摘要
目的 探讨氧化应激在亚慢性氟中毒大鼠肝脏损伤中的作用。方法 在饮水中加入 5 0 ,10 0 ,和 15 0mg/L氟化钠 (NaF)喂饲大鼠 3个月 ,制备亚慢性氟中毒模型。测定染氟各组大鼠肝脏脂质过氧化产物丙二醛 (MDA)的含量及抗氧化酶超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH -Px)的活力 ,同时检测血清中谷丙转氨酶 (SG PT)、谷草转氨酶 (SGOT)的活性。结果 15 0mg/L染氟组大鼠肝脏MDA含量显著高于对照组 (P <0 0 1) ;10 0 ,15 0mg/L染氟组大鼠肝脏SOD活力显著下降 (P <0 0 5 ) ;随染氟剂量增加 ,GSH -Px活力有下降趋势 ;15 0mg/L染氟组SGPT活性显著高于对照组 (P <0 0 1) ,10 0 ,15 0mg/L染氟组SGOT活性显著高于对照组 (P <0 0 1) ,MDA与SGPT之间存在显著正相关 (r=0 46 0 ,P =0 0 0 7)。结论 氟中毒大鼠肝脏内氧化系统与抗氧化系统失衡 ,氧化应激引起的氧化损伤作用可能是氟致大鼠肝毒性的重要原因之一。
Objective To study the effect of oxidative stress on rat's hepatic damage caused by subchronic fluorosis.Methods Rats were given 0,50,100,150?mg/L sodium fluoride in distilled water drinking for three months.The contents of malonyl dialdehyde (MDA),metabolic product of lipid peroxidation and activities antioxidases in fluoride-exposed rat liver were determined.Meanwhile the activities of serum SGPT,SGOT were studied.Results The contents of malonyl dialdehyde (MDA) in rats liver in group of 150?mg/L were significantly higher than control group.The activities of SOD in 100 and 150?mg/L groups were significantly lower than control group and the activities of GSH-Px tended to decrease with the increase of fluoride content in drinking water.The activities of SGPT in 150?mg/L groups were significantly higher than control group.The activities of SGPT in 100 and 150?mg/L groups were significantly higher than control group.There was a significantly positive correlation between MDA and SGPT(r=0.460,P=0.007).Conclusion The balance of oxidative system and anti-oxidative system in rat's liver with fluorosis was broken.The oxidative damage caused by oxidative stress may be the important reason for fluoride-induced hepatic toxicity.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2003年第5期575-576,共2页
Chinese Journal of Public Health
关键词
氟中毒
肝脏
氧化应激
脂质过氧化
fluorosis
liver
oxidative stress
lipid peroxidation
