柴油车尾气颗粒物提取物对V79细胞的毒性  

Toxic Effect of Exhaust Particles Extracts of Diesel Vehicles on V79 Cell

作　　者：刘文彪[1] 董胜璋[1] 林忠宁[1] 任铁玲[1] 余贵英[1] 

机构地区：[1]中山大学公共卫生学院,广东广州510080

出　　处：《环境与健康杂志》2005年第2期119-121,共3页Journal of Environment and Health

摘　　要：目的观察柴油车尾气颗粒物提取物(DEPE)对中国仓鼠肺成纤维细胞(V79)增殖、细胞膜完整性及氧化损伤的毒性。方法DEPE染毒不同浓度或时间后,通过检测V79细胞的细胞生存率、乳酸脱氢酶(LDH)漏出率、谷胱甘肽(GSH)含量、谷胱甘肽过氧化物酶(GSH-PX)活力的变化规律及相互的关系,评价DEPE对细胞的一般毒性和氧化损伤作用。结果在该实验条件下,DEPE可致细胞生存率降低,半数抑制浓度(IC50)约为6400μg/ml;细胞内LDH漏出率增加,GSH含量下降,并伴随着GSH-PX活力升高。结论一定剂量下,DEPE可降低细胞生存率,损伤细胞膜,致细胞氧化损伤。Objective To observe the toxicity of diesel exhaust particles extracts(DEPE) on V79 cell in cell viability, membrane and oxidative stress. Methods Cell exposed different concentrations of DEPE for different time , the change of cell viability, the leakage of intracellular lactate dehydrogenase(LDH), intracellular glutathione(GSH) and glutathione peroxidase (GPX)content were determined respectively, and analyzed the relation between GSH and GPX. Results The results showed that the viability of V79 cell decreased and the leakage rate of lactate dehydrogenase increased gradually in according with the increasing dosage of DEPE,and that DEPE could impair V79 cell by oxidative stress, included intracellular GSH content decreased and the activity of GPX increased, indicating that GPX might play a important role in DEPE induced GSH depletion. Conclusion DEPE may impair cell viability and the cell membrane integrity, also impair cell by oxidative stress.

关 键 词：柴油车尾气颗粒物 乳酸脱氢酶 氧化损伤 

分 类 号：R994.6[医药卫生—毒理学]