Ameliorative effects of glycine on cobalt chloride‐induced hepato‐renal toxicity in rats

BACKGROUND: The important roles of liver and kidney in the elimination of injurious chemicals make them highly susceptible to the noxious activities of various toxicants including cobalt chloride (CoCl(2)). This study was designed to investigate the role of glycine in the mitigation of hepato‐renal toxicities associated with CoCl(2) exposure. METHODS: Forty‐two (42) male rats were grouped as Control; (CoCl(2); 300 ppm); CoCl(2) + Glycine (50 mg/kg); CoCl(2) + Glycine (100 mg/kg); Glycine (50 mg/kg); and Glycine (100 mg/kg). The markers of hepatic and renal damage, oxidative stress, the antioxidant defense system, histopathology, and immunohistochemical localization of neutrophil gelatinase associated lipocalin (NGAL) and renal podocin were evaluated. RESULTS: Glycine significantly reduced the markers of oxidative stress (malondialdehyde content and H(2)O(2) generation), liver function tests (ALT, AST, and ALP), markers of renal function (creatinine and BUN), and decreased the expression of neutrophil gelatinase‐associated lipocalin (NGAL) and podocin compared with rats exposed to CoCl(2) toxicity without glycine treatment. Histopathology lesions including patchy tubular epithelial necrosis, tubular epithelial degeneration and periglomerular inflammation in renal tissues, and severe portal hepatocellular necrosis, inflammation, and duct hyperplasia were observed in hepatic tissues of rats exposed to CoCl(2) toxicity, but were mild to absent in glycine‐treated rats. CONCLUSION: The results of this study clearly demonstrate protective effects of glycine against CoCl(2)‐induced tissue injuries and derangement of physiological activities of the hepatic and renal systems in rats. The protective effects are mediated via augmentation of total antioxidant capacity and upregulation of NGAL and podocin expression.