Antimycin A: An antibiotic substance produced by Streptomyces species. It inhibits mitochondrial respiration and may deplete cellular levels of ATP. Antimycin A1 has been used as a fungicide, insecticide, and miticide. (From Merck Index, 12th ed)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.Rotenone: A botanical insecticide that is an inhibitor of mitochondrial electron transport.Electron Transport: The process by which ELECTRONS are transported from a reduced substrate to molecular OXYGEN. (From Bennington, Saunders Dictionary and Encyclopedia of Laboratory Medicine and Technology, 1984, p270)Hydroxyquinolines: The 8-hydroxy derivatives inhibit various enzymes and their halogenated derivatives, though neurotoxic, are used as topical anti-infective agents, among other uses.Cyanides: Inorganic salts of HYDROGEN CYANIDE containing the -CN radical. The concept also includes isocyanides. It is distinguished from NITRILES, which denotes organic compounds containing the -CN radical.Ubiquinone: A lipid-soluble benzoquinone which is involved in ELECTRON TRANSPORT in mitochondrial preparations. The compound occurs in the majority of aerobic organisms, from bacteria to higher plants and animals.Methacrylates: Acrylic acids or acrylates which are substituted in the C-2 position with a methyl group.Mitochondria: Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)Oligomycins: 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).Succinates: Derivatives of SUCCINIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a 1,4-carboxy terminated aliphatic structure.Cytochromes: 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.Uncoupling Agents: Chemical agents that uncouple oxidation from phosphorylation in the metabolic cycle so that ATP synthesis does not occur. Included here are those IONOPHORES that disrupt electron transfer by short-circuiting the proton gradient across mitochondrial membranes.Quinone Reductases: NAD(P)H:(quinone acceptor) oxidoreductases. A family that includes three enzymes which are distinguished by their sensitivity to various inhibitors. EC 1.6.99.2 (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 1.6.99.5 (NADH dehydrogenase (quinone)) requires NADH, is inhibited by AMP and 2,4-dinitrophenol but not by dicoumarol or folic acid derivatives. EC 1.6.99.6 (NADPH dehydrogenase (quinone)) requires NADPH and is inhibited by dicoumarol and folic acid derivatives but not by 2,4-dinitrophenol.Cytochrome b Group: Cytochromes (electron-transporting proteins) with protoheme (HEME B) as the prosthetic group.Oxidation-Reduction: 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).Amobarbital: A barbiturate with hypnotic and sedative properties (but not antianxiety). Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high. (From Martindale, The Extra Pharmacopoeia, 30th ed, p565)Oxygen Consumption: The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)Succinic Acid: 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)Potassium Cyanide: A highly poisonous compound that is an inhibitor of many metabolic processes, but has been shown to be an especially potent inhibitor of heme enzymes and hemeproteins. It is used in many industrial processes.Mitochondria, Liver: 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)Rhodobacter: A genus of gram-negative bacteria widely distributed in fresh water as well as marine and hypersaline habitats.Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone: A proton ionophore that is commonly used as an uncoupling agent in biochemical studies.Thenoyltrifluoroacetone: Chelating agent and inhibitor of cellular respiration.Cytochromes c1: The 30-kDa membrane-bound c-type cytochrome protein of mitochondria that functions as an electron donor to CYTOCHROME C GROUP in the mitochondrial and bacterial RESPIRATORY CHAIN. (From Enzyme Nomenclature, 1992, p545)Carbonyl Cyanide m-Chlorophenyl Hydrazone: A proton ionophore. It is commonly used as an uncoupling agent and inhibitor of photosynthesis because of its effects on mitochondrial and chloroplast membranes.Oxidoreductases: 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)Ferricyanides: Inorganic salts of the hypothetical acid, H3Fe(CN)6.Dinitrophenols: Organic compounds that contain two nitro groups attached to a phenol.ThiazolesDimercaprol: An anti-gas warfare agent that is effective against Lewisite (dichloro(2-chlorovinyl)arsine) and formerly known as British Anti-Lewisite or BAL. It acts as a chelating agent and is used in the treatment of arsenic, gold, and other heavy metal poisoning.Submitochondrial Particles: The various filaments, granules, tubules or other inclusions within mitochondria.NADH Dehydrogenase: 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 1.6.2.1.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.Mitochondria, Heart: The mitochondria of the myocardium.Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell.Oxidative Phosphorylation: Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds.Adenosine Triphosphate: An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.Diuron: A pre-emergent herbicide.Spectrophotometry: The art or process of comparing photometrically the relative intensities of the light in different parts of the spectrum.NAD: 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)Antimetabolites: Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)Cytochrome c Group: A group of cytochromes with covalent thioether linkages between either or both of the vinyl side chains of protoheme and the protein. (Enzyme Nomenclature, 1992, p539)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.Salicylamides: Amides of salicylic acid.Kinetics: The rate dynamics in chemical or physical systems.Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.Ferrocyanides: Inorganic salts of the hypothetical acid ferrocyanic acid (H4Fe(CN)6).Cytochromes b: Cytochromes of the b group that have alpha-band absorption of 563-564 nm. They occur as subunits in MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III.

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)

*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 ...

*Antimycin A

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 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 ... "Antimycin. A Brief Review of It's Chemistry, Environmental Fate, and Toxicology" (PDF). Ott, Kevin. "Antimycin. A Brief Review ...

*Actinobacteria

Atta, M.A (2009). "Antimycin-A Antibiotic Biosynthesis Produced by Streptomyces Sp. AZ-AR-262: Taxonomy, Fermentation, ...

*Urauchimycin

... s are antimycin antibiotics isolated from marine actinomycete. Novel antimycin antibiotics, urauchimycins A and B, ...

*Streptomyces lusitanus

"Two Antimycin A Analogues from Marine-Derived Actinomycete Streptomyces lusitanus". Marine Drugs. 10 (12): 668-676. doi:10.3390 ...

*Piscicide

Examples of piscicides include rotenone, saponins, TFM, niclosamide and Antimycin A (Fintrol). Historically, fishing techniques ...

*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 pesticides (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 change in morbidity and mortality were ...

*Celastrol

Abu Bakar, M. H.; Cheng, K. K.; Sarmidi, M. R.; Yaakob, H.; Huri, H. Z. (2015). "Celastrol Protects against Antimycin A-Induced ...

*North Cascades National Park Service Complex Fish Stocking Act

"Modification to Mountain Lakes Fishery Management Plan - Piscicide Change from Antimycin to Rotenone". National Park Service - ...

*UQCRFS1

Reconstitution of antimycin-insensitive electron transfer with the iron-sulfur protein and cytochrome c1". J. Biol. Chem. 260 ( ...

*Thenoyltrifluoroacetone

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. ...

*Streptomyces

Antimycin A - compound produced by this bacterium used in piscicides Streptomyces isolates Kämpfer, Peter (2006). "The Family ...

*Rotenone

... is used in biomedical research to study oxygen consumption rate of cells usually in combination with antimycin-D (an ...

*Rainbow trout

This can be done by poisoning rivers with chemicals such as antimycin or rotenone which have been declared safe in the USA by ...

*Histotoxic hypoxia

There are other chemicals that interrupt the mitochondrial electron transport chain (e.g., rotenone, antimycin A) and produce ...

*Superoxide

Oxygen, O2 Ozonide, O− 3 Peroxide, O2− 2 Oxide, O2− Dioxygenyl, O+ 2 Antimycin A - used in fishery management, this compound ...

*List of extremely hazardous substances

Antimony pentafluoride Antimycin A ANTU (Alpha-Naphthylthiourea) Arsenic pentoxide Arsenous oxide Arsenous trichloride Arsine ...

*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 ...

*Edward Slater

He showed that the binding of certain inhibitors of oxidative phosphorylation acting at different sites (antimycin on electron ...

*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 ...
One of distinct genetic alterations in spontaneously immortalized DF-1 cells was found to be dysfunction of p53 and E2F-1 as well as altered antioxidant gene expression (upregulation of MnSOD and downregulation of catalase). We have characterized the
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 ...
The major finding of the present study is that regulation of mitochondrial ROS production varies substantially in the three major fiber types of adult skeletal muscle tissue. Under basal conditions (e.g., non-ADP-stimulated state 4 respiration), free radical leak is significantly higher in WG than in RG or soleus muscle (Fig. 4), whether basal respiration is supported by electrons feeding complex I (low rate of H2O2 production; Fig. 2) or complex II (high rate of H2O2 production; Fig. 3). Remarkably, under conditions that favor high rates of O2−· generation (e.g., in the presence of the complex III inhibitor antimycin A), the absolute rates of H2O2 production in permeabilized WG fibers are nearly as high as those observed in RG muscle and rates in both RG and WG muscle are markedly higher than rates obtained from soleus muscle. This is somewhat counterintuitive, given that the respiratory capacity (Table 1) and mitochondrial content in type IIB (WG) muscle fibers are approximately half of ...
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.
Science & Mathematics / Science, Chemistry & Invention / Topics in microbial chemistry: Antimycin,coenzyme A,kinetin and kinins by Frank Morgan Strong Frank Morgan Strong Wiley; Chapman & Hall (1958) hardback; 166 pages. Contents: Antimycin: Coenzyme A : Kinetin & Kinins :Index : Condition: very clean and good overall. , Used, Rare and Out-Of-Print Books
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.
Simvastatin, but not pravastatin, produced a slow relaxation of the coronary artery, which was independent of the endothelium. The relaxation was attenuated by the mitochondrial complex I inhibitor rotenone (10 μM) and the complex III inhibitor myxothiazol (10 μM), or a combination of the two. The complex III inhibitor antimycin A (10 μM) produced a similar time-dependent relaxation of the porcine coronary artery, which was attenuated by rotenone. Changes in rhodamine 123 fluorescence showed that simvastatin (10 μM) depolarized the membrane potential of mitochondria in both isolated mitochondria and intact blood vessels. Simvastatin and antimycin A both inhibited calcium-induced contractions in isolated blood vessels and calcium influx in smooth muscle cells and this inhibition was prevented by rotenone ...
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 ...
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 ...
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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 ...
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.
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 ...
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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 ...
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 ...
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
Mitochondrial complex III deficiency can be caused by mutations in one of several genes. The proteins produced from these genes either are a part of or help assemble a group of proteins called complex III. The two most commonly mutated genes involved in mitochondrial complex III deficiency are MT-CYB and BCS1L. It is likely that genes that have not been identified are also involved in this condition.. Cytochrome b, produced from the MT-CYB gene, is one component of complex III, and the protein produced from the BCS1L gene is critical for the formation of the complex. Complex III is found in cell structures called mitochondria, which convert the energy from food into a form that cells can use. Complex III is one of several complexes that carry out a multistep process called oxidative phosphorylation, through which cells derive much of their energy. As a byproduct of its action in oxidative phosphorylation, complex III produces reactive oxygen species, which are harmful molecules that can damage ...
Accepted name: quinol cytochrome-c reductase. Reaction: quinol + 2 ferricytochrome c = quinone + 2 ferrocytochrome c + 2 H+. Other name(s): ubiquinol cytochrome-c reductase; coenzyme Q-cytochrome c reductase; dihydrocoenzyme Q-cytochrome c reductase; reduced ubiquinone-cytochrome c reductase; complex III (mitochondrial electron transport); ubiquinone-cytochrome c reductase; ubiquinol-cytochrome c oxidoreductase; reduced coenzyme Q-cytochrome c reductase; ubiquinone-cytochrome c oxidoreductase; reduced ubiquinone-cytochrome c oxidoreductase; mitochondrial electron transport complex III; ubiquinol-cytochrome c-2 oxidoreductase; ubiquinone-cytochrome b-c1 oxidoreductase; ubiquinol-cytochrome c2 reductase; ubiquinol-cytochrome c1 oxidoreductase; CoQH2-cytochrome c oxidoreductase; ubihydroquinol:cytochrome c oxidoreductase; coenzyme QH2-cytochrome c reductase; QH2:cytochrome c oxidoreductase; ubiquinol:ferricytochrome-c oxidoreductase. Systematic name: quinol:ferricytochrome-c ...
The SCOP classification for the a domain/subunit 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.
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.
Looking for online definition of respiratory inhibitor in the Medical Dictionary? respiratory inhibitor explanation free. What is respiratory inhibitor? Meaning of respiratory inhibitor medical term. What does respiratory inhibitor mean?
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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 ...
Buy UBIQUINOL 100mg NOW - 60 softgels Online.UBIQUINOL by Now Foods is the reduced form of CoQ-10 (coenzyme Q10). Scientific studies have shown it to be the most bioavailable form of CoQ-10 currently on the market.
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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 ...
However, we found no difference in the AО 42 protein level between the Vps18 Ohw and Ctrl mice (data not shown). HeВ did not give a specific timeframe for a launch в saying only that the tech is working todayв. If you are currently using a Dedicated server and thinking switching to a VPS we recommend to think twice. You will also have to modify the etcopenvpn file later to point to the correctcrt andkey files. Over 90 of the OMIMs operating expenses go to salary support for MD and PhD science writers and biocurators. As a control, how to build a secure linux server expressing GFPвUVRAG dblA at a similar level to WT Free sms server gateway failed to produce any reactivity with the phosphoвspecific antibodies under any condition. How to configure vpn access on server 2008 can get in touch with our fully qualified technical support via Live Chat, Phone, or Hkw around the clock 24x7x365. ProSpecs products are furnished for LABORATORY RESEARCH USE Bild. If not for antimycin A, the yeast might ...
UQCR10 - UQCR10 (untagged)-Human ubiquinol-cytochrome c reductase, complex III subunit X (UQCR10), transcript variant 1 available for purchase from OriGene - Your Gene Company.
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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Please describe the differences between the two respiratory pathways (aerobic and anaerobic.) I would also like to know more about the net ATP generated from.
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. [4] As a lipid-soluble ...
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Autor: Kleessen, S. et al.; Genre: Zeitschriftenartikel; Im Druck veröffentlicht: 2012; Keywords: flux balance analysis|br/|transfer flavoprotein|br/|metabolic networks|br/|carbon metabolism|br/|escherichia-coli|br/|tca cycle|br/|arabidopsis|br/|systems|br/|growth|br/|dehydrogenases; Titel: Model-based Confirmation of Alternative Substrates of Mitochondrial Electron Transport Chain
This page contains the article- A Complex Dietary Supplement Augments Spatial Learning, Brain Mass, and Mitochondrial Electron Transport Chain Activity in Aging Mice http://www.chiro.org/nutrition/ABSTRACTS/A_Complex_Dietary_Supplement_Augments.shtml
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
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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 ...
Electron transport system or Oxidative phosphorylation: Oxidative phosphorylation is conceptually simple and mechanistically complex. It is seen in the lig
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
Biological Oxidation: Mitochondrial ETC components - This chapter includes the Electron Transport chain components - NAD, FAD, Iron-sulphar proteins and etc
Get an answer for Explain the operation of the electron transport chain in the development ATP and find homework help for other Science questions at eNotes
Save 42% Jarrow Formulas - Ubiquinol QH-absorb 100 mg 60 Softgels Ubiquinol QH-absorb 100 mg Reduced Form Co-Q10 High Absorption & Enhanced Stability Q+ Kaneka - Made with Quality Ubiquinol Gluten Free Cells produce Ubiquinol, the active antioxidant state of CoQ10, which is significantly better absorbed, particularly as we age.* QH-absorb® is a proprietary enhanced-stability formula, clinicallly shown in humans to increase Co-Q10 levels by 215% at 100 mg per day and by 777% over baseline at 300 mg per day.
|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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The ribbed mussel Geukensia demissa inhabits intertidal Spartina grass marshes characterized by sulfide-rich sediments. Sulfide poisons aerobic respiration, and G. demissa may cope in this seemingly inhospitable environment by oxidizing sulfide in gill mitochondria. Well-coupled mitochondria isolated from G. demissa gills were used to investigate sulfide oxidation and ATP synthesis. State 3 respiration, maximally stimulated by 5 micromol l(−)(1) sulfide with a P/O ratio of 0.89 and a respiratory control ratio (RCR) of 1.40, remained refractory to sulfide at higher concentrations except in the presence of salicylhydroxamic acid (SHAM), an inhibitor of alternative oxidases. Sulfide-stimulated ATP production was 3-5 times greater than that stimulated by malate and succinate, respectively, giving an ATP/sulfide ratio of 0.63. The inhibition of sulfide-stimulated respiration and ATP production by the complex III inhibitors myxothiazol and antimycin A, respectively, suggests that electrons enter the ...
From UniProt:. Mitochondrial complex III deficiency, nuclear 4 (MC3DN4): A disorder of the mitochondrial respiratory chain resulting in a highly variable phenotype depending on which tissues are affected. Clinical features include mitochondrial encephalopathy, psychomotor retardation, ataxia, severe failure to thrive, liver dysfunction, renal tubulopathy, muscle weakness and exercise intolerance. [MIM:615159]. ...
With the use of a specially developed incubation chamber the rates of motility, respiration, and fructolysis were measured simultaneously on semen samples. By inhibiting the respiration with antimycin A, and/or the fructolysis with 2-deoxyglucose, the rates of each of the two ATP-producing pathways could be reduced independently. In this way the ratio of the amount of free energy produced by respiration and by fructolysis could be varied at will from 1 to 0. In uninhibited preparations approximately 75% of the free energy derives from respiration, and 25% from fructolysis. By the use of the absolute rates of respiration, fructolysis, and motility, the efficiency of the conversion of free energy into hydrodynamic work was calculated. After correction for the decay of the preparation during the experiment, this conversion efficiency was found to be 30-45% lower for free energy from respiration than for free energy from fructolysis. The difference in distribution of the enzymes for fructolysis and ...
Bcl-2 protein family members are central regulators of apoptosis with mitochondrial sites of action. Treatment-refractory cancers from a variety of sites display high expression of the pro-survival Bcl-XL factor. The Bcl-XL inhibitor 2-methoxy antimycin (2-MeAA) is a promising anticancer agent that kills multidrug-resistant tumor cells with high Bcl-XL expression. The selectivity of targeted therapies for tumor cells versus normal cells is often described as a consequence of tumor cell addiction to the targeted activity (e.g. EGFR antagonists). Bcl-XL expression modifies carbon metabolic flux in several cellular contexts. In the case of Bcl-XL, I propose that the molecular basis of "target addiction" is the superposition of a Bcl-XL metabolic function on the different metabolic states characteristic of tumor and normal cells. The primary aim of this project is to test the hypothesis that metabolic profiles of cancer cells and normal cells are modified by Bcl-XL expression in different ways, and ...
The electron transport system occurs in the cristae of the mitochondria, where a series of cytochromes (enzymes) and coenzymes exist. These cytochromes and coen
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There are actually two forms of the antioxidant compound CoQ-10: ubiquinone and ubiquinol. Both must be present for efficient adenosine triphosphate (ATP) production, which occurs in the energy-producing center of the cell known as the mitochondria,
There are actually two forms of the antioxidant compound CoQ-10: ubiquinone and ubiquinol. Both must be present for efficient adenosine triphosphate (ATP) production, which occurs in the energy-producing center of the cell known as the mitochondria,
CanPrev Ubiquinol 100mg DetailsSupports Cardiovascular HealthPowerful AntioxidantReduces the frequency of migrainesGMO FreeGluten, Dairy, Soy, Wheat, Yeast Free Ubiquinol is an active form of Coenzyme Q10 (CoQ10).
CoQ10 finally comes of age with new Ubiquinol! You know all about the heart-healthy benefits of the vitamin-like nutrient CoQ10, also known as ubiquinone, but did you know that our body has to break this nutrient down to create a useable molecule called ubiquinol? In fact, over 90% of the CoQ10 stored in the body is in the form of ubiquinol. Kaneka Nutrients, the worlds leading manufacturer of pharmaceutical-quality, bio-identical CoQ10, recognized this, and after a decade of research and development, they created the first stabilized, bio-identical supplemental form of Ubiquinol. Produced from 100% natural CoQ10 through a biological fermentation process, Kanekas Ubiquinol achieves higher elevations of circulating CoQ10 in the bloodstream with just a fraction of the dose required when using a regular CoQ10 supplement. ...
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Mitochondria are essential for cellular function, providing ATP for energy and regulating a number of key metabolic processes including apoptosis and calcium homeostasis. The consumption of oxygen by the mitochondrial electron transport chain leads to production of ATP but also to release of electrons that can lead to the generation of free radical species and oxidative damage. Thus, proper function and control of mitochondrial is critical. Mitochondrial function has long been thought to be compromised during aging leading to alter physiologic function and age related pathologies. Our work on sarcopenia described above suggests that altered mitochondrial function and increased generation of reactive oxygen species can contribute to the physiologic decline seen in sarcopenia and ALS. However, in other studies we have shown that altered mitochondrial function can have beneficial effects on metabolism. For example, mice lacking Surf1, a mitochondrial electron transport chain protein assembly ...
* found in: Biapenem, Astilbin, Allicin, aqueous solution, Aristolochic Acid B, Aflatoxin B2, Antimycin A, Aflatoxin M1, 7-Aminoactinomycin D, Aztreonam,..
After the Krebs cycle is completed, oxygen enters the respiration pathway as the electron acceptor at the end of the electron transport chain.
We explain Electron Transport Chain with video tutorials and quizzes, using our Many Ways(TM) approach from multiple teachers.|p|This lesson will describe in detail the processes that occur in the ETC phase of cellular respiration.|/p|
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Oligomycin kills NGF-maintained neurons, but protects NGF-deprived, BAF-saved neurons. (A) To determine the effect of oligomycin on Commitment 2, oligomycin (OL
Suggested Use: As a dietary supplement, take 1 or more softgels daily, preferably with a meal, or as directed by your health care professional. Pure Q10 (Ub
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Materials. Na,K-ATPase α1 subunit monoclonal antibody (clone 464.6) was purchased from Upstate Biotechnology (Lake Placid, New York, USA). GLUT1 antibody was purchased from Chemicon (Temecula, California, USA), ouabain from ICN Biomedicals Inc. (Aurora, Ohio, USA), and ebselen from Alexis Biochemicals (San Diego, California, USA). Leupeptin, catalase-polyethylene glycol (PEG-catalase), antimycin A, rotenone, N-acetyl-L-cysteine (NAC), thenoyltrifluoroacetone (TTFA), t-butyl hydroperoxide (t-H2O2), 1,2-dioleoyl-sn-glycerol (DAG), L-α-phosphatidyl-L-serine (PS), and 1,4-diazabicyclo-[2.2.2] octane (DABCO) were purchased from Sigma-Aldrich (St Louis, Missouri, USA). Bisindolylmaleimide I (Bis) and rat brain PKC were purchased from Calbiochem (San Diego, California, USA). Percoll was purchased from Amersham Pharmacia Biotech (Uppsala, Sweden), GFP polyclonal antibody was purchased from Clontech (Palo Alto, California, USA), and A/G PLUS-Agarose was obtained from Santa Cruz Biotech (Santa Cruz, ...
Respiring rat heart mitochondria were loaded with Ca2+ and then treated with Ruthenium Red. The factors affecting the subsequent Ca2+-efflux were studied. Addition of rotenone or antimycin led to a decline of efflux except at pH values above 7.2, provided the load was less than about 80 nmol per mg of protein. Oligomycin reversed the effect of the respiratory inhibitors. Independently of respiration, efflux was stimulated by the uncoupler trifluoromethyltetrachlorbenzimadazole, by mersalyl and by thyroid hormones. The stimulated efflux could be diminished by ADP, with Mg2+ as cofactor if efflux was rapid. With respiration in progress, efflux could be stimulated by N-ethylmaleimide and 5,5′-dithiobis-(2-nitrobenzoate). The effects of mersalyl and of thyroid hormones could be diminished with dithiothreitol. In the absence of stimulating agents, the Ca2+ efflux was proportional to the load up to some critical amount, this critical amount was decreased by the agents. Thyroxine and mersalyl caused ...
Ubiquinol is the reduced (active antioxidant) state of Co-Q10, the form produced by our cells and is significantly better absorbed as a supplement, particularly as we age.* Jarrow FORMULAS® QH-absorb® is a proprietary enhanced stability formula, which has been clinically shown in humans to increase Co-Q10 levels up to 777% (6.14x) over baseline at 300 mg per day intake. QH-absorb Ubiquinol is the reduced (active) form of Co-Q10, the form which is directly used in human metabolism as a lipid-soluble antioxidant. While standard Co-Q10 (ubiquinone) supplements can be activated in the body, this activation can be less efficient in some individuals, based on age or genetics. Ubiquinol also has superior bioavailability to ubiquinone, as demonstrated in clinical trials. QH-absorb utilizes the Q-absorb natural proliposome lipid-soluble delivery system, which has been clinically shown in humans to increase Co-Q10 levels up to 400% (3.2x) over baseline and is 3-4 times better absorbed than
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4-Heptyl-2,2-dimethyl-[1,3]dioxane | C13H26O2 | CID 557799 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
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Antimycin A - WikipediaAntimycin A - Wikipedia

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 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 ... "Antimycin. A Brief Review of Its Chemistry, Environmental Fate, and Toxicology" (PDF). Ott, Kevin. "Antimycin. A Brief Review ...
more infohttps://en.wikipedia.org/wiki/Antimycin_A

Antimycin AAntimycin A

Solvent vehicles are being tested for effective dissolution of the Antimycin A prior to testing its effects with various fish ...
more infohttps://www.usgs.gov/media/images/antimycin-a-1

Antimycin A | C28H40N2O9 - PubChemAntimycin A | C28H40N2O9 - PubChem

Antimycin A , C28H40N2O9 , CID 14957 - structure, chemical names, physical and chemical properties, classification, patents, ...
more infohttps://pubchem.ncbi.nlm.nih.gov/compound/Antimycin_A

antimycin A1 | C28H40N2O9 - PubChemantimycin A1 | C28H40N2O9 - PubChem

antimycin A1 , C28H40N2O9 , CID 12550 - structure, chemical names, physical and chemical properties, classification, patents, ...
more infohttps://pubchem.ncbi.nlm.nih.gov/compound/antimycin_A1

Quercetin Protects Rat L6 Myocytes from Antimycin A-Induced
Mitochondrial Dysfunction | OMICS InternationalQuercetin Protects Rat L6 Myocytes from Antimycin A-Induced Mitochondrial Dysfunction | OMICS International

We used Antimycin-A to induce cell death in myocyte through mitochondrial dysfunction. We then determined the dose and time of ... Quercetin, Antimycin-A and DMSO were obtained from Sigma Chemical Co (St Louis, MO). PenStrep and DMEM medium were obtained ... Quercetin Protects Rat L6 Myocytes from Antimycin A-Induced Mitochondrial Dysfunction Vijay M Kale* College of Pharmacy, ... Antimycin-A (AMA) damages the mitochondria through inhibition of mitochondrial electron transport. The present study sought to ...
more infohttps://www.omicsonline.org/open-access/quercetin-protects-rat-l6-myocytes-from-antimycin-ainducedmitochondrial-dysfunction-2161-1459-1000202.php?aid=67188

Reversed-phase thin-layer chromatography of homologs of Antimycin-A and related derivativesReversed-phase thin-layer chromatography of homologs of Antimycin-A and related derivatives

Although a base-line resolution of the known four major antimycins Al, A2, A3, and A4 was readily achieved with mobile phases ... a mixture of antimycins A was separated into eight hitherto unreported subcomponents, Ala, Alb, A2a, A2b, A3a, A3b, A4a, and ... Reversed-phase thin-layer chromatography of homologs of Antimycin-A and related derivatives. Journal of Chromatography By:. ... Although a base-line resolution of the known four major antimycins Al, A2, A3, and A4 was readily achieved with mobile phases ...
more infohttps://pubs.er.usgs.gov/publication/1003129

Essay on Antimycin - 648 WordsEssay on Antimycin - 648 Words

How Antimycin Affects the Function of Mitochondria. First, antimycin A binds to the Q site of cytochrome c reductase, ... Antimycin is a mitochondrial inhibitor which is involved in the energy-coupling site of the respiratory system. Antimycin A ... Antimycin Topics: Cellular respiration, Oxidative phosphorylation, Adenosine triphosphate Pages: 3 (648 words) Published: ... Antimycin is now used as a commerical fish toxicant and is the active ingredient in Fintrol, a commerical piscicide used in ...
more infohttp://www.studymode.com/essays/Antimycin-1189703.html

Antimycin A treatment decreases respiratory internal rotenone-insensitive NADH oxidation capacity in potato leaves | BMC Plant...Antimycin A treatment decreases respiratory internal rotenone-insensitive NADH oxidation capacity in potato leaves | BMC Plant...

Desiree) were sprayed with antimycin A, an inhibitor of the cytochrome pathway. Enzyme capacities of NAD(P)H dehydrogenases (EC ... We report a specific decrease in internal rotenone-insensitive NADH dehydrogenase capacity in mitochondria from antimycin A- ... The internal rotenone-insensitive NADH oxidation decreases after antimycin A treatment of potato leaves. However, the decrease ... With the 30 μM antimycin A treatment, the rates were completely insensitive to in vitro addition of antimycin A (data not shown ...
more infohttps://bmcplantbiol.biomedcentral.com/articles/10.1186/1471-2229-4-8

Antimycin A | CTDAntimycin A | CTD

Antimycin A CAS Type 1 Name Butanoic acid, 2(or 3)-methyl-, 3-((3-(formylamino)-2-hydroxybenzoyl)amino)-8-hexyl-2,6-dimethyl-4, ... Antimycin A1 has been used as a fungicide, insecticide, and miticide. (From Merck Index, 12th ed). ...
more infohttp://ctdbase.org/detail.go?type=chem&acc=D000968

Mechanisms involved in the inhibition of glycolysis by cyanide and antimycin A in Candida albicans and its reversal by hydrogen...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 ... MECHANISMS INVOLVED IN THE INHIBITION OF GLYCOLYSIS BY CYANIDE AND ANTIMYCIN A IN CANDIDA ALBICANS AND ITS REVERSAL BY HYDROGEN ... to an activity by which H2O2 can be reduced by electrons flowing from NADH through a pathway that can be inhibited by antimycin ...
more infohttp://www.ifc.unam.mx/publications/mechanisms-involved-inhibition-glycolysis-cyanide-antimycin-candida-albicans-reversal-hydrogen-peroxide-common-feature-candida-species

Alternative pathway activity. Antimycin A-insensitive o | Open-iAlternative pathway activity. Antimycin A-insensitive o | Open-i

Antimycin A-insensitive oxidation of NADPH, NADH and succinate was measured to oxygen in the presence of DTT and pyruvate to ... With the 30 μM antimycin A treatment, the rates were completely insensitive to in vitro addition of antimycin A (data not shown ... With the 30 μM antimycin A treatment, the rates were completely insensitive to in vitro addition of antimycin A (data not shown ... Antimycin A-insensitive oxidation of NADPH, NADH and succinate was measured to oxygen in the presence of DTT and pyruvate to ...
more infohttps://openi.nlm.nih.gov/detailedresult.php?img=PMC424582_1471-2229-4-8-3&req=4

Differential growth inhibition of human diploid fibroblasts by 2-deoxyglucose and antimycin A with ageing in vitro. - Semantic...Differential growth inhibition of human diploid fibroblasts by 2-deoxyglucose and antimycin A with ageing in vitro. - Semantic...

A marked age-dependent response was observed with 2-deoxyglucose but not with antimycin A. The results confirm an increase in ... The relative growth inhibitory effects of 2-deoxyglucose and antimycin A were monitored at five stages during the life-span in ... The relative growth inhibitory effects of 2-deoxyglucose and antimycin A were monitored at five stages during the life-span in ... A marked age-dependent response was observed with 2-deoxyglucose but not with antimycin A. The results confirm an increase in ...
more infohttps://www.semanticscholar.org/paper/Differential-growth-inhibition-of-human-diploid-by-Bittles-Baum/83bc5635fab6849c608f44caee0fb078c8663b62

The Toxoplasma Blog: Genetic Evidence for Cytochrome b Qi Site Inhibition by 4(1H)-quinolone-3-diarylethers and Antimycin in...The Toxoplasma Blog: Genetic Evidence for Cytochrome b Qi Site Inhibition by 4(1H)-quinolone-3-diarylethers and Antimycin in...

Genetic Evidence for Cytochrome b Qi Site Inhibition by 4(1H)-quinolone-3-diarylethers and Antimycin in Toxoplasma gondii ... to possess a Thr222-Pro amino acid substitution that confers 49-fold resistance to ELQ-316 and 19-fold resistance to antimycin ...
more infohttp://toxoplasmaparasite.blogspot.com/2016/12/genetic-evidence-for-cytochrome-b-qi.html

Scutellaria baicalensis Extracts and Flavonoids Protect Rat L6 Cells from Antimycin A-Induced Mitochondrial Dysfunction - omicXScutellaria baicalensis Extracts and Flavonoids Protect Rat L6 Cells from Antimycin A-Induced Mitochondrial Dysfunction - omicX

Antimycin A (AMA) damages mitochondria by inhibiting mitochondrial electron transport and can produce reactive oxygen species ( ... Antimycin A (AMA) damages mitochondria by inhibiting mitochondrial electron transport and can produce reactive oxygen species ( ... Scutellaria baicalensis Extracts and Flavonoids Protect Rat L6 Cells from Antimycin A-Induced Mitochondrial Dysfunction. ... Scutellaria baicalensis Extracts and Flavonoids Protect Rat L6 Cells from Antimycin A-Induced Mitochondrial Dysfunction ...
more infohttps://omictools.com/39348c8f66b0c6cff0344584d3cb0191-protocol

Iron in the structure of Stigmatellin and Antimycin Bound Cytochrome BC1 Complex From Chicken (pdb 3h1i)Iron in the structure of Stigmatellin and Antimycin Bound Cytochrome BC1 Complex From Chicken (pdb 3h1i)

Stigmatellin and Antimycin Bound Cytochrome BC1 Complex From Chicken ... The binding sites of Iron atom in the structure of Stigmatellin and Antimycin Bound Cytochrome BC1 Complex From Chicken (pdb ... Iron in the structure of Stigmatellin and Antimycin Bound Cytochrome BC1 Complex From Chicken (pdb 3h1i). ...
more infohttp://iron.atomistry.com/pdb3h1i.html

SIGMA-ALDRICH -  Grainger Industrial SupplySIGMA-ALDRICH - Grainger Industrial Supply

Antimycin A, Contain 100mg. Brand. SIGMA-ALDRICH. Item #. 45ZE33. Mfr. Model #. A8674-100MG ...
more infohttps://www.grainger.com/category/brand/sigma-aldrich

Agonists, activators, antagonists and inhibitors | AbcamAgonists, activators, antagonists and inhibitors | Abcam

We supply a range of high quality GPCR neurotransmitter ligands, modulators of ligand and voltage-gated ion channels. Find small molecules for your research
more infohttps://www.abcam.com/tag/biochemicals

Products in Biologically Active Small Molecules, Cayman Chemical, UN2811 on Thomas ScientificProducts in Biologically Active Small Molecules, Cayman Chemical, UN2811 on Thomas Scientific

found in: L-779,450, KT195, Citreoviridin, Flibanserin, Antimycin A1, PF-06447475, Colcemid, Epinastine (hydrochloride), ... Antimycin A1 Cayman Chemical. An antibiotic that inhibits complex III of the mitochondrial ETC, preventing electron transport ...
more infohttps://www.thomassci.com/nav/cat1/biologicallyactivesmallmolecules/manufacturer/caymanchemical/unnumber/un2811/0

Products in LKT Labs on Thomas ScientificProducts in LKT Labs on Thomas Scientific

found in: Biapenem, Astilbin, Allicin, aqueous solution, Aristolochic Acid B, Aflatoxin B2, Antimycin A, Aflatoxin M1, 7- ... Antimycin A LKT Labs. Antimycin A was initially produced by Streptomyces. Antimycin A binds cytochrome c reductase, inhibiting ... Antimycin A is used in research models to study mitochondrial respiration and superoxide production. Grade: ≥98% ...
more infohttp://www.thomassci.com/nav/manufacturer/lktlabs/0

Invasive Species | USGS.govInvasive Species | USGS.gov

Comparative Freshwater Fish Toxicity Testing of Antimycin A Researchers are investigating the influence of Antimycin A on Asian ...
more infohttps://www.usgs.gov/centers/wetland-and-aquatic-research-center-warc/science/invasive-species

nature.com searchnature.com search

A New Antibiotic, Antimycin A9, Produced by Streptomyces sp. K01-0031 *Kazuro Shiomi ... Rights & permissionsfor article A New Antibiotic, Antimycin A,sub,9,/sub,, Produced by ,i,Streptomyces,/i, sp. K01-0031 . Opens ...
more infohttp://www.nature.com/search?author=%22Hiroko+Hatano%22&error=cookies_not_supported&code=4d5a69c7-4a95-4c44-bdb8-a3dcde60e1ce

Mitochondrial Electron Transport Chain InhibitorsMitochondrial 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.
more infohttps://www.biovision.com/products/enzyme-inhibitors/mitochondrial-electron-transport-chain-inhibitors.html

Activation of cyclic electron flow by hydrogen peroxide in vivo | PNASActivation of cyclic electron flow by hydrogen peroxide in vivo | PNAS

H2O2 Activates the Antimycin A-Insensitive Pathway.. H2O2-induced CEF was insensitive to antimycin A (Fig. 2B). In addition, ... Infiltration with 20 μM antimycin A was carried out in darkness for 3 h. Successful antimycin A infiltration was confirmed by ... 2B, ANCOVA, P , 0.05, n = 3), well above the observed Ki for inhibition of the antimycin A-sensitive pathway of CEF (51). These ... Infiltration of Leaves with H2O2, Methyl Viologen, and Antimycin A.. To determine the effects of H2O2 on CEF, Col-0 leaves were ...
more infohttps://www.pnas.org/content/112/17/5539?ijkey=132a8a136e1ab95f8d7583cdf86da65d7e705a9a&keytype2=tf_ipsecsha
  • Although a base-line resolution of the known four major antimycins Al, A2, A3, and A4 was readily achieved with mobile phases containing acetate buffers, the separation of the new antibiotic subcomponents was highly sensitive to variation in mobile phase conditions. (usgs.gov)
  • 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. (unam.mx)
  • The internal rotenone-insensitive NADH oxidation decreases after antimycin A treatment of potato leaves.However, the decrease is not due to changes in expression of known nda genes.One consequence of the lower NADH dehydrogenase capacity may be a stabilisation of the respiratory chain reduction level, should the overall capacity of the cytochrome and the alternative pathway be restricted. (nih.gov)
  • Antimycin A-insensitive oxidation of NADPH, NADH and succinate was measured to oxygen in the presence of DTT and pyruvate to assure maximum rates. (nih.gov)
  • H 2 O 2 -dependent CEF was not sensitive to antimycin A or loss of PGR5, indicating that increased CEF probably does not involve the PGR5-PGRL1 associated pathway. (pnas.org)
  • Researchers are investigating the influence of Antimycin A on Asian carp and non-target fishes by measuring the effects of a novel species-specific bait formulation. (usgs.gov)
  • Solvent vehicles are being tested for effective dissolution of the Antimycin A prior to testing its effects with various fish species' blood. (usgs.gov)
  • In aquaculture, Antimycin A is used as an agent to enhance catfish production via selective killing small and more sensitive species. (wikipedia.org)
  • However at 10 ppb, Antimycin A is used as a selective killing agent to kill smaller or more sensitive species that may reduce the yield of commercial farming. (wikipedia.org)
  • Antimycin A is the active ingredient in Fintrol, a chemical piscicide (fish poison) used in fisheries management. (wikipedia.org)
  • Antimycin A was first discovered in 1945 and registered for use as a fish toxicant in 1960. (wikipedia.org)
  • In the early 1960s, it was discovered that antimycin was toxic to fish which led to it being used in many fishery conservation projects across North America. (studymode.com)
  • Antimycin is now used as a commerical fish toxicant and is the active ingredient in Fintrol, a commerical piscicide used in fisheries management and in the catfish industry. (studymode.com)