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目的进一步阐明砷对母体、胎儿、胚胎细胞的影响和验证体外致畸作用。方法用大鼠体内致畸法并结合扫描电镜、组织化学等技术深入探讨了砷的发育毒性和机制。结果Ａｓ２Ｏ３的各剂量组（０，１，４和１０ｍｇ／ｋｇ）均未见母鼠有明显的中毒症状和死亡；胎鼠死亡率分别为１０．２％，１７．４％，２４．８％和６１．１％；骨骼畸形率为１．８９％，３．１２％，１７．２８％和７８．５７％；染毒４８小时后的胚胎畸形率分别为３．１６％，５．３２％，１３．７９％和４０．４８％；扫描电镜观察可见多部位的胚胎表皮细胞受损，细胞表面和细胞连接处出现大小不一的空洞；胚胎畸形表现是神经管未闭、体位异常、肢芽小等；诱生型一氧化氮合成酶组化检查率先证明一氧化氮与胚胎发育异常关系密切，呈明显剂量－反应关系；活体染色表明砷能诱发肢芽细胞过度凋亡；从多角度分析了砷的致畸机理。结论大鼠体内试验证实，砷在胚胎生长发育过程中有致畸作用。
Objective To further elucidate the effects of arsenic on maternal, fetal and embryonic cells and to verify the teratogenic effects in vitro. Methods In vivo teratogenicity in rats and combined with scanning electron microscopy, histochemistry and other techniques in-depth discussion of arsenic developmental toxicity and mechanism. Results As2O3 (0, 1, 4, and 10 mg / kg) did not show any significant toxic symptoms and deaths in maternal mice. The mortality of fetal rats was 10.2%, 17.4% and 24.8% And 61.1% respectively. The rates of skeletal deformities were 1.89%, 3.12%, 17.28% and 78.57%, respectively. The rates of embryo deformities after 48 hours exposure were 3.16% and 5.32% , 13.79% and 40.48%, respectively. Scanning electron microscopy showed that many parts of embryonic epidermal cells were impaired and vacuoles of different sizes appeared on the cell surface and cell junctions. Fetal malformations showed neural tube defects, abnormal position, Buds and so on; Inducible nitric oxide synthase histochemical examination of the first to prove that nitric oxide and embryonic development is closely related to a significant dose-response relationship; living staining shows that arsenic can induce excessive apoptosis of limb bud cells; from a multi-angle The teratogenic mechanism of arsenic has been analyzed. Conclusion In vivo experiments in rats confirmed that arsenic has teratogenic effects during embryonic growth and development.