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Prenatal Ethanol Consumption Alters the Expression of Cellular Retinol Binding Protein and Retinoic Acid Receptor mRNA in Fetal Rat Embryo and Brain
Author(s) -
Grummer Mary A.,
Zachman Richard D.
Publication year - 1995
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1995.tb00995.x
Subject(s) - retinoic acid , embryo , fetus , messenger rna , retinol , chemistry , retinoic acid receptor , ethanol , microbiology and biotechnology , endocrinology , biology , biochemistry , pregnancy , vitamin , genetics , gene
The mechanism by which prenatal ethanol ingestion causes fetal alcohol syndrome (FAS) is unknown. We hypothesize that ethanol disrupts the normal function of retinoids in embryogenesis and differentiation, resulting in FAS. The present work was designed to determine if prenatal ethanol ingestion affects the expression of cellular retinol binding protein (CRBP) and nuclear retinoic acid receptors (RARs). Paired timed pregnant rats were fed a liquid diet, one group treated with 36% of carbohydrate calories replaced with ethanol. Maternal serum retinol concentrations during pregnancy peaked on the 6th day of pregnancy, but no difference was noted between the ethanol and control group. At the 12th and 20th day of gestation, embryos or fetal brain were removed, and RNA was isolated for Northern hybridization. The abundance of CRBP mRNA was significantly elevated by ethanol consumption in both the 12‐day embryo (relative density of control: 1.00 ± 0.10; vs. ethanol: 1.87 ± 0.30, p < 0.05) and 20‐day fetal brain (relative density of control: 1.00 ± 0.09; vs. ethanol: 1.46 ± 0.09, p < 0.01). In the embryo, ethanol ingestion resulted in a decrease in the level of RAR‐β mRNA (control: 1.00 ± 0.05; vs. ethanol: 0.71 ± 0.07, p < 0.01), but had no effect on RAR‐α or RAR‐γ mRNA. In contrast to the embryo, the expression of both the 3.7‐ and 2.7‐kb RAR‐α transcripts was significantly greater in day 20 fetal brain of ethanol‐treated rats (3.7‐kb RAR‐α control: 1.00 ± 0.11; vs. ethanol: 1.65 ± 0.06; p < 0.001;2.7‐kb RAR‐α control: 1.00 ± 0.14; vs. ethanol: 1.74 ± 0.27, p < 0.05), whereas RAR‐β and RAR‐γ expression were not altered. These observations suggest that altered vitamin A function is a potential factor in the embryopathy of prenatal ethanol exposure.