Chronic neurotoxicity of Tetrabromobisphenol A: Induction of oxidative stress and damage to neurons in Caenorhabditis elegans,Chemosphere

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Chronic neurotoxicity of Tetrabromobisphenol A: Induction of oxidative stress and damage to neurons in Caenorhabditis elegans
Chemosphere ( IF 8.1 ) Pub Date : 2024-01-05 , DOI: 10.1016/j.chemosphere.2024.141142
Yunjiang Yu ₁ , Shihui Tan ₂ , Hongzhi Guo ₃ , Xin Hua ₁ , Haibo Chen ₄ , Yue Yang ₁ , Dongli Xie ₁ , Chuan Yi ₅ , Haibo Ling ₅ , Mingdeng Xiang ₁

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Tetrachlorobisphenol A (TCBPA) has been used as an alternative flame retardant in various fields. However, the long-term effects of TCBPA on the nervous system remain unclear. Thus, (L4 larvae) were selected as a model animal to investigate the neurotoxic effects and underlying mechanisms after 10 d of TCBPA exposure. Exposure to TCBPA (0.01–100 μg/L) decreased locomotive behavior in a concentration-dependent manner. In addition, reactive oxygen species (ROS) formation and lipofuscin accumulation were significantly increased, and the expression of was upregulated in the exposed nematodes, indicating that TCBPA exposure induced oxidative damage. Furthermore, 100 μg/L TCBPA exposure caused a reduction in dopamine and serotonin levels, and damage in dopaminergic and serotoninergic neurons, which was further confirmed by the downregulated expression of related genes (e.g., , , , and ). Molecular docking analysis demonstrated the potential of TCBPA to bind to the neurotransmitter receptor proteins DOP-1, DOP-3, and MOD-1. These results indicate that chronic exposure to TCBPA induces neurotoxic effects on locomotive behavior, which is associated with oxidative stress and damage to dopaminergic and serotoninergic neurons.

中文翻译：

四溴双酚 A 的慢性神经毒性：诱导秀丽隐杆线虫神经元氧化应激和损伤

四氯双酚A（TCBPA）已作为替代阻燃剂应用于各个领域。然而，TCBPA 对神经系统的长期影响仍不清楚。因此，选择（L4幼虫）作为模型动物来研究TCBPA暴露10天后的神经毒性作用和潜在机制。暴露于 TCBPA (0.01–100 μg/L) 会以浓度依赖性方式降低运动行为。此外，暴露的线虫中活性氧（ROS）的形成和脂褐素的积累显着增加，并且表达上调，表明TCBPA暴露诱导了氧化损伤。此外，100 μg/L TCBPA 暴露导致多巴胺和血清素水平降低，以及多巴胺能和血清素能神经元损伤，相关基因（例如、、和）表达下调进一步证实了这一点。分子对接分析证明了 TCBPA 与神经递质受体蛋白 DOP-1、DOP-3 和 MOD-1 结合的潜力。这些结果表明，长期接触 TCBPA 会对运动行为产生神经毒性作用，这与氧化应激以及多巴胺能和血清素能神经元的损伤有关。

更新日期：2024-01-05

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