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应用显微解剖、原位杂交组织化学、扫描电镜等技术深入研究了三氧化二砷对大鼠胚胎的发育毒性和神经毒性及ＨＳＰ７０ｍＲＮＡ表达与胚胎神经系统发育的关系。结果表明反映胚胎神经系统发育的头长，神经管未闭、体位异常和脑部形态异常发生率均与染砷剂量和作用时间呈正比关系（Ｐ＜００５）。扫描电镜观察发现大鼠胚胎脑部表皮细胞的微绒毛数量减少，回缩变短，细胞膜表面出现许多小的空洞性病理改变。原位杂交结果表明砷能激发大鼠胚胎产生应激反应，１０ｍｇ／ｋｇ砷诱导的神经管未闭发生率（３５７％）和ＨＳＰ７０ｍＲＮＡ原位表达强度均明显高于４ｍｇ／ｋｇ砷的作用，证明热休克反应具有双重作用，揭示了砷的发育毒性与其剂量和作用时间是否大于细胞内ＨＳＰ７０合成量的自我调控水平有关，同时亦与损害时间发生于胚胎器官形成期的那一时段密切关联。
The effects of arsenic trioxide on the developmental toxicity and neurotoxicity of rat embryos and the relationship between the expression of HSP70mRNA and the development of embryonic nervous system were investigated using microdissection, in situ hybridization histochemistry and scanning electron microscopy. The results showed that the length of head, neural tube, anomalies of body position and abnormal brain morphology, which reflect the development of embryonic nervous system, were in direct proportion to the dose and duration of arsenic exposure (P <005). Scanning electron microscopy showed that the number of microvilli in rat embryonic brain epidermal cells decreased, the contraction shortened, and many small hollow pathological changes appeared on the cell membrane surface. In situ hybridization results showed that arsenic induced a stress response in rat embryos. The incidence of neural tube defects induced by arsenic at 10 mg / kg (35.7%) and HSP70 mRNA expression in situ were significantly higher than that of 4 mg / kg arsenic , Demonstrating that heat shock response has a dual role, revealing that the developmental toxicity of arsenic is related to its dose and duration of action greater than the self-regulation of HSP70 synthesis in the cell and also to the period during which damaging times occur in the embryonic organogenesis .