Objective: The objective of this study was to investigate the effect of silymarin extract from Silybum marianum against nickel-induced alterations in haematological indices, kidney dysfunction and renal antioxidant defence system. Methods:Male albino Wistar rats were divided into four groups seven each. Control, silymarin, nickel and nickel plus silymarin. Silymarin was administrated orally (100 mg/kg b. wt) and nickel as nickel sulfate (NiSO4 6H2 Results:The treatment with nickel led to a significant decrease in body weight with an increase in both absolute and relative kidney weights and a significant increase in renal markers, which confirmed by histopathological alteration. A microcytic anemia was also observed, which was manifested by a reduction of red blood cells count (RBC), hemoglobin (Hb) concentration, platelet counts (Plt), hematocrit and white blood cells counts (WBC). The level of lipid peroxidation was increased. Whereas, GSH concentration and enzymatic antioxidants SOD, GSH-Px and CAT activities were decreased. The co-treatment with methanolic extract of milk thistle attenuated the variation in the hematological and renal markers, decreasing renal lipid peroxidation (p<0.05) with a concomitant increasing reduced glutathione content (p<0.01) and restoring the antioxidant enzymes (SOD, CAT, GSH-Px) in kidney, as well as an improvement in histological changes compared to those previously noticed in nickel group. 0) was given intraperitoneally (20 mg/kg b. wt) at alternative days. The experiment continued for three consecutive weeks. Body weight was recorded regularly. After overnight fasting, animals were killed and serum creatinine, serum urea, serum uric acid, hematological parameters and renal antioxidant markers were determined. Conclusion:To conclude, these findings demonstrated that silymarin extract effectively improved heamatotoxicity and nephrotoxicity caused by nickel.

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Objective: The study was designed to investigate the possible protective role of methionine (Met) in nickel sulfate induced oxidative stress in renal tissue.Methods: Rats were divided into the following groups: Healthy control; L-methionine (Met, 100 mg/kg, orally); nickel sulfate (Ni, 20 mg/kg, intraperitoneally); and combination Ni+Met. The experiment lasted 21 days. Antioxidant and renal function parameters with histological study were performed. Results:In the Ni group, marked renal damage was noticed with the significant elevation in the levels of creatinine, urea, and uric acid in serum. Animals also showed a significant rise in the lipid peroxidation level with a concomitant decrease in glutathione (GSH) and various antioxidant enzymes GSH peroxidase, catalase, and superoxide dismutase. Moreover, these changes in rats given the combined therapy nickel plus methionine were significantly less than those of group nickel, met prevented these alterations and maintained the antioxidant status. Histopathological examination of the kidney tissue proved the protective effect of Met against nickel toxicity. Conclusions:These results demonstrated that methionine augments antioxidant defense against nickel-induced toxicity and provides evidence that it has therapeutic potential as a renoprotective agent.