Hepatotoxicity of maternal ethanol consumption in rat offspring: an assessment with a study of the ontogenetic development of ethanol-oxidizing systems
Rovinski, B.; Hosein, E.A.; Lee, H.; Hin, G.L.; Rastogi, N.K.
Alcohol and Drug Research 7(3): 195-205
1987
ISSN/ISBN: 0883-1386 PMID: 3548738 Document Number: 292344
The effect of chronic maternal ethanol ingestion on the ontogenetic development of rat hepatic ethanol-oxidizing systems was investigated. Alcohol dehydrogenase (ADH) activity was first detected at day 19 of gestation. It then increased rapidly to reach adult levels by day 14 postnatally. The ontogenetic pattern, the specific activity and the affinity of the enzyme for its substrate or cofactor were not affected by chronic maternal ethanol consumption. Hepatic microsomal cytochrome P-450 content was first detected in trace amounts just prior to birth. It then increased rapidly in the first 10 days postnatally. Chronic maternal ethanol ingestion did not affect the developmental pattern but induced an increase in the total amount of P-450 detected throughout the postnatal period studied. Fat accumulation was found in fetal and postnatal livers and appeared to correlate with the emerging ability to oxidize ethanol by fetal ADH. The late appearance of the ADH and microsomal ethanol-oxidizing systems indicates that the fetal liver would be entirely dependent on maternal mechanisms to oxidize in-utero ethanol.