Fetal alcohol exposure: cellular toxicity and molecular events involved in toxicity.
Fetal alcohol exposure: cellular toxicity and molecular events involved in toxicity.
复制标题
胎儿酒精暴露：细胞毒性和毒性涉及的分子事件。
DOI：
10.1111/j.1530-0277.1990.tb01821.x
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Michaelis,EK
中科院分区：
文献类型：
--
作者：
Michaelis,EK
RENATAL ETHANOL exposure leads to develop-P mental delays characterized by decreased growth and differentiation and by visceral and craniofacial malformation. I4 Not all tissues nor all cells are equally susceptible to the detrimental effects of prenatal alcohol exposure nor are the cells undergoing cell division and differentiation the only ones affected by ethanol-induced perturbations during the gestational period. Exposure of the fetus or newborn to alcohol may affect cell replication, cell growth and differentiation, and cell migration. Identifying among the varied actions of ethanol those that are the most likely culprits for the teratogenic effects produced by this alcohol is a very difficult process. Much of the existing clinical and experimental literature reveals that, to a large extent, our understanding of the effects of ethanol on organ and cell development is of a descriptive nature. There are, however, some molecular and cellular mechanisms that have been identified as possible underlying mechanisms for cell toxicity and organ teratogenicity produced by ethanol during the prenatal and perinatal period. In this paper, the emphasis will be placed on probing possible mechanisms for ethanol-precipitated cell damage in several organs, but particularly in the central and peripheral nervous systems. The brain is one of the most frequently affected organs in the clinical condition known as the fetal alcohol syndrome (FAS) or alcohol embryopathy (AE). Even when other teratogenic effects are barely detectable, neurological and behavioral manifestations of prenatal exposure to alcohol are evident. 4, 5
