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在 HepG2 细胞上对[a]pyrene 和 PAH4 的比较毒性分析使用转录组学和代谢组学

Miao Yang¹, Jialin Sun¹, Xin Cao¹

¹Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China; Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China; Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

|April 25, 2025

概括

这项研究表明,PAH4混合物和甲 (BaP) 呈现出类似的肝毒性机制,影响细胞死亡和新陈代谢. 亚利碳化合物受体 (AHR) 信号传导在PAH4毒性中起作用.

科学领域:

环境毒理学环境毒理学
分子毒理学分子毒理学

背景情况:

多环芳 (PAH) 是广泛存在的具有潜在健康风险的污染物.
PAH4 ([a]pyrene,,[a]anthracene,[b]fluoranthene) 是一个用于总PAHs的拟议标记物.
关于PAH4的综合毒性及其与单个PAH相比的差异知之甚少.

研究的目的:

为了研究PAH4.4的肝毒性机制.
为了比较PAH4与[a]pyrene (BaP) 的毒性.
探索基碳化合物受体 (AHR) 信号在PAH4毒性的作用.

主要方法:

使用HepG2细胞模型进行毒性评估.
进行了综合的转录学和代谢学分析.
用人综合生物标志物响应 (IBR) 分析.
使用一种阿里碳化合物受体 (AHR) 抗剂来评估信号通路的参与.

主要成果:

通过P53激活,BaP和PAH4都诱导了细胞毒性,氧化应激和亡.
观察到氧酶增殖器激活受体 (PPAR) 信号和脂质代谢障碍的破坏.
转录组学和代谢组学揭示了共享的毒性机制,影响糖脂和糖脂脂代谢.
IBR分析表明BaP和PAH4的全球毒性相似.
AHR抗剂部分缓解了PAH4诱导的肝毒性.

结论:

BaP和PAH4具有类似的肝毒性机制,包括对亡和脂质代谢的影响.
AHR信号与PAH4混合物的毒性有关.
结果提供了关于PAH混合物的毒理相互作用的见解.

关键词:

在HepG2细胞中.肝毒性肝毒性肝毒性代谢学代谢学代谢学混合物混合物混合物多环芳香碳化合物多环芳香碳化合物文字转录学 (Transcriptomics) 是一个学科.

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