低估的毒性:紫外线放大低剂量Cr (VI) 损伤分子和组织层面的皮肤

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Jie Tang^1,2, Wei Hua², Ruixuan Lu¹

¹Key Laboratory of Green Chemistry & Technology of Ministry of Education, College of Chemistry, Sichuan University, Chengdu, Sichuan 610064, China.

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|September 18, 2025

概括

紫外线 (UV) 照射显著放大了低剂量 (Cr) 的毒性,这是已知的致癌物. 这种协同效应导致分子和组织损伤,需要对环境Cr (VI) 风险评估进行重新评估.

科学领域:

环境毒理学环境毒理学
分子致癌症的产生.
皮肤病学皮肤病学

背景情况:

(VI) [Cr (VI) ]是一种公认的环境致癌物,与DNA损伤和氧化应激有关.
当前的风险评估往往忽略了低剂量的Cr (VI) 与环境因素,特别是紫外线辐射共存.
了解协同毒性对于在现实场景中准确评估风险至关重要.

研究的目的:

为了研究低剂量 (VI) [Cr (VI) ]和紫外线辐射的协同毒性.
阐明Cr (VI) 和UV共暴露效应背后的分子机制.
评估分子和组织层面对皮肤屏障完整性的影响.

主要方法:

利用集成的体外和体内模型来研究Cr (VI) 和UV共暴露.
分析了分子终点,包括DNA和蛋白质损伤,以及反应性氧物种 (ROS) 生成.
评估了皮肤屏障功能的组织水平影响,包括皮肤间的水分流失和角层超结构.

主要成果:

紫外线照射极大地放大了低剂量的CrVI毒性,诱导ROS和随后的DNA/蛋白质裂变.
急性UV-Cr(VI) 联合暴露显著损害了皮肤屏障功能,使皮肤间的水分流失增加了50%.
观察到无组织的角层,表皮厚化,异常的基底细胞激活和炎症细胞透.

结论:

紫外线辐射作为Cr(VI) 毒性的关键增强剂,在分子和组织层面表现出协同作用.
这些发现挑战了传统的基于值的Cr6安全剂量.
需要紧急重新评估暴露在光线下的环境Cr (VI) 风险,这将对公共卫生和法规产生影响.

关键词:

毒性的Cr (VI) 毒性造成DNA/蛋白质损伤.紫外线辐射的辐射细胞亡是细胞的亡.细胞循环停止细胞循环停止有活性氧物种的反应性氧物种.皮肤屏障的功能障碍

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