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目的研究不同水平的砷对小鼠脏器组织脂质过氧化的影响,并观察维生素E(VE)对砷毒作用的干预作用。方法昆明种小鼠按2因素3水平析因实验设计分为9组,不同实验组的动物通过喂饲法给三氧化二砷和VE复制亚慢性砷中毒动物模型。三氧化二砷的分组剂量按照其对小鼠经口半数致死量LD50进行分组,VE按照我国青少年每日推荐量进行分组。2个月后,采用试剂盒,研究砷对小鼠脏器组织中超氧化物歧化酶(SOD)活力、谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MDA)含量的影响以及给于VE处理后的干预作用。结果染毒组动物脏器组织中SOD、GSH-Px活力低于正常对照组动物(P<0.05),MDA含量高于正常对照组(P<0.05);VE处理后动物脏器组织中SOD、GSH-Px活力增强,MDA含量降低(P<0.05)。结论砷能引起小鼠脏器组织中氧化与抗氧化系统失衡,VE可拮抗砷对小鼠脏器氧化水平与抗氧化能力的影响。
Objective To study the effects of different levels of arsenic on lipid peroxidation in mouse organs and to observe the intervention effect of vitamin E on arsenic toxicity. Methods Kunming mice were divided into 9 groups according to the factorial design of 2 factors and 3 levels. Animals of different experimental groups were given animal models of arsenic trioxide and VE for subchronic arsenic poisoning by feeding method. Arsenic trioxide dose group according to its oral LD50 LD50 mice were grouped, VE in accordance with our daily recommended amount of adolescence grouping. After 2 months, the activity of arsenic on the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) Impact and post-VE intervention. Results The activities of SOD and GSH-Px in the viscera tissue of the infected group were lower than those of the normal control group (P <0.05), the content of MDA was higher than that of the normal control group (P <0.05) GSH-Px activity increased, MDA content decreased (P <0.05). Conclusion Arsenic can cause the imbalance of oxidation and anti-oxidation system in mouse organ. VE can antagonize the effect of arsenic on the level of organ oxidation and antioxidant capacity in mice.