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作 者:石玉琴[1] 王玉萍 宋杨[1] 程晋[1] 关霞[1] 杨克敌[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教育部环境与健康重点实验室,湖北武汉430030
出 处:《环境与健康杂志》2010年第1期21-23,F0003,共4页Journal of Environment and Health
基 金:国家自然科学基金资助项目(30671734)
摘 要:目的研究p,p’-DDE在诱导青春前期SD大鼠睾丸细胞凋亡中半胱氨酰天冬氨酸酶(caspase)的作用。方法将22日龄清洁级雄性SD大鼠20只随机分为低(20mg/kg)、中(60mg/kg)、高(100mg/kg)剂量p,p’-DDE染毒组和对照组(玉米油),每组5只。采用腹腔注射染毒,注射容积为10ml/kg,隔天染毒1次,共进行10天。染毒结束后,处死大鼠,分离睾丸、肝、肾、脾、肺器官,称重后计算脏器系数。取睾丸制备组织匀浆,实时荧光定量PCR测定睾丸组织caspase-3、caspase-8、caspase-9mRNA的表达;比色法检测睾丸组织caspase-3、caspase-8、caspase-9的活力。结果各组大鼠体重和睾丸、肾、脾、肺的脏器系数间比较,差异均无统计学意义(P>0.05)。与对照组比较,高剂量p,p’-DDE染毒组大鼠肝脏系数较高,差异有统计学意义(P<0.05)。与对照组比较,高剂量p,p’-DDE染毒组大鼠睾丸组织caspase-3、caspase-8、caspase-9和中剂量p,p’-DDE染毒组大鼠睾丸组织caspase-9表达均升高,差异有统计学意义(P<0.05)。与对照组比较,高剂量p,p’-DDE染毒组大鼠睾丸组织caspase-3、caspase-8、caspase-9活力均较高,差异有统计学意义(P<0.05)。结论p,p’-DDE可能通过启动caspase-8和caspase-9,进而激活下游效应caspase-3的级联反应而诱导睾丸组织细胞凋亡。Objective To investigate the effects of p, p'-DDE on caspase in testis of prepubertal male rats. Methods Twenty male rats (22-day old) were randomly divided into 4 groups, given different concentrations of p, p'-DDE (0,20,60 and 100 mg/kg respectively) in corn oil once every other day by intraperitoneal injection for 10 days, and the volume of injection was 10 ml/kg. After 10 days of treatment,the rats were sacrificed and the organs were weighted, then the testes homogenates were prepared. The mRNA expressions of caspase-3,-8,-9 were determined by real time-PCR,and the activities of caspase-3,-8,-9 were measured with the protocol of assay kit. Results Compared with the control group, no significant changes were seen in body weight, organ coefficient of testes, kidney, spleen and lung,but organ coefficient of liver was increased in group of 100 mg/kg p,p'-DDE . The mRNA expressions of caspase-3,-8,-9 in group of 100 mg/kg p,p'-DDE and caspase-9 in group of 60 mg/kg p,p'-DDE were higher than those of the control group(P〈0.05 ). The activities of caspase-3,-8,-9 were increased in group of 100 mg/kg p, p'-DDE (P〈0.05). Conclusion p, p'-DDE can induce the apoptosis of rat testis through activation of caspase-3 mediated by cleavage of caspase-8 and-9.
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