Abstract
Sodium arsenate induces developmental malformations in a variety of experimental animals. In the golden hamster, the intravenous (or intraperitoneal) administration of 20 mg/kg of sodium arsenate during day 8 to 9 of gestation induces a rather specific spectrum of congenital malformations. This period corresponds to the period of very rapid differentiation and major organogenesis in this animal. The spectrum of defects produced by arsenate in the hamster includes exencephaly, encephaloceles, skeletal defects, and malformations of the genito-urinary system. This teratogenic effect can be significantly reduced by the simultaneous administration of selenium. Recent studies in this laboratory have demonstrated the permeability of the placenta to 74As during the early critical stages of embryogenesis and the distribution of this isotope in maternal, placental and embryonic tissues. We have also recently demonstrated the marked potentiation of the teratogenic effect of sodium arsenate by subjecting the mothers to short periods of hyperthermia immediately following the administration of subteratogenic or minimal teratogenic levels of arsenate.