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目的探讨牛磺酸(Tau)和维生素C(Vit-C)对锰致大鼠氧化损伤的影响,为阐明锰中毒的发病机制和防治提供依据。方法 Wistar大鼠32只,随机分为4组,分别为对照组、单纯染锰组、Tau和Vit-C干预组。对照组大鼠腹腔注射生理盐水,其余各组腹腔注射29.685 mg/kg Mn Cl2溶液。腹腔注射后2h,对照组和单纯染锰组大鼠隔日皮下注射生理盐水,Tau干预组隔日皮下注射125.15 mg/kg Tau,Vit-C干预组隔日皮下注射704.52 mg/kg Vit-C。每周染锰5次,1次/d,染毒4周。共计染锰20次,Tau和Vit-C干预各10次。测定肝、脑和肾组织还原型谷胱甘肽(GSH)、丙二醛(MDA)的含量和谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)的活力。结果与对照组比较,单纯染锰组大鼠肝脏、脑和肾组织MDA含量增加,肝肾组织GSH含量降低。脑组织GSH含量和GSH-Px活力有下降趋势,但统计学差异不明显。Tau干预组大鼠与单纯染锰组相比,肝脏、脑和肾组织MDA含量下降,GSH含量增加。脑和肾组织GSHPx活力增高,脑组织SOD活力增高。Vit-C干预组大鼠与单纯染锰组相比,大鼠肝脏MDA含量有下降趋势,脑和肾组织MDA含量明显下降。虽然大鼠肝脏、脑和肾组织GSH含量增加,但统计学差异不明显。仅肝组织GSH-Px活力明显增加。结论锰可使大鼠产生氧化损伤,Tau和Vit-C对锰致大鼠氧化损伤有一定的拮抗作用。
Objective To investigate the effects of taurine (Tau) and vitamin C (C-C) on oxidative damage induced by manganese in rats and provide basis for elucidating the pathogenesis and prevention of manganese poisoning. Methods Thirty-two Wistar rats were randomly divided into 4 groups: control group, Mn-only group, Tau and Vit-C intervention groups. Rats in control group were injected intraperitoneally with normal saline, and the other groups were intraperitoneally injected with 29.685 mg / kg MnCl2 solution. Rats in control group and manganese-only group were injected subcutaneously with saline every other day after intraperitoneal injection. Rats in Tau group were injected subcutaneously with 125.15 mg / kg Tau every other day, Vit-C intervention group were subcutaneously injected with 704.52 mg / kg Vit-C every other day. Manganese 5 times a week, 1 / d, 4 weeks. A total of 20 times with manganese, Tau and Vit-C intervention 10 times. The content of glutathione (GSH), malondialdehyde (MDA) and the activity of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in liver, brain and kidney were measured . Results Compared with the control group, the contents of MDA in the liver, brain and kidney of the rats with manganese alone increased and the contents of GSH in the liver and kidney decreased. GSH content in brain tissue and GSH-Px activity decreased, but the statistical difference was not obvious. Tau intervention group compared with the simple manganese group, the liver, brain and kidney MDA content decreased, GSH content increased. Brain and kidney tissue increased GSHPx activity, increased brain SOD activity. Compared with pure manganese group, the content of MDA in liver of rats in Vit-C intervention group decreased and MDA content in brain and kidney decreased significantly. Although the content of GSH in liver, brain and kidney of rats increased, the difference was not obvious. Only liver tissue GSH-Px activity was significantly increased. Conclusion Manganese can cause oxidative damage in rats, and Tau and Vit-C can antagonize manganese-induced oxidative damage in rats.