阿里尔碳化合物受体激活介导脊椎动物中多二乙醇的急性死亡性和发育毒性:对毒性等效因子框架的机制见解和影响
Rui Zhang1, Jian Zhai2, Qiuxuan Wu1
1School of Water Conservancy and Environment, University of Jinan, Jinan 250022, China.
Environmental science & technology
|December 5, 2025
概括
多二乙烯 (PCDE) 在脊椎动物中引起毒性,主要是通过酸受体 (AHR) 激活. 这项研究证实了AHR是关键的调解者,对于这些二氧化类化合物的生态风险评估至关重要.
科学领域:
- 环境毒理学环境毒理学
- 有毒性的分子机制.
- 生态毒理学 生态毒理学
背景情况:
- 在脊椎动物中,多二乙烯 (PCDE) 的毒理机制尚未完全理解.
- PCDE是环境污染物,具有生物积聚的潜力和与二氧化的结构相似性.
研究的目的:
- 为了研究是否阿里碳化合物受体 (AHR) 激活调解PCDE诱导的急性致死性和发育性毒性.
- 评估不同脊椎动物物种中PCDE同源的二氧化类活性.
主要方法:
- 野生类型,转基因 (Tg(cyp1a:gfp) 和Ahr2-null斑马鱼对11种环境PCDE原体的暴露.
- 在转基因斑马鱼幼虫中通过GFP诱导激活Ahr2的证实.
- 在斑马鱼,鸟类和老鼠模型中进行体外物种特异性光酶记者基因 (LRG) 测试.
主要成果:
- 与野生类型相比,Ahr2-null斑马鱼的死亡率和形明显降低,证实Ahr2是PCDE毒性的主要媒介.
- 在体外测试显示了斑马鱼,鸟类和老鼠模型中PCDE的显著的二氧化类活性,物种间的强度变化高达27,000倍.
- 一些PCDE的相对强度与已知的二氧化类化合物相当或超过.
结论:
- AHR激活是脊椎动物PCDE毒性背后的主要分子机制.
- 结果为PCDE的生态风险评估提供了关键数据.
- 由于其类似于二氧化碳的特性和生物积累潜力,PCDE值得考虑将其纳入全球毒性等效因子框架.
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