摘要
目的 探讨丙烯腈的毒作用机制。方法 采用小鼠静式吸入染毒方法 ,观察小鼠全血、心脏、肝脏、肾脏的丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)活力及全血谷胱甘肽过氧化物酶 (GSH Px)活力的变化。结果 低、中、高染毒剂量组心脏、肝脏MDA水平显著高于对照组 ,中、高剂量组显著高于低剂量组 ,而心脏SOD活力高剂量组显著低于对照组和低剂量组 ,肝脏SOD活力各染毒组显著低于对照组 ,中、高剂量组显著低于低剂量组。肾脏的MDA含量及SOD活力各组差异均无显著性 ;全血GSH Px活力显著下降 ,并呈剂量 效应关系 ,各染毒组全血MDA含量升高。结论 丙烯腈可能具有形成自由基、促进机体脂质过氧化。
Objective To explore the toxicity mechanism of acrylonitrile.Methods Mice were exposed to acrylonitrile by inspiration in a static total enclosure chamber.The malondialdehyde(MDA)level and superoxide dismutase(SOD)activity in liver,heart and kidney and the glutathione peroxidase(GSH Px)activity in blood were observed in the study.Results MDA levels of heart and liver in low,middle and high dose group were significantly higher than that in control group,and that in high dose group were also significantly higher than low dose group.The SOD activity of heart in high dose group was significantly lower than that in control and low dose group.The SOD activity of liver in middle and high dose group was significantly lower than that in control and low dose group.MDA and SOD levels of kidney did not change after exposure to acrylonitrile.The activity of GSH Px in blood decreased remarkably and showed a dose effect relationship.Conclusion Acrylonitrile could induce lipid peroxidation and decrease the capability of antioxidase(SOD,GSH Px).
出处
《中国工业医学杂志》
CAS
北大核心
2002年第5期260-261,共2页
Chinese Journal of Industrial Medicine