LOWER SERUM THYROXINE LEVELS IN RATS FOLLOWING PRENATAL EXPOSURE TO ETHANOL
LOWER SERUM THYROXINE LEVELS IN RATS FOLLOWING PRENATAL EXPOSURE TO ETHANOL
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DOI：
10.1111/j.1530-0277.1990.tb00503.x
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发表时间：
1990-06-01
期刊：
影响因子：
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通讯作者：
BELLISARIO, RL
中科院分区：
文献类型：
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作者：
HANNIGAN, JH;BELLISARIO, RL
胎儿酒精综合症(FAS)以生长不良、发育迟缓和智力低下而闻名。在动物中，出生前接触酒精会改变解剖、生理和神经化学成熟，并产生与儿童相似的行为变化。由于甲状腺激素是正常的躯体和神经成熟的关键营养因子，而且胎儿甲状腺激素受到母亲急性酒精摄入的深刻影响，我们推测出生前酒精暴露的出生后影响可能与甲状腺激素的异常发育有关。我们在这里报道，子宫内暴露于酒精的年轻大鼠血清总甲状腺素(T4)浓度显著低于正常和配对喂养的对照组大鼠。结果表明，产前酒精暴露可能会损害甲状腺发育，而不仅仅是营养不良或发育迟缓。总T4水平降低可能是产前酒精暴露的致畸结果，这可能导致发育受损、神经组织改变和行为功能障碍。
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.