Hannigan J H, Bellisario R L
Center for Behavioral Teratology, State University of New York, Albany 12222.
Alcohol Clin Exp Res. 1990 Jun;14(3):456-60. doi: 10.1111/j.1530-0277.1990.tb00503.x.
Fetal alcohol syndrome (FAS) is noted for poor growth, developmental delays, and mental retardation. In animals, prenatal alcohol exposure alters anatomical, physiological, and neurochemical maturation and produces behavioral changes similar to those in children. Since thyroid hormones are critical trophic factors for normal somatic and neural maturation, and since fetal thyroid hormones are profoundly affected by acute maternal ethanol administration, we hypothesized that postnatal effects of prenatal alcohol exposure may be related to abnormal thyroid hormone development. We report here that young rats exposed to alcohol in utero have significantly lower serum total thyroxine (T4) concentrations than normal and pair-fed control rats. The results suggest prenatal ethanol exposure may compromise thyroid development in ways not attributable to undernutrition or developmental delays alone. Lowered total T4 levels may be a teratogenic outcome of prenatal alcohol exposure, which could contribute to impaired growth, altered neural organization, and behavioral dysfunction.
胎儿酒精综合征（FAS）以生长发育迟缓、智力发育迟缓为特征。在动物中，孕期酒精暴露会改变解剖学、生理学和神经化学成熟过程，并产生与儿童相似的行为变化。由于甲状腺激素是正常躯体和神经成熟的关键营养因子，且胎儿甲状腺激素会受到母体急性乙醇给药的严重影响，我们推测孕期酒精暴露的产后影响可能与甲状腺激素发育异常有关。我们在此报告，子宫内暴露于酒精的幼鼠血清总甲状腺素（T4）浓度显著低于正常和配对喂养的对照大鼠。结果表明，孕期乙醇暴露可能以并非仅归因于营养不良或发育迟缓的方式损害甲状腺发育。总T4水平降低可能是孕期酒精暴露的致畸后果，这可能导致生长受损、神经组织改变和行为功能障碍。
