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Prostaglandin Synthesis Inhibitors Block Alcohol‐Induced Fetal Hypoplasia
Author(s) -
Pennington Sam,
Allen Zebetta,
Runion Jane,
Farmer Pam,
Rowland Lisa,
Kalmus Gerhard
Publication year - 1985
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.1530-0277.1985.tb05578.x
Subject(s) - ethanol , alcohol , pregnancy , fetus , endocrinology , medicine , prostaglandin , hypoplasia , growth retardation , abstinence , fetal alcohol syndrome , prostaglandin e2 , fetal growth , teratology , chemistry , biology , biochemistry , genetics , psychiatry
Alcohol‐induced growth retardation is a fetal effect consistently associated with maternal ethanol consumption. In humans, those infants whose mothers consume even a limited amount of ethanol during pregnancy have a significant incidence of growth inhibition. The molecular mechanism responsible for this growth deficiency is unknown, and prevention depends on maternal abstinence during pregnancy. The data reported here suggest that ethanol‐mediated increases in tissue prostaglandin (PG) E levels (PGE 1 plus PGE 2 ) are correlated with the growth retardation. Further, simultaneous administration of PG synthesis inhibitors with the alcohol blocks the rise in tissue PG levels and protects against the alcohol‐induced hypoplasia.