邻苯二甲酸酯暴露的大鼠尿液生物标志物研究

建立了检测尿液中邻苯二甲酸酯类化合物(PAEs)共同水解产物邻苯二甲酸(PA)的分析方法;通过雄性成年SD大鼠代谢试验,检测了邻苯二甲酸二丁酯(DBP)和邻苯二甲酸二(2-乙基己基)酯(DEHP)单独暴露、以及联合暴露条件下大鼠尿液中PA总量,并分析了PA与暴露总量之间的关系.结果显示,随着暴露剂量的增大,尿液中排出的PA总量也不断增大;DBP单独暴露、DEHP单独暴露以及两者联合暴露时尿液PAEs代谢物平均排泄总量占摄入量的百分比分别为65.04%、55.00%和38.35%;大鼠尿液中PA的摩尔总量与DBP、DEHP、以及两者联合暴露的摩尔量之间的相关系数分别为0.92(P<0.01)、0.56(P<0.01)、0.93(P<0.01).尿液水解后的PA能够反映PAEs类物质的总暴露水平,将来可能作为一种潜在的暴露生物标志物用于人群的PAEs暴露监测.     

Potential neoplastic effects of parathion-methyl on rat liver

The mutagenic and carcinogenic effects of parathion-methyl were examined by bacterial reverse assay and a long term experiment with Wistar rats. The potential mutagenic effect of parathion-methyl in Salmonella typhimurium TA100 bacterial cells was observed without rat liver S9 metabolic activation. Parathion-methyl was further investigated for pathological changes in rat pancreas and liver. The long-term rat experiments showed that parathion-methyl exposure for 3 months can cause pathological changes in rat pancreases acinar cells and pancreatic hepatocytes. Atypical acinar cell focuses (AACF) were determined in the liver and pancreas of the rats. The results from short-term Ames test and long-term rat experiments suggest that parathion-methyl would be potential carcinogenic.     

抗氧化剂对二氧化硫诱导的大鼠心脏线粒体损伤的缓解作用

采用Wistar大鼠作为模型进行整体动物染毒，SO₂组动式吸入SO₂（7mg/m³）28d，每天4h；SO₂+NALC（N-乙酰半胱氨酸）组吸入同样条件的SO₂，且自SO₂染毒之日起隔天腹腔注射50mg/kg b.w.NALC，对照组吸入新鲜空气并注射生理盐水.采用荧光定量PCR技术检测心脏组织中氧化磷酸化复合体亚基CO1和ATP6以及核转录因子PGC1-α、NRF1、TFAM的mRNA转录水平；并采用Western blot技术检测3种线粒体调控基因的蛋白表达.结果发现，在吸入SO₂后，核转录因子PGC1-α、NRF1、TFAM的mRNA转录和蛋白表达水平显著降低，并且2种亚基CO1和ATP6的mRNA转录水平也显著下降，而抗氧化剂NALC处理能够明显缓解3种核转录因子及2种复合体亚基表达水平的下降.提示SO₂暴露通过下调PGC1-α、NRF1、TFAM表达来影响线粒体DNA的转录，干扰氧化磷酸化重要组分的合成，该过程发生机制可能与自由基的产生相关，而抗氧化剂的使用可有效缓解SO₂诱导的心脏线粒体损伤作用.     

Potential neoplastic e ects of parathion-methyl on rat liver

The mutagenic and carcinogenic e ects of parathion-methyl were examined by bacterial reverse mutation assay and a long-term experiment with wistar rats. The potential mutagenic e ect of parathion-methyl in Salmonella typhimurium TA100 bacterial cells was observed without rat liver S9 metabolic activation. Parathion-methyl was further investigated for pathological changes in rat pancreas and liver. The long-term rat experiments showed that parathion-methyl exposure for 3 months can cause pathological changes in rat pancreases acinar cells and pancreatic hepatocytes. Atypical acinar cell focuses (AACF) were determined in the liver and pancreas of the rats. The results from short-term Ames test and long-term rat experiments suggested that parathion-methyl would be potential carcinogenic.     

甲醛吸入染毒致大鼠多组织器官氧化损伤效应研究

大鼠吸入甲醛 (13 5mg m3 ) ,连续染毒 7d ,每天 4h .染毒结束后 ,测定组织器官 (肺、脑、肝和外周血 )中还原型谷胱甘肽(GSH)含量、谷胱甘肽过氧化物酶 (GSH PX)活力、超氧化物歧化酶 (SOD)活性及脂质过氧化产物丙二醛 (MDA)含量 ,以探讨甲醛对机体的脂质过氧化作用及机体的抗氧化损伤机制 .实验结果表明甲醛吸入组大鼠外周血GSH、GSH PX和MDA水平显著高于对照组 (P <0 0 5 ) ,而甲醛吸入组和对照组相比较 ,大鼠肺、肝、脑组织中的GSH含量、GSH PX活力、SOD活性、MDA含量以及外周血中SOD活性均未见显著性差异 .由此认为 ,外周血抗氧化物GSH、GSH PX活力和脂质过氧化产物MDA水平可望成为甲醛早期暴露的生物效应指标 .