Developmental thyroid hormone disruption: Prevalence, environmental contaminants and neurodevelopmental consequences
Developmental thyroid hormone disruption: Prevalence, environmental contaminants and neurodevelopmental consequences
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DOI：
10.1016/j.neuro.2011.11.005
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发表时间：
2012-08-01
期刊：
影响因子：
3.4
通讯作者：
Koibuchi, Noriyuki
中科院分区：
文献类型：
--
作者：
Gilbert, Mary E.;Rovet, Joanne;Koibuchi, Noriyuki
甲状腺激素（TH）对生长和发育，特别是大脑发育至关重要。有许多环境因素导致循环TH的边际减少。虽然很明显，严重的发育性甲状腺功能减退症对神经发育是非常有害的，但关于中度甲状腺功能减退症的后果的信息较少。环境污染物引起的低水平TH破坏的影响尚未确定。本文是2011年夏天在中国西安举行的第13届国际神经毒理学协会会议上四位特邀演讲者的摘要。玛丽吉尔伯特和乔安妮·罗维特概述了甲状腺激素在大脑发育中的作用，并回顾了关于产前和产后早期甲状腺轴中断的神经学后遗症的人类和动物数据。陈祖培指出，碘缺乏是包括中国在内的许多国家TH不足和智力低下的常见原因。本文综述了目前我国碘缺乏症的发病率和神经系统的预后，以及最近实施的碘化计划消除这一智力低下病因的有效性。Joanne Rovet描述了妊娠期间和先天性甲状腺功能减退症条件下TH破坏的影响。出生时甲状腺功能正常，但在子宫内经历TH不足的儿童，在脑成像中显示出微妙的认知障碍和异常。尽管及早发现和治疗，但出生时患有甲状腺疾病的儿童也存在缺陷。不同模式的认知影响，结果从产前与产后TH不足。玛丽吉尔伯特报告了环境污染物对动物大脑发育的甲状腺干扰作用。结果的神经生理，行为，结构和分子的改变，伴随着甲状腺轴的适度扰动进行了审查。Noriyuki Koibuchi描述了接触持久性有机污染物时TH介导的信号传导的分子目标。多氯联苯（PCBs）和多溴联苯醚（PBDEs）是普遍存在的环境污染物，在受体水平上破坏TH信号传导。这些化学物质的这种作用可能导致这些化学物质对大脑功能的负面影响。总之，流行病学，临床前和动物研究已经清楚地确定了TH在大脑发育中的关键作用。需要开展更多的工作来了解甲状腺轴低水平扰动的影响，以评估与环境污染物对甲状腺作用相关的风险。爱思唯尔公司出版
Thyroid hormones (TH) are critical for growth and development and particularly brain development. There are numerous environmental agents that lead to marginal reductions of circulating TH. Although it is clear that severe developmental hypothyroidism is profoundly detrimental to neurodevelopment, there is less information regarding the consequences of modest degrees of thyroid. The impact of low level TH disruptions induced by environmental contaminants has not been defined. This paper is a synopsis from four invited speakers who presented at the 13th International Neurotoxicology Association meeting held in Xi'an, China during the summer of 2011. An overview of the role of TH in brain development and a review of human and animal data on the neurological sequelae of disruption of the thyroid axis in the pre- and early post-natal periods were presented by Mary Gilbert and Joanne Rovet. Iodine deficiency, a common cause of TH insufficiency and mental retardation in many countries, including China, was addressed by Zupei Chen. In this presentation the current incidence of iodine deficiency and neurological outcome in China and the efficacy of recently implemented iodinization programs to eliminate this cause of mental retardation were reviewed. Joanne Rovet described the impact of TH disruption during pregnancy and under conditions of congenital hypothyroidism. Children born with normal thyroid function, but who experienced TH insufficiency in the womb, display subtle cognitive impairments and abnormalities in brain imaging. Despite early detection and treatment, deficiencies also exist in children born with thyroid disorders. Different patterns of cognitive effects result from prenatal versus postnatal TH insufficiency. Mary Gilbert reported on the effects of environmental contaminants with thyroid disrupting action on brain development in animals. Results of neurophysiological, behavioral, structural and molecular alterations that accompany modest perturbations of the thyroid axis were reviewed. Noriyuki Koibuchi described molecular targets of TH-mediated signalling accompanying exposure to persistent organic pollutants. Both polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are prevalent environmental contaminants that disrupt TH signalling at the receptor level. This action by these chemical classes could contribute to the negative impact of these chemicals on brain function. In summary, epidemiological, preclinical and animal research has clearly identified the critical role of TH in brain development. Additional work is required to understand the impact of low level perturbations of the thyroid axis to evaluate the risk associated with environmental contaminants with thyroid action. Published by Elsevier Inc.