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探究食物污染物在自闭症谱系障碍中的作用:对重金属、农药和霉菌毒素的综合分析

Investigating the role of food pollutants in autism spectrum disorder: a comprehensive analysis of heavy metals, pesticides, and mycotoxins.

作者信息

Nehzomi Zahra Shamsipour, Shirani Kobra

机构信息

Department of Toxicology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2025 Mar;398(3):2511-2533. doi: 10.1007/s00210-024-03551-4. Epub 2024 Oct 28.

DOI:10.1007/s00210-024-03551-4
PMID:39466439
Abstract

Food pollutants, including heavy metals, pesticides, and mycotoxins, have been proposed as potential risk factors for autism spectrum disorder (ASD) during pregnancy and early childhood. This paper examines the impact of food pollutants on ASD risk. A systematic search through PubMed, Google Scholar, and Sciverse yielded studies from 1990 to present. Research indicates elevated levels of heavy metals in children with ASD, linking pesticides and toxins to brain development disruptions. Mycotoxins, specifically, show a correlation with ASD and can contaminate food, posing a threat to neurodevelopment. Strategies like choosing organic foods and reducing exposure to toxins may benefit individuals with ASD and those vulnerable to the disorder. Further research is essential to comprehend the food pollutant-ASD relationship and devise effective exposure reduction strategies.

摘要

包括重金属、农药和霉菌毒素在内的食物污染物,已被认为是孕期和幼儿期自闭症谱系障碍(ASD)的潜在风险因素。本文探讨了食物污染物对自闭症谱系障碍风险的影响。通过PubMed、谷歌学术和Sciverse进行的系统检索,得到了1990年至今的研究。研究表明,自闭症谱系障碍儿童体内的重金属含量升高,农药和毒素与大脑发育紊乱有关。具体而言,霉菌毒素与自闭症谱系障碍存在关联,并且会污染食物,对神经发育构成威胁。选择有机食品和减少接触毒素等策略,可能会使自闭症谱系障碍患者以及易患该疾病的人受益。进一步的研究对于理解食物污染物与自闭症谱系障碍之间的关系以及制定有效的减少接触策略至关重要。

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本文引用的文献

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Medicina (Kaunas). 2024 Mar 14;60(3):479. doi: 10.3390/medicina60030479.
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Mycotoxins in Cereal-Based Products and Their Impacts on the Health of Humans, Livestock Animals and Pets.谷物制品中的真菌毒素及其对人类、家畜和宠物健康的影响。
Toxins (Basel). 2023 Jul 28;15(8):480. doi: 10.3390/toxins15080480.
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Aflatoxin B1 Exacerbates Genomic Instability and Apoptosis in the BTBR Autism Mouse Model via Dysregulating DNA Repair Pathway.
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