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- W103632922 abstract "Chloroethanols are toxic chemicals used in the industry and also formed as a result of the metabolism of several widely used halogenated hydrocarbons. The effect of 2-chloroethanol (CE), 2,2-dichloroethanol (DCE) and 2,2,2-trichloroethanol (TCE) on rat liver mitochondrial respiration was studied. Rat liver mitochondria were prepared in a mitochondrial isolation medium consisting of 250 mM sucrose, 10 mM Tris-HCl and 1 mM EDTA. Respiration of the mitochondrial suspension was determined with an oxygen electrode at 25C and the polarographic buffer consisted of 250 mM mannitol, 10 mM KCl, 10 mM K{sub 2}HPO{sub 4}, 5 mM MgCl{sub 2}, 0.2 mM EDTA and 10 mM Tris-HCl. With succinate as the respiratory substrate and using chloroethanols, CE stimulated respiration by 28.2 {plus minus} 6.5% and DCE by 202.7 {plus minus} 8.2% while TCE inhibited mitochondrial respiration. The effect of change in the concentration of chloroethanols on mitochondrial respiration was also studied. CE showed maximum stimulation at 600 mM, DCE at 150 mM and TCE at 30 mM. Respiratory stimulation was independent of mitochondrial protein concentration. Chloroethanols inhibited mitochondrial respiration when glutamate-malate was used as the respiratory substrate. Estimation of adenosine triphosphate (ATP) generation showed that chloroethanols inhibited the synthesis of ATP. These results indicatemore » that chloroethanols stimulate mitochondrial respiration by uncoupling oxidative phosphorylation and that the uncoupling potency is proportional to the extent of chlorination.« less" @default.
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- W103632922 date "1991-03-11" @default.
- W103632922 modified "2023-09-28" @default.
- W103632922 title "Uncoupling of oxidative phosphorylation in rat liver mitochondria by chloroethanols" @default.
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