关键词: Benz[a]anthracene Embryonic exposure Neuro-immune Proteomics analysis Social behavior Zebrafish

Mesh : Animals Zebrafish Water Pollutants, Chemical / toxicity Benz(a)Anthracenes / toxicity Social Behavior Behavior, Animal / drug effects Receptors, Aryl Hydrocarbon / metabolism Embryo, Nonmammalian / drug effects

来  源:   DOI:10.1016/j.scitotenv.2024.172615

Abstract:
Benz[a]anthracene (BaA), a prevalent environmental contaminant within the polycyclic aromatic hydrocarbon class, poses risks to both human health and aquatic ecosystems. The impact of BaA on neural development and subsequent social behavior patterns remains inadequately explored. In this investigation, we employed the zebrafish as a model to examine the persisting effects of BaA exposure on social behaviors across various developmental stages, from larvae, juveniles to adults, following embryonic exposure. Our findings indicate that BaA exposure during embryogenesis yields lasting neurobehavioral deficits into adulthood. Proteomic analysis highlights that BaA may impair neuro-immune crosstalk in zebrafish larvae. Remarkably, our proteomic data also hint at the activation of the aryl hydrocarbon receptor (AHR) and cytochrome P450 1A (CYP1A) pathway by BaA, leading to the hypothesis that this pathway may be implicated in the disruption of neuro-immune interactions, contributing to observable behavioral disruptions. In summary, our findings suggest that early exposure to BaA disrupts social behaviors, such as social ability and shoaling behaviors, from the larval stage through to maturity in zebrafish, potentially through the detrimental effects on neuro-immune processes mediated by the AHR-CYP1A pathway.
摘要:
奔驰[a]蒽(BaA),多环芳烃类别中普遍存在的环境污染物,对人类健康和水生生态系统都构成了风险。BaA对神经发育和随后的社会行为模式的影响仍未充分探索。在这次调查中,我们采用斑马鱼作为模型来研究BaA暴露对不同发育阶段社会行为的持续影响,从幼虫身上,从青少年到成年人,胚胎暴露后。我们的发现表明,在胚胎发生过程中接触BaA会导致成年后持续的神经行为缺陷。蛋白质组学分析强调BaA可能会损害斑马鱼幼虫的神经免疫串扰。值得注意的是,我们的蛋白质组学数据也暗示了芳香烃受体(AHR)和细胞色素P4501A(CYP1A)途径的激活,导致这种途径可能与神经免疫相互作用的破坏有关的假设,导致可观察到的行为中断。总之,我们的研究结果表明,早期接触BaA会破坏社会行为,比如社交能力和浅滩行为,从斑马鱼的幼体阶段到成熟,可能通过对AHR-CYP1A途径介导的神经免疫过程的有害影响。
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