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Uncouplers, mitochondrial

Crompton, M., McGuinness, O. and Nazareth, W. (1992). The involvement of cyclosporin A binding proteins in regulating and uncoupling mitochondrial energy transduction. Biochim. Biophys. Acta. 1101, 214. [Pg.70]

Leite AZ, Sipahi AM, Damiao AO, Coelho AM, Garcez AT, Machado MC, Buchpiguel CA, Lopasso FP, Lordello ML, Agostinho CL, Laudanna AA Protective effect of metronidazole on uncoupling mitochondrial oxidative phosphorylation induced by NSAID A new mechanism. Gut 2001 48 163-167. [Pg.65]

The major types of adipose tissue are (1) white adipose tissue, which manufactures, stores, and releases lipid and (2) brown adipose tissue, which dissipates energy via uncoupled mitochondrial respiration. Obesity research includes evaluation of the activity of adrenergic receptors and their effect on adipose tissue with respect to energy storage and expenditure or thermogenesis. [Pg.676]

Certain foreign compounds can cause changes in body temperature, which may become a toxic response if they are extreme. Substances such as 2,4-dinitrophenol and salicylic acid will raise body temperature, as they uncouple mitochondrial oxidative phosphorylation. Thus, the energy normally directed into ATP during oxidative phosphorylation is released as heat. Substances that cause vasodilation may cause a decrease in body temperature. [Pg.236]

Uncouplers. Uncouplers dissociate electron transport from photophosphorylation. Both noncyclic and cyclic phosphorylation are inhibited, but electron transport reactions are either unaffected or stimulated. Because uncouplers relieve the inhibition of electron transport imposed by energy transfer inhibitors, they are considered to act at a site closer to the electron transport chain than the site of phosphate uptake. In Figure 2, they are shown (site 2) as dissipating some form of conserved energy represented as on the noncyclic and cyclic ATP-gener-ating pathways. Perfluidone is the only herbicide identified to date that functions as a pure uncoupler at pH 8.0 (2). Compounds that uncouple photophosphorylation also uncouple mitochondrial oxidative phosphorylation. [Pg.64]

PFOA is thought to induce peroxisome proliferation and interfere with mitochondrial metabolic pathways. Direct measurements revealed that PFOA uncouple mitochondrial respiration by increasing... [Pg.1939]

The belief that alcoholics are more susceptible to the toxicity of 2,4-DNP during occupational exposure (Perkins 1919) may indicate an interaction with ethanol (and possibly other alcohols) or it may simply be a function of the compromised physiological state of alcoholics. 2,4-DNP appears to markedly increase the rate of ethanol metabolism in rat liver slices by 100-160% (Videla and Israel 1970) and in rats in vivo by 20-30% (Israel et al. 1970). Because 2,4-DNP uncouples mitochondrial electron transport from oxidative phosphorylation, the oxidation of NADH to NAD is accelerated in the mitochondria. Reoxidation of NADH rather than the activity of alcohol dehydrogenase is the rate-limiting step in the metabolism of ethanol, and, therefore, the metabolic effect of 2,4-DNP enhances the clearance of ethanol (Eriksson et al. 1974). Because 2,4-DNP is known to augment the rate of respiration and perspiration, 2.7-8.2% of the initial dose of ethanol was also eliminated by expiration and cutaneous evaporation in the rat (Israel et al. 1970). [Pg.139]

Two mechanisms for the toxicity of 6-OHDA have been proposed. First, auto-oxidation could generate ROS and subsequently oxidize unsaturated fatty acids of lipids or thiol groups of proteins. Second, 6-OHDA uncouples mitochondrial oxidative phosphorylation (Wagner and Trendelenburg, 1971). Whether the neurotoxicity of 6-OHDA can be attributed to the production of ROS or dihydroxyindoles (for a review, see Thoe-nen and Tranzer, 1973) is not yet defined. Degeneration of nigrostriatal neurons after intracerebral injections of 6-OHDA to rats is potentiated by administration of iron (Ben-Shachar and Youdim,... [Pg.461]

Arsenate (pentavalent) uncouples mitochondrial oxidative phosphorylation by a mechanism whereby arsenate substitutes for inorganic phosphate in the formation of ATP, with subsequent formation of an unstable arsenate ester that is hydrolyzed rapidly. This process is termed arsenolysis. [Pg.1138]

However, an indirect effect on MTs has been proposed for dinitro-anilines and amiprophos-methyl mediated by effects on Ca " levels. Dinitroanilines were shown to inhibit Ca uptake by mitochondria, thus possibly increasing cytoplasmic Ca ", which would inhibit tubulin polymerization. Propham and chlorpropham also inhibited uptake by mitochondria, but less so than the dinitroanilines. Therefore, an indirect effect on MT asssembly and function cannot be excluded for the N-phenylcarbamates. A possible mechanism by which the iV-phenylcarba-mates could affect Ca levels has already been discussed—namely, a direct or indirect effect on electron transport (Section 5.1). There are also several reports that dinitroanilines can inhibit or uncouple mitochondrial electron transport. [Pg.148]

Many inhibitors of substrate oxidations, substrate transport, electron transport, and ATP synthesis are known including many well-known toxins (see Sherratt, 1981 Harold, 1986 Nicholls and Ferguson, 1992). These are not discussed here except to mention specific uncouplers of oxidative phosphorylation. Classic uncouplers such as 2,4-dinitrophenol have protonated and unprotonated forms, both of which are lipid soluble and cross the inner mitochondrial membrane discharging the proton gradient. This prevents ATP synthesis and stimulates respiration. [Pg.135]

Uncouplers of oxidative phosphorylation Compounds that uncouple oxidative phosphorylatiou from electron transport in the inner mitochondrial membrane. Most are weak lipophilic acids that can run down the proton gradient across this membrane. [Pg.334]

Uncouplers (eg, dinitrophenol) are amphipathic (Chapter 14) and increase the petmeabihty of the lipoid inner mitochondrial membrane to protons (Figure 12—8), thus teducing the electtochemical potential and shott-citcuiting the ATP synthase. In this way, oxidation can proceed without phosphotylation. [Pg.97]

Nucleic acids are not the only biomolecules susceptible to damage by carotenoid degradation products. Degradation products of (3-carotene have been shown to induce damage to mitochondrial proteins and lipids (Siems et al., 2002), to inhibit mitochondrial respiration in isolated rat liver mitochondria, and to induce uncoupling of oxidative phosphorylation (Siems et al., 2005). Moreover, it has been demonstrated that the degradation products of (3-carotene, which include various aldehydes, are more potent inhibitors of Na-K ATPase than 4-hydroxynonenal, an aldehydic product of lipid peroxidaton (Siems et al., 2000). [Pg.330]

FIGURE 8.9 Mitochondrial 02 and H2S consumption from non-limiting 02 to anoxic conditions, (a) Isolated mitochondria were exposed to repeated bouts of 12.5 pM H2S until anoxia was achieved, (b) At higher 02 levels, both 02 and H2S consumption events are coincident, but as the 02 levels decline the events become uncoupled and 02 consumption is limited first. The multiphasic kinetics of 02 consumption may result from transient inhibition of cytochrome c oxidase by H2S. Under anoxia, H2S consumption continues at a low level (after [36] reproduced with permission of the Company of Biologists). [Pg.253]

Casteilla et al. [26] suggested that mitochondrial superoxide production is modulated by uncoupling proteins. It has also been proposed [27] that the production of superoxide by... [Pg.751]

Uncoupling is a specific toxic effect that takes place in energy-transducing membranes (photosynthetically active membranes, inner mitochondrial... [Pg.239]


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See also in sourсe #XX -- [ Pg.71 ]




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