从塞舌尔儿童发展研究营养队列2中,暴露于产前MeHg的儿童的KEAP1多态和神经发育结果
Helena Korres de Paula1, Tanzy M Love2, Daniela Pineda1
1Division of Occupational and Environmental Medicine, Lund University, Lund 22185, Sweden.
Neurotoxicology
|October 20, 2023
概括
KEAP1中的遗传变异,但不是NFE2L2,与暴露于甲基的儿童的神经发育差异有关. 这些发现强调了遗传因素在中的作用.
科学领域:
- 环境健康 环境健康
- 神经科学是一个神经科学.
- 遗传学 是一个遗传学.
背景情况:
- 人类甲基 (MeHg) 的新陈代谢因遗传因素而有所不同.
- 核因子E2相关因子2 (NRF2) 和其调节器KEAP1影响MeHg代谢和神经毒性.
- 了解这些遗传变异对于评估与产前暴露相关的风险至关重要.
研究的目的:
- 研究NFE2L2 (NRF2) 和KEAP1的遗传变异与儿童神经发育结果之间的关联.
- 评估与这些遗传多态性相关的产前暴露带来的风险.
- 检查鱼类消费量较高的人群中20个月和7岁时的结果.
主要方法:
- 研究了塞舌尔的一个母婴队列 (营养队列2).
- 对1285名儿童进行了NFE2L2和KEAP1多态的基因型鉴定.
- 产前的MeHg暴露通过带血中的水平进行测量;神经发育通过20个月和7年的标准化测试进行评估.
主要成果:
- 没有发现NFE2L2或KEAP1多态度与血度或20个月的神经发育之间的显著关联.
- 在7岁时,KEAP1多态 (rs8113472和rs9676881) 与精神运动功能,社会沟通和认知有显著的关联.
- 特定的KEAP1变异与更糟糕和更好的神经发育结果有关.
结论:
- 在NFE2L2中的遗传变异与MeHg水平或神经发育无关.
- KEAP1多态性与暴露于MeHg高水平的儿童的神经发育差异有关.
- 这些发现表明KEAP1在中介暴露对神经发育的影响方面发挥了作用.
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