Vitamin A attenuates PFOS-induced neurotoxicity and alters early proximity patterns to conspecifics in zebrafish larvae.

IF 2.9 3区医学 Q2 BEHAVIORAL SCIENCES

Frontiers in Behavioral Neuroscience Pub Date : 2025-06-05 eCollection Date: 2025-01-01 DOI:10.3389/fnbeh.2025.1564694

Peiyun Jiang, Jingyu Wang, Xiaoying Wang, Li Zou, Di Wu, Qu Xu, Yue Jiang, Mengmeng Yao, Qin Hong, Xia Chi

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引用次数: 0

Abstract

Introduction: Perfluorooctane sulfonic acid (PFOS), a persistent perfluoroalkyl substance with ubiquitous environmental distribution and bioaccumulative potential, has raised significant public health concerns due to its association with neurodevelopmental disorders. This study investigates vitamin A's neuroprotective capacity against PFOS-induced toxicity, particularly focusing on social behavior deficits-a core phenotype of autism spectrum disorder (ASD).

Methods: Zebrafish larvae were exposed to 1 μM or 5 μM PFOS (with/without 5 nM vitamin A co-treatment) from 24-144 hours post-fertilization (hpf). Control groups received 0.01% DMSO (vehicle) or 5 nM vitamin A alone. Developmental parameters (body length, heart rate), locomotor activity (total distance moved), and neurobehavioral endpoints (conspecific interaction) were quantified using automated tracking systems (ViewPoint ZebraLab). Neurochemical alterations were assessed through qPCR (dopaminergic genes) and AO staining (apoptosis).

Results: PFOS exposure (5 μM) significantly increased inter-individual distance (IID) and reduced physical contact frequency during social interaction tests. Neurochemical analyses revealed concurrent dopamine transporter downregulation and apoptosis-related gene activation . Vitamin A co-treatment attenuated these effects.

Discussion: Our findings demonstrate that PFOS disrupts early social neurodevelopment through dopaminergic dysregulation and apoptotic signaling, while vitamin A exhibits counteractive potential. this study elucidates the impact of PFOS exposure on zebrafish social behavior and brain development. while highlighting the neuroprotective potential of vitamin A against PFOS exposure, These findings have significant guiding implications for the development of public health policy and provide a scientific foundation for comprehending the neurotoxicity of PFOS and developing effective intervention measures.

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维生素A减轻全氟辛烷磺酸引起的神经毒性，并改变斑马鱼幼虫对同种生物的早期接近模式。

导语：全氟辛烷磺酸（PFOS）是一种持久性全氟烷基物质，具有无处不在的环境分布和生物蓄积性，由于与神经发育障碍有关，引起了重大的公共卫生关注。本研究探讨了维生素A对全氟磺酸引起的毒性的神经保护能力，特别是关注社会行为缺陷-自闭症谱系障碍（ASD）的核心表型。方法：斑马鱼幼鱼受精后24-144小时分别暴露于1 μM或5 μM的全氟辛烷磺酸（加/不加5 nM维生素A）中。对照组分别给予0.01% DMSO（对照剂）或单独给予5 nM维生素A。使用自动跟踪系统（ViewPoint ZebraLab）对发育参数（体长、心率）、运动活动（总移动距离）和神经行为终点（同向相互作用）进行量化。通过qPCR（多巴胺能基因）和AO染色（细胞凋亡）评估神经化学变化。结果：全氟辛烷磺酸暴露（5 μM）显著增加了个体间距离（IID），降低了社会互动测试中的身体接触频率。神经化学分析显示同时存在多巴胺转运蛋白下调和凋亡相关基因激活。维生素A联合治疗减轻了这些影响。讨论：我们的研究结果表明，全氟辛烷磺酸通过多巴胺能失调和凋亡信号通路破坏早期社会神经发育，而维生素A则表现出对抗潜能。本研究阐明了全氟辛烷磺酸暴露对斑马鱼社会行为和大脑发育的影响。这些发现对公共卫生政策的制定具有重要的指导意义，并为理解全氟辛烷磺酸的神经毒性和制定有效的干预措施提供了科学依据。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Behavioral Neuroscience BEHAVIORAL SCIENCES-NEUROSCIENCES

CiteScore

4.70

自引率

3.30%

发文量

506

审稿时长

6-12 weeks

期刊介绍： Frontiers in Behavioral Neuroscience is a leading journal in its field, publishing rigorously peer-reviewed research that advances our understanding of the neural mechanisms underlying behavior. Field Chief Editor Nuno Sousa at the Instituto de Pesquisa em Ciências da Vida e da Saúde (ICVS) is supported by an outstanding Editorial Board of international experts. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide. This journal publishes major insights into the neural mechanisms of animal and human behavior, and welcomes articles studying the interplay between behavior and its neurobiological basis at all levels: from molecular biology and genetics, to morphological, biochemical, neurochemical, electrophysiological, neuroendocrine, pharmacological, and neuroimaging studies.