摘要
用大鼠全胚胎培养法并结合电镜技术探讨了硒与砷、氟、甲基汞之间是否存在交互作用及作用类型。结果表明三者均能诱发体外培养的胚胎发育异常,并呈剂量反应关系。加入0.5μg/ml硒后明显拮抗1.0μg/ml砷、10μg/ml氟和0.4μg/ml汞的致畸性及胚胎毒性,但不能缓解3.0μg/ml砷和20μg/ml氟的发育毒性,主要呈现砷、氟的独立作用。脏层卵黄囊(VYS)是硒抗砷、氟致畸效应的主要位点之一,1.0μg/ml砷和10μg/ml氟所导致VYS超微结构的病理改变在相应联合组均消失。然而,汞和硒+汞对VYS结构无明显的损害作用,说明≤0.4μg/ml汞能迅速通过VYS而直接攻击胚胎细胞。结果提示,VYS结构与功能紊乱是砷、氟致畸的重要机制之一,也与硒、砷、氟之间拮抗作用的机制有关。
Whole embryo culture technique and electron microscopy were used to study interaction of arsenic,fluoride and mentylmercury with selenium in vitro during early organogenesis of rat embryos.Results showed arsenic,fluoride and menthylmercury could induce death,malformation and retardation in embryonic growth and development in vitro,with an apparent dose-effect relationship.After the addition of 0.5 μg/ml selenium,the teratogenicity and embryotoxicity of 1.0μg/ml arsenic,10μg/ml fluoride and 0.4μg/ml menthylmercury were significantly antagonized.However,because selenium could not ameliorate developmental toxicity of 3.0μg/ml arsenic and 20μg/ml fluoride,the results were independent effect of arsenic or fluoried.Visceral yolk sac(VYS) was an important 'target' site of selenium antagonism of arsenic or fluoride induced teratogenesis in vitro.All pathological changes of VYS induced by 1.0μg/ml arsenic and 10μg/ml fluoride have disappered with selenium added in rat serum cluture in vitro.Menthylmercury didn't damage ultrastructures of VYS with or without selenium.It is evident that menthylmercury can quickly pass through VYS and directly attack embryos.The results suggest that:1)disorders of VYS structure and function were one of teratogenic mechanisms of arsenic or fluoride and 2) would be related to mechanism of interaction between selenium and arsenic or fluoride.
出处
《癌变.畸变.突变》
CAS
CSCD
1996年第5期267-272,共6页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
国家自然科学基金
关键词
硒
砷
氟
甲基汞
致畸作用
全胚胎培养
selenium
arsenic
fluoride
menthylmercury
malfomation
whole embryo culture
in vitro