Captopril ameliorates toxicity induced by paraquat in mitochondria isolated from the rat liver.

The aim of the present study was to show the abilities of captopril as a thiol ACEi (angiotensin converting enzyme inhibitor), on mitochondria toxicity due to paraquat. Mitochondrial isolation from rat liver was divided into 4 groups. Group 1 was considered as control, group 2 received paraquat (5 mM), group 3 received captopril (0.08 mM) and group 4 received paraquat (5 mM)+captopril (0.08 mM). Lipid peroxidation, catalase activity, GSH (reduced glutathione) and GSSG (oxidized glutathione) concentrations were determined in isolated rat liver mitochondria. Simultaneous treatment of mitochondria with captopril (0.08 mM)+paraquat (5 mM) significantly ameliorate the mitochondria toxicity induced by paraquat (5 mM) alone. The results confirm antioxidant effect of captopril. This effect appears to be attributable to the Sulfhydryl Groups (SH) in the compound which may be due to captopril abilities to scavenge reactive oxygen species. The results indicate that captopril may prevent oxidative stress induced by paraquat.