Willhite C C, Ferm V H
Adv Exp Med Biol. 1984;177:205-28. doi: 10.1007/978-1-4684-4790-3_9.
A variety of species, including the human, have been shown to be susceptible to the embryotoxic effects of inorganic arsenic. Malformations of the axial skeleton, neurocranium, viscerocranium, eyes, and genitourinary systems as well as prenatal death followed a bolus dose of trivalent or pentavalent inorganic arsenic. Trivalent arsenic was more teratogenic than pentavalent arsenic; in contrast, the methylated metabolites of arsenic possessed only limited teratogenic activity. Administration of inorganic arsenic to mammals results in concentration of arsenic within the placenta and small amounts are deposited within the embryo. Studies concerning the pathogenesis of arsenic-induced axial skeletal lesions revealed early failure of neural fold elevation and a subsequent, persistent failure of closure of the neural tube. Physical factors, drugs and heavy metals may modify the response to a teratogenic dose of inorganic arsenic. Medical problems associated with industrial or agricultural arsenicalism are most often typified by chronic exposure; future studies should emphasize those routes of administration and types of exposure that are characteristic of arsenic intoxication.
包括人类在内的多种物种已被证明对无机砷的胚胎毒性作用敏感。给予一剂三价或五价无机砷后，会出现轴向骨骼、脑颅、面颅、眼睛和泌尿生殖系统的畸形以及产前死亡。三价砷比五价砷的致畸性更强；相比之下，砷的甲基化代谢产物仅具有有限的致畸活性。给哺乳动物施用无机砷会导致砷在胎盘内聚集，少量砷会沉积在胚胎中。关于砷诱导的轴向骨骼病变发病机制的研究表明，神经褶抬高早期失败，随后神经管闭合持续失败。物理因素、药物和重金属可能会改变对致畸剂量无机砷的反应。与工业或农业砷中毒相关的医学问题通常以慢性暴露为典型；未来的研究应强调那些砷中毒特有的给药途径和暴露类型。
