Di-n-butyltindichloride uncouples oxidative phosphorylation in rat liver mitochondria.
In this study di-n-butyltindichloride (DBTC) was found to inhibit alpha-ketoacid-stimulated response of rat liver mitochondria to the addition of ADP and the uncoupler carbonyl cyanide p-trifluoromethoxyphenyl hydrazone (FCCP). The alpha-ketoglutarate oxidation was already inhibited at a level of 0.8 nmol DBTC/mg protein. When succinate was used as substrate together with rotenone, the State 3 and FCCP stimulated oxidation were not inhibited by DBTC. But from a level of 8.3 nmol DBTC/mg protein, the State 4 respiration was increased. It is concluded that in low amounts DBTC specifically blocks alpha-ketoacid dehydrogenases, but higher concentrations of this compound uncouples oxidative phosphorylation. However, this uncoupling will be masked when the NADH production from substrate oxidation is decreased by DBTC as will be in case of alpha-ketoacids.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism*; D009947:Organotin Compounds / Q000633:toxicity*; D010085:Oxidative Phosphorylation / Q000187:drug effects*; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D014475:Uncoupling Agents / Q000633:toxicity*
D009947:Organotin Compounds; D014475:Uncoupling Agents; D000244:Adenosine Diphosphate; C020735:dibutyldichlorotin