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作 者:段燕英[1] 陈国元[1] 季佳佳[1] 鲁燕[1] 虎凤仙[2] 柴莲花[2] 刘卫东[2] 刘四海[2] 邬堂春[1]
机构地区:[1]华中科技大学同济医学院公共卫生学院劳动卫生与环境卫生学系环境与健康教育部重点实验室,武汉430030 [2]华中科技大学同济医学院公共卫生学院预防医学实验教学中心
出 处:《卫生研究》2007年第4期401-403,共3页Journal of Hygiene Research
基 金:国家自然科学基金资助项目(No.30471442)
摘 要:目的检测二硫化碳(CS2)对大鼠睾丸c-myc表达水平的影响。方法取健康Wistar雄性大鼠36只随机分为6组,以不同浓度CS2(0、50、250、1250mg/m3)静式吸入染毒,共10周。另设1250mg/m3(CS2)加VitE(250mg/kg)组和单纯VitE(250mg/kg)组,作为实验干预组,VitE拌入饲料。染毒结束后,处死动物取出睾丸组织制备组织匀浆,分别测定各组超氧化的歧化酶(SOD)、丙二醛(MDA)含量。蛋白定量后用WesternBlot法检测c-myc表达水平。结果睾丸中SOD活力下降,MDA含量上升,前者在各个浓度时与对照组比较均有显著差异(P<0.01),后者在最高浓度时与对照组比较有显著差异(P<0.01)。c-myc的表达出现双向变化,即在低浓度时被抑制,中、高浓度时被诱导,且最高浓度时与对照组比较有显著差异(P<0.05)。当用VitE干预后,SOD活性回升(P<0.05),MDA含量下降(P<0.01),c-myc的表达明显降低(P<0.05)。结论脂质过氧化可能参与了CS2对大鼠睾丸c-myc表达的调节。Objective To survey the expression of c-myc of teticles in rats exposed to carbon disulfide( CS2 ) and the possible mechanism of effects on it. Methods 36 wistar male rats were randomly divided into six groups. Four groups were exposed to CS2 at the dose of O, 50, 250 and 1250mg/m^3 . The other two groups were treated at the dose of 1250 mg/ m^3 CS2 plus VitE(250mg/kg diet) and VitE(250mg/kg diet) respectively. After 10-week esposures, rats were sacrificed and the SOD activity and MDA content and the c-myc expressions in testicles were determined. Results When compared with the control group, SOD activities of testicles in the exposure group were decreased significantly ( P 〈 0.01 ), MDA contents of testicles were increased significantly at the concentration of 1250mg/m^3 CS2 ( P 〈 0.01). The expression of cmyc of testicles present biphasic, and decreased at the concentraton of 50mg/m^3 CS2 and increased at the other concentrations and higher than these of controls at the concentration of 1250mg/m^3 CS2 significantly( P 〈 0.05). After treatment of CS2 combined with antioxidant VitE, SOD activity of testicles increased (P 〈 0.05), MDA content of testicles decreased( P 〈 0.01 ) and c-myc expression of testicles decreased consequently( P 〈 0.05). Conclusion the modulation of c-myc expression in testicles of rats treated with CS2 could be associated with lipid peroxidation induced by CS2.
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