Zidenberg-Cherr S, Benak P A, Hurley L S, Keen C L
Department of Nutrition, University of California, Davis 95616.
Drug Nutr Interact. 1988;5(4):257-74.
Excessive ethanol intake during pregnancy can cause birth defects in humans and is referred to as fetal alcohol syndrome (FAS). Because of the characteristic changes that are similar in FAS and zinc (Zn) deficiency, we have examined the role of Zn nutriture in the teratogenicity of ethanol in Sprague-Dawley rats. Female Sprague-Dawley rats were adapted to liquid diets containing Zn at 2 micrograms/ml (LZn), 30 micrograms/ml (AZn), or 300 micrograms/ml (HZn); ethanol contributed either 0% or 36% of kilocalories. Ethanol consumption resulted in reduced fetal growth and retarded skeletal development. Ethanol had no effect on whole body fetal Zn concentrations; however, copper (Cu) deficiency was induced in the HZn fetuses. Ethanol consumption resulted in higher than normal fetal liver CuZnSOD activity in the LZn and AZn groups. Fetuses from HZn dams showed no ethanol effect on CuZnSOD activity, suggesting that the low availability of Cu to the fetus prevented the increase in CuZnSOD activity in response to ethanol. The increase in the activity of fetal CuZnSOD in LZn and AZn groups is consistent with the concept that the metabolism of ethanol results in free radical generation in fetal tissue. Because excessive free radical levels may result in tissue damage, this may be one mechanism contributing to the expression of FAS.
孕期过量摄入乙醇会导致人类出生缺陷，这被称为胎儿酒精综合征（FAS）。由于FAS与锌（Zn）缺乏存在相似的特征性变化，我们研究了锌营养状况在乙醇对斯普拉格-道利大鼠致畸作用中的作用。将雌性斯普拉格-道利大鼠适应含锌量分别为2微克/毫升（低锌，LZn）、30微克/毫升（适宜锌，AZn）或300微克/毫升（高锌，HZn）的液体饮食；乙醇提供0%或36%的千卡热量。摄入乙醇导致胎儿生长减缓以及骨骼发育迟缓。乙醇对胎儿全身锌浓度没有影响；然而，高锌组胎儿出现了铜（Cu）缺乏。在低锌和适宜锌组中，摄入乙醇导致胎儿肝脏铜锌超氧化物歧化酶（CuZnSOD）活性高于正常水平。高锌组母鼠所产胎儿的CuZnSOD活性未受乙醇影响，这表明胎儿可利用的铜含量低，阻碍了CuZnSOD活性因乙醇而升高。低锌和适宜锌组胎儿CuZnSOD活性的增加与乙醇代谢导致胎儿组织中产生自由基的概念相符。由于过量的自由基水平可能导致组织损伤，这可能是导致FAS表现的一种机制。
