摘要
[目的 ]探索SO2 吸入染毒的氧化损伤作用及其毒理作用的机制。 [方法 ]研究SO2 吸入对小鼠肝、肺、肾、心、脾、脑、胃、小肠及睾丸 9种脏器谷胱甘肽过氧化物酶 (GSH Px)活性的影响。小鼠每天吸入染毒 6h ,连续 7d ,浓度分别为 (2 2± 2 )mg/m3 和 (64± 3 )mg/m3 。 [结果 ]在SO2 浓度为 (2 2± 2 )mg/m3 时 ,雄鼠肺中GSH Px活性显著升高 ,肾和肝略有升高 ,其余脏器均有所降低 ,其中心脏降低尤为显著 ;雌性的GSH Px活性普遍升高 ,其中肺和脑显著升高。在SO2 浓度为 (64± 3 )mg/m3 时 ,雌、雄小鼠各器官中GSH Px活性均下降 ,雄鼠在肝、肺、肾、心、脑、胃、肠及睾丸中的下降达到显著性水平 (P <0 0 5或P <0 0 1) ,且降低程度大于雌鼠。 [结论 ]SO2 可引起小鼠不同脏器细胞内抗氧化酶 (GSH Px)活性的改变 ,导致机体抗氧化损伤的能力下降 。
In order to study oxidation damage of SO 2 and mechanism of its toxicological role in mammals. After exposure to SO 2 at different concentrations,the activities of glutathione peroxidase (GSH Px) in nine organs (liver,lung,kidney,heart,spleen,brain,stomach,small intestine and testicle) from mice were investigated. For male mice,the increases of GSH Px activities were caused by SO 2 at low concentration (22±2 mg/m 3) in lungs (significant);while the decrease of GSH Px activities were caused by low SO 2 exposure in heart (significant) and in other organs (not significant). For female mice,SO 2 at 22±2 mg/m 3 caused increase of GSH Px activities in all organs tested,but only the increase of GSH Px activities in lungs and brains were statistically significant. SO 2 at higher concentration (64±3 mg/m 3) caused decrease of GSH Px activities in all organs tested in mice of both sexes,and the decrease of GSH Px activities in liver,lung,kidney,heart,brain,stomach,intestine and testicle in male mice were statistically significant. [Conclusion] SO 2 might cause decrease of GSH Px activities in various organs of mice in a dose dependent manner . The decrease in activities of the antioxidant enzyme might predispose the organism to increase free radical damage,and to reduce protection against lipid peroxidation.
出处
《环境与职业医学》
CAS
北大核心
2003年第1期6-9,共4页
Journal of Environmental and Occupational Medicine
基金
国家自然科学基金资助项目 (编号 :30 0 70 647)
山西省自然科学基金资助项目
