone and antimycin A, on the glomerular filtration barrier by using immunohistochemistry and Northern blotting and quantitating the resulting proteinuria. (elsevier.com)
- Urinary protein excretion increased significantly in the rotenone- and antimycin-A-treated groups during perfusion. (elsevier.com)
- We have used an in vitro model of anoxia/ischemia, causing severe ATP depletion by using the combination of a mitochondrial respiration inhibitor (antimycin A), a non-metabolizable glucose analog (2-deoxyglucose), and a calcium ionophore (A23187) in human renal cells to mimic the ischemic phase of renal ischemic reperfusion injury ( 15 ). (asnjournals.org)
- Cyanide-insensitive respiration was enhanced by addition of antimycin A to the incubation mixture, but repressed by the addition of cycloheximide, emetine, puromycin (cytosolic translation inhibitors), carbonylcyanide-m-chlorophenylhydrazone (uncoupler) and actinomycin D (transcription inhibitor). (elsevier.com)
- Succinate and glucose respiration were inhibited by 2-heptyl-4-hydroxyquinoline-N-oxide, antimycin A and myxothiazol, suggesting the presence of a bc1 complex.KCN inhibition curves in the presence of ascorbate-TMPD, succinate or glucose were biphasic, with KCN-sensitive and -resistant oxidases. (indjst.org)
- Cerebral but not RGC-5 or neuroblastoma cells increased superoxide production in response to the complex I inhibitor rotenone, while neuroblastoma but not cerebral or RGC-5 cells dramatically decreased superoxide production in response to the complex III inhibitor antimycin A. Immunoblotting and real-time quantitative PCR of METC components demonstrated different patterns of expression among the three different sources of neuronal mitochondria. (biomedcentral.com)
- Transfection of HT1299luc cells with NDI1 abolished the ATP decline observed in nontransfected HT1299luc cells after administration of either complex I inhibitor rotenone or BAY 87-2243 C but had no effect on ATP decline after treatment of Ht1299luc-NDI1 cells with complex III inhibitor antimycin A (Fig.?6D). (biotechnologysymposium.com)
- The positions of the four iron centers within the bc 1 complex and the binding sites of the two specific respiratory inhibitors antimycin A and myxothiazol were identified. (elsevier.com)
- The light-induced acidification of the cytoplasm was not observed in the presence of the cytochrome respiratory chain inhibitors antimycin A and mucidin. (microbiologyresearch.org)
- es antimycin, whereas aurachin D is different from either antimycin or myxothiazol. (archive.org)
- SHAM is effective against A. castellanii and Acanthamoeba polyphaga only when used in conjunction with antimycin A, an inhibitor of the conventional cytochrome respiratory pathway. (strath.ac.uk)
- Antimycin is an electron transport chain inhibitor. (pharmaguideline.com)
- that are unable to grow in the presence of antimycin A an inhibitor of complex III of the standard electron transport chain. (rmrfotoarts.com)
- Antimycin A or AntA (an electron transport chain blocker, 10 M in DMSO) was used as a positive control and consequently improved the DHE oxidation levels by 2.6-fold higher than the control group (data not shown). (ivachtin.com)
- Non-mitochondrial OCR was measured after injection with 5?M Antimycin A and subtracted from basal and maximal OCR measurements. (ac-devd-cho.com)
- 11. Antimycin A shows selective antiproliferation to oral cancer cells by oxidative stress-mediated apoptosis and DNA damage. (nih.gov)
- We performed a short-term (60 min) compound treatment with two known inhibitors of oxidative phosphorylation, Antimycin A and CCCP. (moleculardevices.com)
- Physiological Concentration of Exogenous Lactate Reduces Antimycin A Triggered Oxidative Stress in Intestinal Epithelial Cell Line IPEC-1 and IPEC-J2 In Vitro. (helsinki.fi)
- Rox is the residual oxygen consumption in the ROX state, due to oxidative side reactions, estimated after addition of antimycin A (inhibitor of CIII). (oroboros.at)
- An antimycin A concentration of 0.07 micromoles per gram of mitochondrial protein is effective. (pharmaguideline.com)
- Antimycin A (Ama) inhibits Complex III (CIII) at the Q o level and could increase the H 2 O 2 flux. (oroboros.at)
- Antimycin A" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (ucdenver.edu)
- In this paper we report the first case of antimycin A resistance in a protozoan parasite that is attributable to a mutation in the mitochondrial apocytochrome b (CYb) gene. (ed.ac.uk)
- We selected for, and isolated, a mutant Leishmania tarentolae strain that is resistant to antimycin A. This resistance was evident at the levels of the in vitro growth and enzymatic activity of the cytochrome bc1 complex. (ed.ac.uk)
- Schnaufer, A , Sbicego, S & Blum, B 2000, ' Antimycin A resistance in a mutant Leishmania tarentolae strain is correlated to a point mutation in the mitochondrial apocytochrome b gene ', Current Genetics , vol. 37, no. 4, pp. 234-41. (ed.ac.uk)
- Compared with the corresponding parental cells, the SP cells of SWCNT-transformed and H460 cells acquired apoptosis resistance to various chemotherapy including antimycin A, cisplatin, doxorubicin and etoposide. (cdc.gov)
- ATP depletion preconditioning (1 h of antimycin A and 2-deoxyglucose treatment followed by 1 h of recovery), adenosine, an A 1 adenosine receptor selective agonist, or an A 2a adenosine receptor selective agonist significantly attenuated subsequent severe ATP depletion injury of HK-2 cells. (asnjournals.org)
- Mitophagy in U2OS cells was performed 16C20 h after depolarization with antimycin A and OA by following -TOMM20 staining by immunofluorescence. (labsmart.net)
- Subfractionation studies showed that cytochrome b 5 (cyt b5), which has been considered to be a typical ER protein, was localized in both the endoplasmic reticulum membrane (ER) and the outer membrane of mitochondria in cauliflower (Brassica olracea) cells and was a component of antimycin A-insensitive NADH-cytochrome c reductase system in both membranes. (elsevier.com)
- Similar to antimycins, it acts similarly. (pharmaguideline.com)
- While these compounds all inhibited oxygen consumption, only those that exert an effect prior to (rotenone) or at (antimycin a) the point of mitochondrial superoxide formation inhibited LDCL. (nih.gov)
- The dependence of brain mitochondria reactive oxygen species production on oxygen level is linear, except when inhibited by antimycin A. . J Neurochem. (cornell.edu)
- Although multiple electrofishing removals in a summer was an effective tool, it became evident that a chemical approach using the piscicide Antimycin A would be the most cost-effective and efficient for larger streams with deeper pools that could not be electrofished. (nps.gov)
- In contrast, in the presence of inhibitors of Cyclic Electron Flow (CEF) like Antimycin A (AA) and rotenone, the oscillation of F PSI /F PSII was either abolished or severely dampened. (ias.ac.in)
- De leverede en blodprøve og havde deres anonymiserede kliniske data knyttet til deres biospecimen. (marjolein-teepen.com)
- This graph shows the total number of publications written about "Antimycin A" by people in this website by year, and whether "Antimycin A" was a major or minor topic of these publications. (ucdenver.edu)
- Answer the following questions about Antimycin A in a few paragraphs. (mycoursebay.com)