Abstract
Initial experiments involving mouse development employed single IP injections of 45 mg/kg sodium arsenate on one of days 6-12 of gestation and produced a spectrum of developmental defects. Embryotoxicity was indicated by high prenatal mortality and decreased fetal weights. A chelating agent, 2,3-dimercaptopropanol (BAL), was then employed in an attempt to alleviate the adverse effects of prenatal arsenate. BAL was administered 4 hr before, concurrently with, or 4 hr after arsenate. All BAL treatments diminished arsenate-induced gross malformations and growth retardation; the concurrent treatment alleviated skeletal malformation. Injection of rats IP with arsenate has also been reported to result in teratogenicity, including renal agenesis. Further reports indicated that 40 mg/kg arsenate administered to mice by gavage on days 9–11 increased prenatal mortality, reduced fetal weights, and was associated with minor malformations. According to our recent work, however, single oral doses of arsenate must be around 120 mg/kg to cause prenatal toxicity. Multiple doses of 60 mg/kg on 3 days had little effect. Sodium arsenite has also been found to be fetotoxic and teratogenic. Such effects were seen at IP doses of 10–12 mg/kg.
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Selected References
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