氧化应激导致6PPD和其他轮胎添加剂在A549人类肺上皮细胞中的DNA损伤
Samuel Hyman1,2, Rea Bilić3, Annie Jensen3
1Department of Earth and Environmental Science, Centre for Atmospheric Science, School of Natural Sciences, The University of Manchester, Manchester, UK. samuel.hyman@postgrad.manchester.ac.uk.
Scientific reports
|October 13, 2025
概括
轮胎添加剂如p-phenylenediamines (PPDs) 和benzothiazoles (BTs) 通过耗尽谷和破坏DNA来损害人类肺细胞. N-乙-L-氨酸 (NAC) 可以防止这些影响,建议针对轮胎添加剂毒性的潜在缓解策略.
科学领域:
- 环境科学 环境科学
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 轮胎添加剂,包括p-phenylenediamines (PPDs) 和benzothiazoles (BTs),是广泛存在的环境污染物.
- 这些化合物已在城市空气和人体中检测到,但它们对人体细胞的毒理影响仍未得到充分研究.
研究的目的:
- 研究特定轮胎添加剂对人类气膜肺细胞的毒理作用 (A549).
- 评估这些化合物引起的细胞毒性,氧化应激和DNA损伤.
主要方法:
- A549细胞暴露于各种轮胎添加剂:6PPD,6PPD-Q,DPPD,BTZ和MBT.
- 进行的测试包括细胞毒性,谷氨 (GSH) 枯竭和DNA链断裂分析.
- 研究了N-乙-L-氨酸 (NAC) 对6PPD诱导的损伤的保护作用.
主要成果:
- 所有测试的轮胎添加剂都在24小时暴露后以度依赖的方式引起了显著的谷氨耗尽和诱导DNA链断裂.
- N-乙-L-氨酸 (NAC) 有效地减轻了GSH耗尽和6PPD引起的DNA损伤.
- 观察到的效应发生在超过典型环境空气水平的度下,但考虑到在尘埃,排水和废水中的环境检测,这些效应是相关的.
结论:
- 轮胎添加剂通过各种暴露途径 (吸入,摄入,皮肤) 对人类气膜细胞构成风险.
- 谷氨耗尽和DNA损伤是轮胎添加剂毒性的关键机制.
- NAC显示出作为保护剂的潜力,可以防止6PPD的不良影响.
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