The mode of action of p,p'=DDT on mammalian mitochondria.
In rats treated with single, sublethal doses of p,p'-DDT oxidative phosphorylation efficiency, respiratory activity and "latent" ATPase activity in liver and brain mitochondria were determined. A time- and dose-dependent decrease in oxidative phosphorylation efficiency was found. Time-dependent suppression of respiratory activity in state 3 was noticed and a stimulation of mitochondrial ATPase activity 24 h after DDT treatment in liver and brain mitochondria was found. The correlation between time-dependent changes in the brain mitochondrial fraction and distribution of DDT in brain after a single, oral dose is discussed. It is suggested that changes in mitochondria were caused by DDT and its metabolites. It is concluded that the uncoupling of oxidative phosphorylation especially in brain mitochondria could be responsible for some DDT intoxication symptoms in mammals.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D003634:DDT / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D008297:Male; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects*; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D013997:Time Factors
D003634:DDT; D000251:Adenosine Triphosphatases