Growth, enzymes and hormonal changes in offspring of alcohol-fed rats.
Consumption of ethanol by rats during pregnancy reduces the body and brain weight of their fetuses and pups. The reduction is greater if the offspring are kept with their alcohol-fed mothers rather than with control surrogate mothers during lactation. The activity of several enzymes of the neuronal cell membranes (Na+, K+-ATPase, Ca2+-ATPase, acetylcholinesterase, 5'-nucleotidase) is also reduced. This decrease in enzyme activity may be related to the decrease in neuronal development and could produce profound alterations in brain function. Altered hypothalamic-hypophysial function may be partly responsible for developmental anomalies found in the fetal alcohol syndrome. The levels of plasma luteinizing hormone are lower in pups exposed prenatally to ethanol, and prolactin levels are much higher. Concentrations of ethanol were essentially the same in maternal blood and in the fetus. Acetaldehyde levels in the placenta, amniotic fluid and the remaining fetal tissue at days 15 and 19 of gestation were about 40-50% of those in maternal blood. Acetaldehyde may be important in the pathogenesis of the fetal alcohol syndrome.
D000079:Acetaldehyde / Q000097:blood; D000818:Animals; D002462:Cell Membrane / Q000201:enzymology; D004798:Enzymes / Q000378:metabolism*; D000431:Ethanol / Q000494:pharmacology*; D005260:Female; D006128:Growth / Q000187:drug effects*; D007986:Luteinizing Hormone / Q000097:blood*; D009474:Neurons / Q000201:enzymology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011388:Prolactin / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains
D004798:Enzymes; D000431:Ethanol; D011388:Prolactin; D007986:Luteinizing Hormone; D000079:Acetaldehyde