环境的亲氧化剂诱导了人类角质细胞中改变的包膜蛋白质配置
Lo-Wei Lin1, Blythe P Durbin-Johnson2, David M Rocke2
1Department of Environmental Toxicology, University of California, Davis, California 95616, USA.
概括
环境的亲氧化剂可以破坏皮肤屏障蛋白,改变角状包裹 (CEs). 这项研究揭示了DMNQ,MLS和TCDD等特定药物如何影响CE形成和蛋白质概况,突出了细胞氧化还原状态的作用.
科学领域:
- 皮肤病学 皮肤病学
- 生物化学 生物化学
- 毒理学 毒理学 毒理学
背景情况:
- 角形外 (CEs) 对于皮肤屏障功能至关重要,由转谷氨酶介导的蛋白质交叉链接形成.
- 氧化损伤还可以导致CE中的蛋白质交叉链接,这与酶过程不同.
- 环境亲氧化剂已被证明可以将细胞蛋白质纳入CEs.
研究的目的:
- 研究环境亲氧化剂 (DMNQ,MLS,TCDD) 诱导CE形成并改变CE蛋白质组的机制.
- 为了比较这些亲氧化剂与已知的诱导剂,X537A.的影响.
- 阐明细胞氧化还原状态在CE形成中的作用.
主要方法:
- 使用DMNQ,MLS,TCDD和X537A诱导CE.
- 分析CE蛋白质配置文件和识别蛋白质添加物.
- 评估与CE形成相关的膜透性.
- 检测特定蛋白质,如CYP1A1和CE前体.
主要成果:
- DMNQ和MLS诱导了与膜透相关的CE形成,类似于X537A.
- 由DMNQ诱导的CE显示出与X537A相似的蛋白质配置,因为它不形成 adducts.
- 由于反应性碳基因形成蛋白质添加物,MLS诱导了CE蛋白质组的显著变化.
- 由TCDD诱导的CE含有CE前体和CYP1A1,这表明基碳化合物受体 (AhR) 的激活.
结论:
- 环境的亲氧化剂可以显著改变表皮CE蛋白质组.
- 通过亲氧化剂改变CE的机制各不相同,涉及膜透,蛋白质添加物形成或AhR激活.
- 细胞的氧化还原状态在角化包裹的形成和完整性中起着至关重要的作用.
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