摘要
目的探讨亚硒酸钠(Na2SeO3)和N-乙酰半胱氨酸(NAC)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、Na2SeO3干预组和NAC干预组。对照组大鼠腹腔注射生理盐水,其余各组腹腔注射150μmol/kgMnCl2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,Na2SeO3干预组隔日皮下注射10μmol/kg Na2SeO3,NAC干预组隔日皮下注射1 mmol/kg NAC。每周染锰5次,1次/d,染毒4周。共计染锰20次,Na2SeO3和NAC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,染锰大鼠肝、脑和肾组织MDA含量显著升高,肝肾组织GSH含量降低。Na2SeO3和NAC干预均使脑和肾组织MDA含量显著降低。Na2SeO3干预组大鼠肾GSH含量显著增加,肝GSH-Px和SOD活力降低。NAC干预组大鼠脑SOD活力显著降低。结论锰可使大鼠产生氧化损伤,Na2SeO3和NAC对锰致大鼠氧化损伤有一定的拮抗作用。
Objective To study the effects of sodium Selenite（Na2 SeO3 ）and N-acetylcysteine（NAC）on oxidative damage induced by manganese so as to probe into the mechanism of manganese poisoning and to provide criteria for its control. Methods 32 Wistar rats were randomly divided into four groups, i. e. the control, MnCl2, Na2SeO3 intervention and NAC intervention groups. The control group was intraperitoneally（ip） injected with normal saline and other three groups were ip injected with 150 μmol/kg manganese chloride（MnCl2 ）, Two hours later, the control and MnCl2 groups were subcutaneously （sc） injected with normal saline, while Na2SeO3 and NAC intervention groups were sc injected with 10 μmol/kg Na2 SeO3 and 1 mmol/kg NAC respectively in every other day. All groups were administrated 5 times a week for four weeks, including a total of 20 times MnCl2 administration, 10 times Na2 SeO3 and NAC intervention. The levels of reduced glutathione（GSH）and malonydialdehyde（MDA）, activities of glutathione peroxidase （GSH-Px）and superoxide dismutase（SOD）in the liver, brain and kidney of rats were measured, Results Compared with the control group, the levels of MDA of liver, brain and kidney in the manganese exposed group increased significantly, while GSH levels of liver and kidney in the manganese exposed group decreased significantly. Na2SeO3 and NAC intervention caused the decrease of MDA contents in rat brain and kidney treated with manganese. Na2SeO3 intervention resulted in the increase of GSH levels in kidney, reduction of GSH-Px and SOD activities in the liver of rats. NAC intervention caused the reduction of SOD activities in the brain of rats. Conclusions Manganese resulted in oxidative injury in experimental rats. Treatment with Na2 SeO3 and NAC can antagonize oxidative damage induced by manganese in certain extent.
出处
《工业卫生与职业病》
CAS
CSCD
北大核心
2007年第6期321-324,共4页
Industrial Health and Occupational Diseases
基金
辽宁省教育厅科学研究基金资助项目(2004C025)
