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Effects in the mouse and rat of prenatal exposure to arsenic.

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.
AuthorsR D Hood, G T Thacker, B L Patterson
JournalEnvironmental health perspectives (Environ Health Perspect) Vol. 19 Pg. 219-22 (Aug 1977) ISSN: 0091-6765 [Print] United States
PMID908302 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Teratogens
  • Dimercaprol
  • Arsenic
Topics
  • Abnormalities, Drug-Induced
  • Animals
  • Arsenic (administration & dosage, antagonists & inhibitors, pharmacology)
  • Dimercaprol (pharmacology)
  • Dose-Response Relationship, Drug
  • Female
  • Fetal Death (etiology)
  • Fetal Growth Retardation (chemically induced)
  • Fetus (drug effects)
  • Mice (embryology)
  • Pregnancy
  • Rats (embryology)
  • Teratogens
  • Time Factors

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