PROTECTIVE EFFECTS OF RUTIN ON SODIUM ARSENITE-INDUCED HEPATO-RENAL TOXICITY IN WISTAR RATS
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Sodium arsenite is a toxic metalloid compound widely distributed in the environment through contaminated water, industrial effluents, and pesticides. Exposure to arsenic compounds has been associated with severe oxidative damage, particularly affecting the liver and kidneys. This study investigated the protective effect of rutin, a natural flavonoid with potent antioxidant properties, on sodium arsenite–induced hepato-renal toxicity in Wistar rats. Thirty-five (35) male Wistar rats were randomly divided into five groups of seven animals each. Group 1 served as the control and received corn oil only; Group 2 received 50mg/kg of rutin dissolved in distilled water; Group 3 received sodium arsenite (10 mg/kg body weight) dissolved in distilled water; Group 4 received rutin (25 mg/kg) and sodium arsenite (10 mg/kg) and; while Group 5 received rutin (50 mg/kg) and sodium arsenite (10 mg/kg). After the treatment period, blood samples were collected for biochemical analysis of liver and kidney function biomarkers- aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), urea, and creatinine. The results showed that sodium arsenite administration caused a significant increase (p < 0.05) in serum levels of AST, ALT, ALP, LDH, urea, and creatinine compared to the control group, indicating hepatic and renal impairment. However, co-administration of rutin led to a dose-dependent decrease in these biomarkers, bringing their values closer to the normal range. This suggests that rutin effectively mitigated the biochemical alterations induced by sodium arsenite. In conclusion, the findings demonstrate that rutin possesses potent antioxidant and protective properties capable of ameliorating sodium arsenite–induced liver and kidney toxicity in Wistar rats. This implies that rutin may have potential therapeutic applications in preventing heavy-metal-induced oxidative damage in humans.
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