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Journal of Kerman University of Medical Sciences. 2006; 13 (3): 132-140
in Persian | IMEMR | ID: emr-77870

ABSTRACT

The aim of the present study was to show the capability of captopril as a thiol ACEi [angiotensin converting enzyme inhibitor], in suppressing mitochondrial toxicity due to paraquat. In this study, rats liver mitochondria were isolated with buffer using refrigerated centrifuge. In order to obtain the minimum toxic dose of paraquat and the effective dose of captopril, different concentrations of paraquat [1 to 100mM]and captopril [0.08 to 1mM]were investigated by determining LC [50], viability indices, lipid peroxidation, mitochondrial swelling, catalase activity, GSH and GSSG. Simultaneous treatment of mitochondria with captopril [0.08mM] and paraquat [5mM] significantly ameliorate the mitochondrial toxicity of paraquat [5mM] alone. Our results show that captopril is a effective antioxidant. The antioxidative action of captopril appears to be attributable to the sulphahydryl group [SH] in the compound. This effect may be due to captopril abilities to scavenge reactive oxygen species. Our results indicate that Captopril can ameliorate oxidative stress induced by paraquat and therefore, can be used for the prevention and treatment of diseases caused by environmental toxins


Subject(s)
Animals , Paraquat/toxicity , Mitochondria, Liver , Oxidative Stress , Rats
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