Prostaglandin synthesis inhibitors block alcohol-induced fetal hypoplasia.
Prostaglandin synthesis inhibitors block alcohol-induced fetal hypoplasia.
复制标题
前列腺素合成抑制剂可阻止酒精引起的胎儿发育不全。
DOI：
10.1111/j.1530-0277.1985.tb05578.x
复制
发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Kalmus,G
中科院分区：
文献类型：
--
作者：
Pennington,S;Allen,Z;Runion,J;Farmer,P;Rowland,L;Kalmus,G
酒精引起的生长迟缓是一种与母体乙醇消耗始终相关的胎儿效应。在人类中，母亲在怀孕期间摄入少量乙醇的婴儿也有显着的生长抑制发生率。造成这种生长缺陷的分子机制尚不清楚，预防取决于母亲在怀孕期间的禁欲。这里报告的数据表明，乙醇介导的组织前列腺素 (PG) E 水平（PGE1+ PGE2）增加与生长迟缓相关。此外，同时给予 PG 合成抑制剂和酒精可以阻止组织 PG 水平的上升，并防止酒精引起的发育不全。
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 (PGE1plus PGE2) 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.