Wong Sarah, Giulivi Cecilia
University of California, Department of Molecular Biosciences, 1089 Veterinary Medicine Dr., 3009 VetMed3B, Davis, CA 95616, USA.
CNS Neurol Disord Drug Targets. 2016;15(5):614-23. doi: 10.2174/1871527315666160413122624.
Autism spectrum disorders (ASD) are a growing concern with more than 1 in every 68 children affected in the United States by age 8. Limited scientific advances have been made regarding the etiology of autism, with general agreement that both genetic and environmental factors contribute to this disorder.
To explore the link between exposure to PBDE, mitochondrial dysfunction and autism risk.
Perinatal exposures to PBDEs may contribute to the etiology or morbidity of ASD including mitochondrial dysfunction based on (i) their increased environmental abundance and human exposures, (ii) their activity towards implicated in neuronal development and synaptic plasticity including mitochondria, and (iii) their bioaccumulation in mitochondria.
In this review, we propose that PBDE, and possibly other environmental exposures, during child development can induce or compound mitochondrial dysfunction, which in conjunction with a dysregulated antioxidant response, increase a child's susceptibility of autism.
自闭症谱系障碍（ASD）日益受到关注，在美国每68名8岁儿童中就有超过1人受其影响。关于自闭症的病因，科学进展有限，人们普遍认为遗传和环境因素都与这种疾病有关。
探讨接触多溴二苯醚、线粒体功能障碍与自闭症风险之间的联系。
围产期接触多溴二苯醚可能导致ASD的病因或发病，包括线粒体功能障碍，基于以下几点：（i）它们在环境中的丰度增加以及人类接触增加；（ii）它们对包括线粒体在内的神经元发育和突触可塑性的影响；（iii）它们在线粒体中的生物蓄积。
在本综述中，我们提出在儿童发育过程中，多溴二苯醚以及可能的其他环境暴露可诱导或加重线粒体功能障碍，这与抗氧化反应失调一起，增加了儿童患自闭症的易感性。
