二氧化硫致小鼠脑胃蛋白质氧化损伤作用  

Oxidation effect of sulfur dioxide inhalation on protein in brain and stomach tissues in mice

作　　者：解静芳[1] 许丽娟[1] 韩琦[1] 郝婷娟[1] 孟紫强[2] 

机构地区：[1]山西大学环境与资源学院环境科学研究室,山西太原030006 [2]山西大学环境医学与毒理学研究所

出　　处：《中国公共卫生》2011年第3期320-321,共2页Chinese Journal of Public Health

基　　金：国家自然科学基金(30740037)

摘　　要：目的探讨SO2吸入后对小鼠脑和胃蛋白的氧化损伤程度和毒作用机制。方法将小鼠随机分为14,28,56 mg/m33个剂量组分别进行SO2吸入染毒,用2,4-二硝基苯肼(DNPH)比色法和氯化钾十二烷基磺酸钠(KC l-SDS)沉淀法分别测定脑组织和胃组织蛋白质的羰基含量(PCO)和DNA-蛋白质交联率(DPC)。结果 SO2可导致雌、雄小鼠脑细胞PCO和DPC升高,且呈现明显的剂量-效应关系(复相关系数r2≥0.984 0);SO2浓度为14、28、56 mg/m3时,脑PCO分别升高17.4%、38.2%和72.9%,DPC分别升高15.2%、22.1%和42.8%;在SO2浓度为28,56 mg/m3时升高具有统计学意义(P<0.05);雌性小鼠脑细胞DPC升高较雄性小鼠明显;SO2未引起雌、雄小鼠胃细胞PCO和DPC的明显改变。结论 SO2吸入可致雌、雄小鼠脑PCO和DPC升高,产生氧化损伤,但未引起小鼠胃PCO和DPC明显改变。Objective To research the level of protein oxidation damage induced by SO2 inhalation and the mechanism of its toxicological effect on protein in brain and stomach tissues in mice.Methods After exposure to SO2 inhalation at 3 different concentrations（14,28,and 56 mg/m^3）,the levels of protein carbonyl（PCO） and DNA-protein crosslinks（DPC） were analyzed with spectrophotometric 2.4-dinitrophenylhydrazine（DNPH） assay and potassium chlorine-sodium dodecyl sulfate（KCl-SDS） assay.Results SO2 could cause the formation of PCO and DPC in brain of mice in a dose-effect relationship（r2≥ 0.984 0）.The contents of PCO in the brain increased by 17.4%,38.2%,and 72.9% when the concentration of SO2 were 14,28,and 56 mg/m^3,respectively,while the contents of DPC increased by 15.2%,22.1%,and 42.8%.But only when the concentrations of SO2 were 28 and 56 mg/m3,the PCO and DPC contents were significantly higher than those of the control group（P0.05）.The inerease of DPC in the female mice was higher than that of in the male mice.But the increases of PCO and DPC in stomach after SO2 inhalation were not statistically significant.Conclusion SO2 inhalation could significantly increase the levels of PCO and DPC in brain,but not in stomach in mice.

关 键 词：二氧化硫 羰基 DNA-蛋白质交联 氧化损伤 

分 类 号：Q591.2[生物学—生物化学]