摘要
目的探讨大气细颗粒物(PM2·5)对大鼠脑组织的毒性作用机制。方法将32只雄性Wistar大鼠随机分为低、中、高(1·5,7·5,37·5mg/kg)3个剂量染毒组和生理盐水对照组。气管注入染毒后24h处死大鼠,测定脑组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性和谷胱甘肽(GSH)、硫代巴比妥酸反应物(TBARS)含量。结果经PM2·5染毒后大鼠脑组织的SOD、CAT活性出现显著的剂量依赖性下降趋势;高浓度组GSH含量显著降低;GSH-Px活性在不同剂量染毒后虽出现下降趋势,脂质过氧化水平(LPO)也有所升高,但与对照组之间差异无统计学意义。各染毒组SOD/TBARS比值显著降低(P<0·05),TBARS/GSH-Px比值则在高浓度染毒后较对照组明显升高(P<0·05)。结论PM2·5可引起大鼠脑组织的氧化损伤,是一种神经毒性因子。
Objective To investigate the toxicological mechanism of airborne fine particulate （PM2.5） on brains of rats.Methods 32 male wistar rats were randomly divided into PM2.5 exposure groups at different concentration （1.5,7.5,37.5mg/kg） and control group instilled with physiological saline. Rats were killed 24 h after instillation, and the lzvels of thiobarbituric acid reactive substance （TBARS）, Glutathione （GSH） and activities of superoxlde dismutase （SOD）, Glutathione peroxidase （GSH-Px）, Catalase （CAT） were measured. Results The activities of SOD and CAT decreased with PM2.5 concentration in a dose-depenent manner （P〈0.05）. PM2.5 instillation at 37.5mg/kg caused statistically significant decrease of GSH level. （P〈0.05）. The changes of GSH-Px activities and TBARS levels at all concentration were not statistically significent in comparison with control group. SOD/TBARS decreased significantly at all concentrations, and TBARS/GSH-Px increased significently at 37.5mg/kg concentration （P〈0.05）. Conclusion PM2.5 could cause oxidative damage to brains of rats. It was a neural toxin.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2005年第8期990-991,共2页
Chinese Journal of Public Health
基金
国家自然科学基金重点项目(30230310)
山西省自然科学基金(20031092)
