We studied the effect of oral supplementation with L-ascorbic acid (50 mg/100 g body weight) on nickel sulfate (2.0 mg/100 g body weight, i.p.) induced lipid peroxidation in the testes of Wister strain male albino rats. Testicular lipid peroxide and glutathione (GSH) levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated. Nickel sulfate treatment significantly increased the level of testicular lipid peroxide and decreased all antioxidant enzymes activities and GSH concentration. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on testicular lipid peroxide and GSH concentration as well as antioxidant enzymatic defense system.

We studied the effect of oral supplementation with L-ascorbic acid (50 mg /100 g body weight (BW) on nickel sulfate (2.0 mg/ 100 g BW, i.p)-induced lipid peroxidation and histopathology in the lung of Wister strain male albino rats. Lipid peroxide and glutathione levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), were estimated. Nickel sulfate administration significantly increased the level of lipid peroxides and decreased all antioxidant enzyme activities. Nickel sulfate treatment also induced (a) loss of normal characteristics and architectural organization, (b) inflammation in bronchioles, (c) alveolar congestion, (d) alveolar cell hyperplasia, and (e) congestion in the lumen. The simultaneous administration of L-ascorbic acid and nickel sulfate improved both lipid peroxidation and the histopathology of lung when compared with rats receiving nickel sulfate alone. The results indicate that L-ascorbic acid prevents nickel-induced alteration of antioxidant defense mechanisms and histopathology of lung tissue.

Nickel is an abundant carcinogenic and nephrotoxic metal whose activity leads to renal impairment. Previous studies have shown a protective effect of simultaneous vitamin C administration on acute and chronic nickel toxicity. However, very little research relating to the effect of vitamin C pretreatment in preventing nickel-induced acute nephrotoxicity is available. Therefore, the present study aimed to determine the efficiency of vitamin C (VC) pretreatment in preventing acute renal toxicity of nickel. Mice were pretreated orally with vitamin C (16.6 mg kg-1 body weight, b.w.) for seven consecutive days, prior to intraperitoneal (i.p.) administration of nickel chloride at different doses (3, 5, and 10 mg Ni kg-1 b.w.) for an exposure period of 24 hours. Thereafter, animals were killed and kidney tissue and blood samples were taken for histological examination and biochemical marker analyses. Vitamin C pretreatment alone did not alter the levels of serum kidney markers (creatinine, urea, and uric acid). However, treatment with Ni alone showed a significant increase in the levels of serum creatinine, urea, and uric acid with marked necrotic epithelial cells and infiltration by inflammatory cells in kidney sections as compared to the control group. Pretreatment with vitamin C and treatment with Ni at all doses tested for 24 hours showed a significant decrease in the levels of serum creatinine, urea, and uric acid, as well as an improvement in histological changes compared to those previously seen in the group treated with Ni alone. It is concluded that vitamin C pretreatment effectively improved renal function and tissue damage caused by nickel.