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[目的]探讨甲基汞致大鼠脑氧化损伤及牛磺酸对氧化损伤的保护作用。[方法]将24只健康清洁级Wistar大鼠按体质量随机分为4组,每组6只,分别为对照组、低剂量染汞组、高剂量染汞组和牛磺酸干预组。周一至周五每天进行染毒,对照组腹腔注射生理盐水,低剂量染汞组腹腔注射4μmol/kg氯化甲基汞,高剂量染汞组和牛磺酸干预组腹腔注射12μmol/kg氯化甲基汞;每周一、三、五染毒前2 h进行预处理,对照组、低剂量染汞组和高剂量染汞组皮下注射生理盐水,牛磺酸干预组皮下注射1 mmol/kg的牛磺酸;连续进行4周,最后一次染毒后,处死大鼠。取大脑皮质测定:活性氧(ROS)、巯基、羰基、丙二醛(MDA)的含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-px)的活性及细胞凋亡率。[结果]与对照组比较,低、高汞组大鼠的体质量增长幅度降低(P<0.05,P<0.01);ROS分别是其1.8和3.9倍(均P<0.01);SOD和GSH-px的活性均降低;巯基的含量降低;羰基的含量升高;MDA增加;细胞凋亡率分别升高3.4和10.0倍。牛磺酸干预组与高剂量染汞组比较,ROS的生成量降低了17%;SOD、GSH-px的活性有不同程度的升高;巯基、羰基和MDA的含量也有不同程度的改变;细胞凋亡率为高汞组的44%。[结论]甲基汞可导致脑氧化损伤,牛磺酸对甲基汞所致氧化损伤具有一定的保护作用。
[Objective] To explore the protective effect of methylmercury on oxidative damage of brain and taurine in rats. [Method] Twenty-four healthy Wistar rats were randomly divided into 4 groups according to body weight, with 6 rats in each group. They were control group, low-dose mercury stain group, high-dose mercury stain group and taurine intervention group. The rats in the control group were intraperitoneally injected with normal saline. The low dose of mercury in the group was injected intraperitoneally with 4 μmol / kg methylmercury methylmercury, the high dose of the mercury group and the taurine intervention group were intraperitoneally injected with 12 μmol / kg of chloride The rats in the control group, the low-dose mercury-stained group and the high-dose mercury-exposed group were injected subcutaneously with normal saline and the taurine-treated group was subcutaneously injected with 1 mmol / kg of bovine serum Sulfonic acid; 4 consecutive weeks, after the last exposure, rats were sacrificed. The levels of reactive oxygen species (ROS), sulfhydryl, carbonyl and malondialdehyde (MDA), the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) Apoptosis rate. [Result] Compared with the control group, the growth of body weight of rats in low and high mercury groups decreased (P <0.05, P <0.01), the levels of ROS increased 1.8 and 3.9 times respectively (all P <0.01) px activity were reduced; the content of sulfhydryl reduced; carbonyl content increased; MDA increased; apoptotic rates were increased 3.4 and 10.0 times. Compared with the high-dose group, the production of ROS reduced by 17%, the activity of SOD and GSH-px increased in different degree, and the content of thiol, carbonyl and MDA also changed to some extent. The apoptosis rate was 44% in the high mercury group. [Conclusion] Methylmercury can cause cerebral oxidative damage, and taurine has some protective effects on methylmercury induced oxidative damage.