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PubMed · 8108564

Chemical teratogenesis.

M R Juchau
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Abstract

This review has briefly summarized what is currently known concerning the mechanisms whereby several groups of chemicals regarded as "recognized" human teratogens elicit their respective teratogenic effects. It is evident that the extent of our understanding of mechanisms for individual chemicals varies dramatically from that of a reasonably good understanding for methotrexate and other folic acid antagonists to that of virtually no understanding for the most widely recognized human teratogen, thalidomide. Even with methotrexate, however, much remains to be learned pertaining to mechanisms--i.e., the critical links in the chain of events between dihydrofolate reductase inhibition and the manifestation of specific abnormalities. Nevertheless, we can take some comfort in being able to say that we understand the primary causative mechanism. For thalidomide, as well as several others the chemical represents both a shame and a challenge--a challenge that should be addressed with our most serious efforts.

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Abnormalities, Drug-InducedAnimalsHumansTeratogensJournal ArticleResearch Support, U.S. Gov't, P.H.S.Review

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BibTeXRIS

M R Juchau. 1993. Chemical teratogenesis.. https://doi.org/10.1007/978-3-0348-7150-1_3

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PubMed1995

Teratogenicity of high vitamin A intake.

BACKGROUND: Studies in animals indicate that natural forms of vitamin A are teratogenic. Synthetic retinoids chemically similar to vitamin A cause birth defects in humans; as in animals, the defects appear to affect tissues derived from the cranial neural crest. METHODS: Between October 1984 and June 1987, we identified 22,748 pregnant women when they underwent screening either by measurement of maternal serum alpha-fetoprotein or by amniocentesis. Nurse interviewers obtained information on the women's diet, medications, and illnesses during the first trimester of pregnancy, as well as information on their family and medical history and exposure to environmental agents. We obtained information on the outcomes of pregnancy from the obstetricians who delivered the babies or from the women themselves. Of the 22,748 women, 339 had babies with birth defects; 121 of these babies had defects occurring in sites that originated in the cranial neural crest. RESULTS: For defects associated with cranial-neural-crest tissue, the ratio of the prevalence among the babies born to women who consumed more than 15,000 IU of preformed vitamin A per day from food and supplements to the prevalence among the babies whose mothers consumed 5000 IU or less per day was 3.5 (95 percent confidence interval, 1.7 to 7.3). For vitamin A from supplements alone, the ratio of the prevalence among the babies born to women who consumed more than 10,000 IU per day to that among the babies whose mothers consumed 5000 IU or less per day was 4.8 (95 percent confidence interval, 2.2 to 10.5). Using a smoothed regression curve, we found an apparent threshold near 10,000 IU per day of supplemental vitamin A. The increased frequency of defects was concentrated among the babies born to women who had consumed high levels of vitamin A before the seventh week of gestation. CONCLUSIONS: High dietary intake of preformed vitamin A appears to be teratogenic. Among the babies born to women who took more than 10,000 IU of preformed vitamin A per day in the form of supplements, we estimate that about 1 infant in 57 had a malformation attributable to the supplement.

Abnormalities, Drug-Induced↗