Preventive effect of zinc on nickel-induced oxidative liver injury in rats

Abstract

The present study was undertaken to evaluate the protective effect of zinc against nickel-induced oxidative liver injury in rats. Male albino rats were randomly divided into four different groups, where the first group was served as a control, whereas the remaining groups were respectively treated with zinc sulphate (227mg zinc/l in drinking water), nickel sulphate (2mg/100g b.w./ day, intraperitoneally), and a combination of nickel sulphate and zinc sulphate. The treatment of all groups was lasted for three consecutive weeks. Liver dysfunction parameters represented by glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT) and alkaline phosphatase (GOT), serum glucose, total protein and albumin levels were estimated. Liver glutathione (GSH), catalase and glutathione peroxidase values were also determined in liver as indicators of oxidative damage. Exposure of rats to nickel caused a significant decrease in body weight and an increase in liver weight compared to the controls. Nickel treatment was also led to high glucose concentration and produced oxidative liver injury characterized by increasing GPT, GOT and ALP activities. Meanwhile nickel administration decreased serum total protein and albumin in the animals. In addition liver glutathione level, catalase and glutathione peroxidase activities were diminished due to high lipid peroxidation. However, the administration of zinc with nickel resulted in a remarkable improvement of the investigated values comparison with rats treated with nickel alone. Liver histological studies have confirmed the changes observed in biochemical parameters and proved the beneficial role of zinc. In conclusion, nickel led to liver dysfunction and hepatic lipid peroxidation in animals, but simultaneous treatment with zinc offers a relative protection against nickel induced oxidative liver injury and lipid peroxidation probably due to its antioxidant properties.