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Effect of melatonin on carbon tetrachloride- induced kidney injury in wistar rats
Abstract
Exposure to carbon tetrachloride (CCl4) induces acute and chronic renal injuries as well as oxidative stress in rats. The aim of this study was to evaluate the effect of exogenous melatonin (MEL) treatment on CCl4-induced oxidative stress and nephrotoxicity in rats using histopathological and biochemical parameters. Serum creatinine, blood urea nitrogen (BUN), nitrite and albumin concentrations were
measured for the evaluation of renal function. Antioxidant status in the kidney tissue was estimated by determining the activities of superoxide dismustase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and glutathione-S-transferase (GST) as well as thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) levels. For histopathological evaluation, kidney of all rats were excised and processed for light microscopy. CCl4 caused elevated level of TBARS and marked depletion of renal endogenous antioxidant enzymes. Furthermore, severe deterioration of renal function was observed in CCl4-treated rats as assessed by increased serum creatinine, BUN levels and decreased creatinine and urea clearance as compared with the control rats.
MEL treatment positively ameliorated the alterations in these biochemical variables in the CCl4 + MEL-treated rats. MEL markedly reduced elevated TBARS and nitrite, significantly attenuated renal dysfunction, increased the levels of antioxidant enzymes. Kidney sections of CCl4-treated group showed, changes in microanatomy. In contrast, these deleterious histopathological alterations resulting from CCl4 nephrotoxin were absent after MEL treatment in CCl4 + MEL group of rats. In conclusion, our results
demonstrated that MEL through its antioxidant activity effectively ameliorated CCl4- induced nephrotoxicity. (Afr. J. Biomed. Res. 10: 153 – 164)
measured for the evaluation of renal function. Antioxidant status in the kidney tissue was estimated by determining the activities of superoxide dismustase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and glutathione-S-transferase (GST) as well as thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) levels. For histopathological evaluation, kidney of all rats were excised and processed for light microscopy. CCl4 caused elevated level of TBARS and marked depletion of renal endogenous antioxidant enzymes. Furthermore, severe deterioration of renal function was observed in CCl4-treated rats as assessed by increased serum creatinine, BUN levels and decreased creatinine and urea clearance as compared with the control rats.
MEL treatment positively ameliorated the alterations in these biochemical variables in the CCl4 + MEL-treated rats. MEL markedly reduced elevated TBARS and nitrite, significantly attenuated renal dysfunction, increased the levels of antioxidant enzymes. Kidney sections of CCl4-treated group showed, changes in microanatomy. In contrast, these deleterious histopathological alterations resulting from CCl4 nephrotoxin were absent after MEL treatment in CCl4 + MEL group of rats. In conclusion, our results
demonstrated that MEL through its antioxidant activity effectively ameliorated CCl4- induced nephrotoxicity. (Afr. J. Biomed. Res. 10: 153 – 164)
