Department of Nutrition, University of California, Davis, Davis, CA 95616, USA.
Biofactors. 2010 Mar-Apr;36(2):125-35. doi: 10.1002/biof.89.
There is increasing evidence that human pregnancy outcome can be significantly compromised by suboptimal maternal nutritional status. Poor diet results in a maternal-fetal environment in which the teratogenicity of other insults such as alcohol might be amplified. As an example, there is evidence that zinc (Zn) can interact with maternal alcohol exposure to influence the risk for fetal alcohol spectrum disorders (FASD). Studies with experimental animals have shown that the teratogenicity of alcohol is increased under conditions of Zn deficiency, whereas its teratogenicity is lessened when animals are given Zn-supplemented diets or Zn injections before the alcohol exposure. Alcohol can precipitate an acute-phase response, resulting in a subsequent increase in maternal liver metallothionein, which can sequester Zn and lead to decreased Zn transfer to the fetus. Importantly, the teratogenicity of acute alcohol exposure is reduced in metallothionein knockout mice, which can have improved Zn transfer to the conceptus relative to wild-type mice. Consistent with the above, Zn status has been reported to be low in alcoholic women at delivery. Preliminary data from two basic science and clinical nutritional studies that are ongoing as part of the international Collaborative Initiative on Fetal Alcohol Spectrum Disorders support the potential role of Zn, among other nutritional factors, relative to risk for FASD. Importantly, the nutrient levels being examined in these studies are relevant to general clinical populations and represent suboptimal levels rather than severe deficiencies. These data suggest that moderate deficiencies in single nutrients can act as permissive factors for FASD, and that adequate nutritional status or intervention through supplementation may provide protection from some of the adverse effects of prenatal alcohol exposure.
越来越多的证据表明，母体营养状况不佳会显著影响妊娠结局。不良的饮食会导致母体-胎儿环境中，其他如酒精等致畸因素的致畸作用可能会放大。例如，有证据表明锌（Zn）可以与母体酒精暴露相互作用，影响胎儿酒精谱系障碍（FASD）的风险。实验动物研究表明，在缺锌的情况下，酒精的致畸性会增加，而当动物在酒精暴露前给予补充 Zn 的饮食或 Zn 注射时，其致畸性会减轻。酒精可以引发急性期反应，导致母体肝脏金属硫蛋白增加，从而将 Zn 隔离，并导致向胎儿的 Zn 转移减少。重要的是，金属硫蛋白敲除小鼠的急性酒精暴露致畸性降低，相对于野生型小鼠，其向胚胎的 Zn 转移能力可以提高。与上述情况一致，在分娩时的酗酒女性中，Zn 状态报告较低。正在进行的两项基础科学和临床营养研究的初步数据作为胎儿酒精谱系障碍国际合作倡议的一部分，支持 Zn 等营养因素与 FASD 风险之间的潜在作用。重要的是，这些研究中检查的营养水平与一般临床人群相关，代表的是次优水平，而不是严重缺乏。这些数据表明，单一营养素的中度缺乏可以作为 FASD 的许可因素，而充足的营养状况或通过补充进行干预可能会为预防产前酒精暴露的一些不良影响提供保护。
