Effect of naringenine on oxidative damage and apoptosis in liver and kidney in rats applied chronic mercury chloride

Mercury chloride is a heavy metal type that causes the formation of free radicals, causing hepatotoxicity, nephrotoxicity and apoptosis. In this study, the effects of naringenin on oxidative stress and apoptosis in liver and kidney of rats exposed to mercury chloride were investigated. In the study, 41 male 2-month-old Wistar-Albino rats were divided into 5 groups. 1st group; control group, group 2; naringenin-100, group 3; mercury chloride, group 4; mercury chloride + naringenin-50, group 5; mercury chloride + naringenin-100. 1 ml/kg saline i.p. to the control, 0.4 mg/kg/day mercury (II) chloride i.p. to the second group, 50 and 100 mg/kg naringenin prepared in corn oil was given by gavage to naringenin groups, applications lasted for 20 days. At the end of the applications; when mercury chloride and the control group were compared, increase in plasma urea and in plasma, liver and kidney MDA levels and decrease in GSH levels were observed (p<0.001). Increase in kidney (p<0.001) and blood (p<0.01) SOD, kidney (p <0.001) and blood GSH-Px (p<0.01) and kidney GST activities (p<0.001), decrease in liver CAT activity (p<0.01), histopathological changes and increase in caspase-3 levels detected (p<0.05). When treatment groups and mercury chloride were compared, naringenin; decreased the AST, ALT, LDH (p<0.01), urea and creatinine in plasma, the MDA levels in liver, kidney and plasma, and both naringenin doses in blood, 100 mg/ kg naringenin in liver and kidney increased above control values GSH levels (p<0.001). Naringenin decreased kidney and blood SOD, blood and kidney GSH-Px, kidney GST activities (p<0.001), histopathological changes and caspase-3 (p<0.05). In conclusion it has been determined that naringenin is protective and therapeutic against oxidative damage and apoptosis in liver and kidney, and 100 mg/kg naringenin is more effective in preventing histopathological changes and apoptosis.