RESUMO
Stannous chloride (SnCl2) is widely used in daily human life to conserve soft drinks, in food manufacturing and biocidal preparations. It had genotoxicity, immunotoxicity, neurotoxicity and oxidative stress. Therefore, the present experiment was carried out to determine the effectiveness of l-ascorbic acid (AA) in alleviating the toxicity of SnCl2 on some enzyme activities and oxidative damage in male New Zealand white rabbits. Six rabbits per group were assigned to 1 of 4 treatment groups: 0 mg AA and 0 mg SnCl2/kg BW (control); 40 mg AA/kg BW; 20 mg SnCl2/kg BW (1/500 LD50); 20 mg SnCl2 plus 40 mg AA/kg BW. Rabbits were orally administered the respective doses every other day for 12 weeks. Liver and kidney specimens were processed for histopathologic studies. Results obtained showed that SnCl2 significantly (P < 0.05) induced free radicals in rabbit liver, testes, kidney, lung, brain and heart. While, the activity of glutathione S-transferase (GST) and the level of sulfhydryl groups (SH-group) were decreased (P < 0.05) in all tested organs except brain and heart. Aspartate aminotransferase (AST) activity was increased (P < 0.05) in liver and decreased in testes, but alanine aminotransferase (ALT) did not change. The activities of alkaline phosphatase (AlP) and acid phosphatase (AcP) were decreased (P < 0.05) in liver, testes, kidney and lung. Also, the activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma of rabbits treated with SnCl2 compared to control group. Histopathologic studies showed marked changes in hepatocytes as well as proliferation of duct epithelium, dilatation and congestion of blood vessels as well as mononuclear inflammatory infiltrate. The kidney were also severely affected by SnCl2 the Bowman's space was increased, with infiltration of renal parenchyma by mononuclear inflammatory infiltrate and changes in cells lining convoluted tubule. Ascorbic acid alone significantly decreased the levels of free radicals, and increased the activity of GST and the levels of SH groups in tested organs except brain and heart. While, the rest of the tested parameters were not affected. Results showed that AA alleviated the harmful effects of SnCl2. This was proved histopathologically by the great improvement in liver and kidney histology where hepatocytes retained normal architecture with mild dilatation and congestion of blood vessels. Bowman's space of kidney was almost normal, with normal lining of proximal and distal convoluted tubules. In conclusion AA could be effective in the protection against stannous chloride toxicity.
