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.