锌、硒对砷诱导金属硫蛋白合成影响的研究

Study of zinc,selenium on arsenic induced metallothionein synthesis in mice

目的:探讨锌、硒对砷诱导金属硫蛋白合成的影响。方法:采用亚慢性毒性实验方法,分别测定小鼠肝脏中金属硫蛋白(MT)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力。结果:砷低剂量组、单纯锌组和单纯硒组肝脏MT含量升高,高于对照组和砷高剂量组(P<0.05)。随着砷染毒剂量的增加,小鼠肝脏组织中MDA含量增加,SOD、GSH-Px活性降低,且呈剂量-效应关系。结论:亚砷酸钠能够诱导小鼠产生金属硫蛋白,金属硫蛋白含量与抗氧化能力存在相关性,锌、硒能抑制MDA生成量,提高SOD、GSH-Px活性,增加抗氧化能力,从而拮抗砷毒性。

Objective： To explore zinc, selenium on arsenic induced metallothionein synthesis in mice, Methods： Subchronic toxicity experiment was applied. Then the mice organic contents of metallothionein （MT） and lipid peroxides degradation product malondialdehyde （MDA）, the total superoxide dismutase （SOD） activities and glutathione peroxidase （GSH-Px） activities in liver were determined individually. Results： Compared with the control group and high arsenic group, the MT contents of liver were higher in low arsenic, Zn and Se groups, while liver MT contents had statistically results （P〈0.05）. The results showed that with the increases of exposure levels of arsenic, the contents of MDA increased and the activities of SOD and GSH-Px decreased and showed a dose-effect manner. Conclusion： Arsenic can induce metallothionein protein. MT has correlation to anti-lipid peroxidation. Zinc and selenium could decrease the contents of MDA and increase the activities of SOD and GSH-Px significantly, which can increase anti-lipid peroxidation ability and against arsenic toxicity.