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为进一步揭示砷的致畸性、胚胎毒性和作用机制，采用胚胎活体染色和原位ＤＮＡ末端标记等技术探讨了不同剂量砷是否能诱导孕９．５天龄大鼠的胚胎细胞发生凋亡（程序性细胞死亡）及其凋亡与畸胎形成的关系。结果表明随着砷浓度（０、１、４和８ｍｇ／ｋｇ）的增高，畸胎率和死胎率分别由２．６％和０上升到３５．７％和２３．８％，呈明显剂量－反应关系。活体染色发现在胚胎脑、眼、体节、肢芽和腮弓等部位出现大量散在的凋亡细胞，与畸形发生部位相一致。原位ＤＮＡ末端标记进一步证实砷能诱发器官形成期胚胎细胞凋亡，８ｍｇ／ｋｇ砷染毒后，凋亡阳性率高达５５．６％（Ｐ＜０．０５），表明凋亡与畸胎发生关系密切，这是砷致畸作用的重要机制之一。实验结果还发现胚胎细胞坏死亦与畸胎形成有关。
In order to further reveal the teratogenicity, embryotoxicity and mechanism of arsenic toxicity, we explored whether different doses of arsenic could induce apoptosis of embryonic cells of 9.5-day-old pregnant rats by using live embryo staining and in situ DNA end labeling Programmed cell death) and its relationship with the formation of teratogenicity. The results showed that with the increase of arsenic concentrations (0, 1, 4 and 8 mg / kg), the rate of teratogenicity and stillbirth increased from 2.6% and 0 to 35.7% and 23.8% Reaction relationship. In vivo staining revealed a large number of scattered apoptotic cells in embryonic brain, eye, body segments, limb buds and the arch of the paw, consistent with the site of deformity. In situ DNA end labeling further confirmed that arsenic induced apoptosis of embryonic cells during organogenesis, and the apoptotic rate was as high as 55.6% (P <0.05) after exposure to 8 mg / kg arsenic, indicating apoptosis and teratogenicity Close relationship, which is one of the important mechanisms of arsenic teratogenic effect. Experimental results also found that embryonic cell necrosis also associated with teratogenicity.