Hypothesis: Prenatal Ethanol‐Induced Birth Defects and Retinoic Acid
- 1 June 1991
- journal article
- Published by Wiley in Alcohol, Clinical and Experimental Research
- Vol. 15 (3) , 565-567
- https://doi.org/10.1111/j.1530-0277.1991.tb00561.x
Abstract
A hypothesis is presented to explain the biochemical basis of ethanol‐induced birth defects. Prenatal ethanol exposure causes central nervous system and limb abnormalities in humans and in animals. Retinoic acid and didehydroretinoic acid are known to play an important role in the central nervous system and limb developments. Ethanol is known to inhibit the formation of retinoic acid from retinol and deplete hepatic retinoid levels. It is hypothesized that ethanol reduces the levels of retinoic acid in the developing embryo either by inhibiting conversion of retinol to retinoic acid and/or by depleting the level of retinol, thereby causing central nervous system and limb abnormalities.Keywords
This publication has 26 references indexed in Scilit:
- Maternal Genetic Effects on Ethanol Teratogenesis and Dominance of Relative Embryonic Resistance to MalformationsAlcohol, Clinical and Experimental Research, 1990
- Prenatal alcohol exposure: Comparability of effects in humans and animal modelsNeurotoxicology and Teratology, 1990
- Identification of a receptor for the morphogen retinoic acidNature, 1987
- A human retinoic acid receptor which belongs to the family of nuclear receptorsNature, 1987
- Major limb malformations following intrauterine exposure to ethanol: Two additional cases and literature reviewTeratology, 1986
- Aspirin Reduces Alcohol‐Induced Prenatal Mortality and Malformations in MiceAlcohol, Clinical and Experimental Research, 1984
- Hepatic Vitamin A Depletion in Alcoholic Liver InjuryNew England Journal of Medicine, 1982
- Prenatal ethanol exposure in mice: Teratogenic effectsTeratology, 1979
- The effects of moderate alcohol consumption during pregnancy on fetal growth and morphogenesisThe Journal of Pediatrics, 1978
- RECOGNITION OF THE FETAL ALCOHOL SYNDROME IN EARLY INFANCYThe Lancet, 1973