摘要
选动情间期SD种雌性大鼠,分别皮下注射5和10mg/kg CdC12及生理盐水1.0ml/kg。染毒后第6天用戊巴比妥麻醉,再静脉注射0.5和2.0μg/kg LHRH。结果表明,LHRH能使垂体和血清中LH含量升高。另一试验,动情间期SD大鼠,皮下注射10mg/kg CdCl_2后第6天,注射LHRH后,血清LH和孕酮水平明显升高,能部分恢复排卵功能。实验结果提示,Cd^(2+)中止排卵过程似乎在于使垂体释放LH减少,进而使LH对卵巢黄体功能的支持减退,这可能是Cd^(2+)阻断孕酮作用的途径之一。
Groups of SD rats were given cadmium chloride ( CdCl2 ) at 5, 10 mg/kg b.w.or 0.9% Nad solution at 1.0 mg/kg subcutaneously on the day of diestrus Ⅱ.Six days later(proe-streus), they were anesthetized with pentobarbital and injected intravenously with 0.5 or 2.0 μg/kg LHRH. Their blood was collected for LH determination. The second batch of the rats pretreated with 10 mg/kg CdCl2 and treated with 4 μg/kg LHRH was allowed to recover from the ansthesia and checked for ovulation on the next day ( estrus ) . In the rats pretreated with 10 mg/kg CdCl2, the LH content of pituitary gland was found reducd remarkably, while those preteated with Cd++, the ovulation was found recovered, which received supplementary LHRH. It is concluded that Cd++-induced anovulation is associated with the altered function of the pituitary gland and ovary, which can restored by excess LHRH.
出处
《卫生毒理学杂志》
CSCD
1992年第1期1-3,共3页
Journal of Health Toxicology