Aim of the present study was planned to determine the protective role of
naringin in attenuating the toxicity induced by
nickel sulfate in rat liver. In this investigation
nickel sulfate (20mg/kg
body weight) was administered intraperitoneally for 20days to induce toxicity.
Naringin was administered orally (20, 40 and 80mg/kg
body weight) for 20days with intraperitoneal administration of
nickel sulfate. Liver injury was measured by the increased activities of serum hepatic
enzymes namely
aspartate transaminase,
alanine transaminase,
alkaline phosphatase, gamma glutamyl
transferase,
lactate dehydrogenase and total
bilirubin along with increased elevation of lipid peroxidation markers, thiobarbituric reactive
acid substances,
lipid hydroperoxides,
protein carbonyl content and conjugated dienes. The toxic effect of
nickel was also indicated by significantly decreased activities of enzymatic
antioxidants like
superoxide dismutase,
catalase,
glutathione peroxidase,
glutathione-S-transferase,
glutathione reductase and
glucose-6-phosphate dehydrogenase and non-enzymatic
antioxidants like
reduced glutathione, total sulfhydryl groups,
vitamin C and
vitamin E levels were significantly decreased.
Naringin administered at a dose of 80mg/kg
body weight significantly reversed the activities of hepatic marker
enzymes, decreasing
lipid peroxidative markers, increasing the
antioxidant cascade and decreasing the
nickel concentration in the liver. The effect at a dose of 80mg/kg
body weight was more pronounced than that of other two doses (20 and 40mg/kg
body weight). All these changes were supported by histopathological observations. These results clearly demonstrate that
naringin has the potential in alleviating the toxic effects of
nickel in rat liver.