| Objective: To investigate the effects of zinc on the arsenic poisoning mice biological effects on mice with arsenic poisoning of zinc on lipid metabolism and cell apoptosis in for the role of arsenic poisoning mechanism to provide a scientific basis. Methods: Selection of health Kunming mice were divided into five groups (negative control group, the positive control group, three zinc intervention group), the use of oral gavage, for six weeks after gavage, a xanthine Determination of the oxidation organizations Superoxide dismutase (SOD) activity; thiobarbituric acid (TBA) Determination in malondialdehyde (MDA) content; Chemical assay (DNTB) of the Organization of glutathione peroxidase (GSH-Px) activity; respectively flame and graphite furnace atomic absorption spectrophotometry of the Organization of arsenic and zinc content; determination of liver free fatty acid (FFA) composition; determination of nitrate reductase nitric oxide content; immunohistochemical determination of the apoptotic factor fas, fasL expression. Results: (1) the positive control group, the intervention group and the negative control group mice were compared with varying degrees of weight loss, lower coefficient of organs, liver and kidney tissue Higher seeing an increase in arsenic accumulation of chronic arsenic poisoning performance. And the positive control group, low, negative in the intervention group and the control group of mice had a significant difference (P<0.05). (2) compared with the negative control group, the intervention group decreased activity of GSH-PX, and the differences are statistically significant (P<0.01) in the intervention group increased MDA, and the differences are statistically significant (P<0.05). SOD activity in the intervention group were lower, low-arsenic + zinc and arsenic in the zinc group and the negative control group had a significant difference (P<0.05). Zinc intervention group compared with the positive control group, GSH-PX activity increased, MDA reduced, and the difference is statistically significant. (3)the negative control group compared to the positive control group, and low zinc intervention group mouse liver fatty acid composition of unsaturated fatty acids increased polyunsaturated fatty acids decreased, the difference was significant (P<0.01) and high-zinc intervention group mouse liver fatty acid composition of saturated fatty acids decreased, polyunsaturated fatty acids increased, the difference was significant (P<0.01) compared with the corresponding experimental groups, the intervention group mouse liver fatty acid composition of saturated fatty acids decreased, polyunsaturated fatty acids increase in monounsaturated fatty acids increase, and with the zinc, and high-zinc intervention group is the difference between statistical significance (P<0.01). With higher doses of zinc intervention, the intervention group mouse liver fatty acid composition be reduced in saturated fatty acids, polyunsaturated fatty acids increase, and a dose - effect relationship. (4) With the intervention group to the increase in zinc, Fas, FasL expression was decreased gradually. Low in zinc + arsenic group of Fas, FasL expression rate and the negative control group, the differences were statistically significant (P<0.05), and high-zinc + arsenic group rate and the expression of Fas-positive compared to the control group, the difference with statistical significance (P<0.01), middle - and high-arsenic + zinc group FasL expression rate and the positive control group, the differences were statistically significant (P<0.05). NO content in the liver and Fas, FasL expression was positively correlated, and Zn contents of Fas and FasL expression rate was negatively correlated. Conclusion: (1) Intake of arsenic can be excessive lipid peroxidation induced by the body, liver and kidney tissue MDA levels increased, SOD and GSH-Px activity decreased. (2) Intake of excessive arsenic can lead to liver tissue FFA composition change, that is, unsaturated fatty acids increase in polyunsaturated fatty acids decrease. (3) Arsenic can increase NO mice, Fas, FasL expression was increased, and promote apoptosis of the liver. (4) Zinc could antagonize accumulation of arsenic-induced lipid peroxidation in the body, the role of apoptosis and the fatty acid composition of the arsenic poisoning caused by the oxidative damage and apoptosis is a protective effect.
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