Abstract
The organochloride insecticide DDT (2,2-bis(p-chlorophenyl)-1,1-trichloroethane) depresses the phosphorylation efficiency of mitochondria as inferred from the decrease of respiratory control ratio (RCR) and P/O ratio, perturbations of transmembrane potential (delta psi) fluctuations associated with mitochondrial energization and phosphorylative cycle induced by ADP. DDT depresses the delta psi developed by energized mitochondria and prevents complete repolarization, that is delayed and resumed at a lower rate. The inhibitory action of DDT on phosphorylation efficiency may result from: (1) a direct effect on the ubiquinol-cytochrome c segment of the redox chain; (2) direct action on the ATP-synthetase complex; (3) partial inhibition of the phosphate transporter. DDT preferentially interacts with phosphorylation process in relation to respiration. High concentrations of DDT induce destruction of the structural integrity of mitochondria.
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