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同时暴露于双甲和会通过向下丘脑-垂体-甲状腺轴和PPAR通路来增强斑马鱼的肝毒性

Le Zhang¹, Qiang Li², Yingying Tang¹

¹College of Environmental Science and Engineering, Guangzhou University, Guangzhou, 510006, China.

Environmental pollution (Barking, Essex : 1987)

|August 28, 2025

概括

双A (BPA) 和 (As) 会导致肝脏损伤和甲状腺功能受损. 同时暴露会加剧这些毒性影响,强调需要评估环境风险.

科学领域:

环境毒理学
肝病学
内分泌学

背景情况:

双A (BPA) 和 (As) 是广泛存在的污染物,具有已知的代谢破坏性和重叠的肝脏目标.
BPA和As同时暴露的联合肝毒性作用和分子机制尚不清楚.

研究的目的:

在斑马鱼中研究BPA和As的单独和联合肝毒性作用.
阐明BPA和As诱导的肝损伤的分子机制,包括对下丘脑-垂体-甲状腺 (HPT) 轴和脂质代谢的影响.

主要方法:

斑马鱼被暴露在BPA和/或As中28天.
通过组织病理学,肝功能测试和氧化应激标记来评估肝损伤.
通过转录基因分析探索分子机制,重点关注HPT轴激素和过氧体增殖器激活受体 (PPAR) 信号.

主要成果:

暴露于BPA和/或As导致严重的肝损伤,肝功能受损,氧化应激和脂质代谢失调.
同时接触BPA和As会加剧氧化应激和脂质功能障碍.
暴露于BPA和/或As会扰乱HPT轴,降低关键激素水平 (TRH,TSH,T3,T4) 并改变基因表达.
转录组分析显示PPAR信号通路因BPA和/或As而受到干扰.

结论:

在斑马鱼中,BPA和As独立引起肝毒性,同时暴露导致副作用的增加.
肝毒性可能是由HPT轴和PPAR信号通路的同时破坏引起的.
这项研究提供了关于BPA和As联合毒性的关键机制见解,强调了评估同时暴露风险的重要性.

关键词:

脂肪代谢的调节失调混合物氧化损伤有毒性转录组

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