Abstract
Objective: Cadmium chloride is an environmental pollutant, known for inducing cytotoxicity via oxidative stress, DNA damage and apoptotic activities. This study evaluated the hepatoprotective potentials of L-arginine against cadmium-chloride induced toxicity in adult Wistar rats.
Methods: Twenty-five (25) adult Wistar rats were randomized into five groups (n=5): a control group given standard rat chow and water ad libitum; a toxicant group administered cadmium chloride orally at 5 mg/kg body weight/day; and two treatment groups receiving cadmium chloride (5 mg/kg) co-administered orally with L-arginine at 100, and 200 mg/kg body weight/day, respectively and a positive control group administered 200 mg/kg L-arginine only, for twenty-eight days. Hepatotoxicity was assessed via histopathological examination of liver tissue, evaluation of hepatic functional parameters notably serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase activities, Also, antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase were assessed alongside hepatic malondialdehyde levels.
Results: Co-administration of L-arginine attenuated inflammatory changes and preserved hepatic architecture, with the high dose showing near-complete tissue recovery, significantly reduced serum alanine aminotransferase and aspartate aminotransferase levels, decreasing malondialdehyde concentrations, and restored antioxidant enzyme activities.
Conclusion: These findings demonstrate that oral L-arginine at high dose significantly ameliorates cadmium chloride-induced hepatotoxicity by restoring antioxidant defense and suppressing oxidative damage, supporting its potential as a possible therapeutic agent in heavy metal-induced hepatoxicity.