Aflatoxin B1 (AFB1) and G1 (AFG1) have been evaluated for activity toward energy-linked reduction of endogenous nicotinamide nucleotides by succinate and vitamin K3 during anaerobic reversed electron transfer in isolated rat liver mitochondria. These toxins induced a concentration-dependent inhibition involving three possible sites: succinate dehydrogenase, ATPase, and the reaction sequence between respiratory complex 1 and the nonphosphorylated high-energy intermediate or state (X∼I or ΔψH−). AFG1 appears slightly more potent than AFB1. These findings are discussed in terms of the mechanisms of aflatoxin involvement with mitochondrial oxidative phosphorylation.
Biochemical Medicine 09/1981; 26(1):1-7. DOI:10.1016/0006-2944(81)90023-5