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Abstract

Iron overload has toxic effects on the body. Hepatotoxicity is a common finding in iron-overloaded patients, resulting from iron deposition in hepatocytes. Angiotensinɪɪ is involved in developing hepatic damage through its prooxidative properties. Therefore, the current study aimed to investigate the therapeutic effect of the ACE inhibitor, lisinopril, against ferrous sulfate-induced hepatic functional disorders and histological damages in rats, due to its inhibitory effect on angiotensin II and its ability to scavenge free radicals in-vitro. 23 male adult rats were randomly classified into three groups and treated as follows: Normal control group: received daily 1 ml/day distilled water as an intraperitoneal injection for 14 days, Iron overload non-treated group: received ferrous sulfate at a daily dose of 30 mg/kg/day i.p. for 14 days, Iron overload treated with lisinopril group: received ferrous sulfate at a dose of 30 mg/kg/day followed by lisinopril at a dose of 1 mg/kg/day daily i.p. for 14 days. Compared to the control group, administration of ferrous sulfate resulted in liver dysfunction, as evidenced by significantly higher serum hepatic markers levels, increased malondialdehyde levels, and histological damages. Treatment with lisinopril significantly reversed the elevated serum hepatic enzyme levels and lipid peroxidation marker in the liver. All these changes were corroborated by histological observations of the liver (P<0.05). Our study suggests that lisinoprilprotects against iron overload-induced hepatotoxicity through inhibition of lipid peroxidation.