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.