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产前暴露于甲状腺干扰物及其对大脑发育的不良影响的证据。

Evidence for Prenatal Exposure to Thyroid Disruptors and Adverse Effects on Brain Development.

作者信息

Demeneix Barbara A

机构信息

CNRS/UMR7221, Muséum National d'Histoire Naturelle/Université Paris-Sorbonne, Paris, France.

出版信息

Eur Thyroid J. 2019 Dec;8(6):283-292. doi: 10.1159/000504668. Epub 2019 Nov 15.

DOI:10.1159/000504668
PMID:31934553
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6944944/
Abstract

Thyroid hormone regulates vital processes in early brain development such as neuronal stem cell proliferation, migration, and myelination. The fetal thyroid is not fully functional until mid-pregnancy (18-20 weeks), so placental transfer of maternal thyroid hormones during early pregnancy is crucial, as is the maternal iodine status. The volume of chemical production has increased 300-fold since the 1970s. Thus, chemical exposure is ubiquitous; every child born today has dozens of man-made xenobiotic compounds in its blood. Increasing evidence from both epidemiological and animal or in vitro studies demonstrates that many of these chemicals have the potential to interfere with thyroid hormone availability and action at different physiological levels. These chemicals are found in numerous consumer products and include certain plastics, pesticides, perfluorinated compounds, and flame retardants. The last decades have seen exponential increases in neurodevelopmental disease including autism spectrum disorder and attention deficit/hyperactivity disorder. We hypothesize that prenatal exposure to mixtures of thyroid hormone-disrupting chemicals, with iodine deficiency potentially exacerbating the situation, has a strong probability of contributing to this increased incidence of neurodevelopmental disease, but could also entail a surreptitious, but socio-economically consequential, loss of IQ. Thyroid hormone receptor actions can modulate gene transcription, most often through epigenetic mechanisms. Thus, interference with epigenetic regulations is increasingly thought to link neurodevelopmental disease and IQ loss to thyroid hormone disruption.

摘要

甲状腺激素调节早期大脑发育中的重要过程,如神经元干细胞增殖、迁移和髓鞘形成。胎儿甲状腺直到妊娠中期(18 - 20周)才完全发挥功能,因此妊娠早期母体甲状腺激素的胎盘转运至关重要,母体碘状态也是如此。自20世纪70年代以来,化学品产量增长了300倍。因此,化学物质暴露无处不在;如今出生的每个孩子血液中都有数十种人造外源性化合物。越来越多的流行病学、动物或体外研究证据表明,这些化学物质中的许多都有可能在不同生理水平上干扰甲状腺激素的可用性和作用。这些化学物质存在于众多消费品中,包括某些塑料、农药、全氟化合物和阻燃剂。在过去几十年中,包括自闭症谱系障碍和注意力缺陷多动障碍在内的神经发育疾病呈指数级增长。我们推测,产前暴露于破坏甲状腺激素的化学物质混合物中,碘缺乏可能会使情况恶化,很有可能导致神经发育疾病发病率的增加,但也可能导致智商的悄悄下降,而这在社会经济方面会产生后果。甲状腺激素受体的作用通常通过表观遗传机制调节基因转录。因此,越来越多的人认为对表观遗传调控的干扰将神经发育疾病和智商下降与甲状腺激素紊乱联系起来。

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