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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。
Using rat’s whole embryo culture method combined with electron microscopy to investigate whether there is an interaction between selenium and arsenic, fluorine, methylmercury and the type of action. The results showed that all three could induce abnormal embryonic development in vitro and showed a dose-response relationship. Adding 0.5μg/ml selenium significantly antagonized the teratogenicity and embryotoxicity of 1.0μg/ml arsenic, 10μg/ml fluoride and 0.4μg/ml mercury, but could not alleviate 3.0μg/ml arsenic and 20μg/ml fluoride. The developmental toxicity mainly presents the independent effects of arsenic and fluorine. The visceral yolk sac (VYS) is one of the major sites of selenium-induced arsenic and fluoride teratogenic effects. The pathological changes of VYS ultrastructure caused by 1.0 μg/ml arsenic and 10 μg/ml fluoride disappeared in the corresponding joint group. However, mercury and selenium+mercury have no obvious damage to VYS structure, indicating that ≤0.4μg/ml mercury can directly attack embryonic cells through VYS. The results suggest that structural and functional disorders of VYS are one of the important mechanisms of arsenic and fluoride-induced teratogenesis, and are also related to the mechanism of antagonism between selenium, arsenic, and fluoride.