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人体皮肤纤维细胞细胞系-Hs6868中T-2菌毒素诱导的DNA损伤
Edyta Janik-Karpinska1, Michal Ceremuga2, Marcin Niemcewicz1
1Biohazard Prevention Centre, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.
International journal of molecular sciences
|October 14, 2023
概括
T-2毒素是一种强大的三甲基菌毒素,会在人体皮肤细胞中引起DNA损伤. 这项研究揭示了其基因毒性机制,与DNA病变和改变的炎症和修复基因表达相关.
科学领域:
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- T-2毒素是一种来自Fusarium物种的强有力的三甲基菌毒素.
- 它对人类和动物产生有毒作用,具有显著的皮肤毒性.
- 了解其在皮肤细胞中的基因毒性机制至关重要.
研究的目的:
- 研究人类皮肤纤维细胞-Hs68细胞中T-2毒素诱导的基因毒性的分子机制.
- 评估DNA损伤和炎症和修复基因表达的变化.
- 为了阐明T-2毒素暴露和细胞反应之间的关系.
主要方法:
- 人体皮肤纤维细胞-Hs68细胞被T-2毒素 (0.1,1,10μM) 治疗了24h和48h.
- 性彗星测定用于检测DNA链断裂和性性部位.
- 分析了炎症 (TNF,INFG,IL1A,IL1B) 和修复基因 (LIG1,LIG3,FEN,XRCC1,APEX) 的mRNA表达.
主要成果:
- 在Hs68细胞中,T-2毒素诱导了DNA性性部位和链断裂.
- 与毒素度和暴露时间相关的DNA损伤水平.
- 炎症基因的mRNA水平增加,而LIG3降低,APEX增加.
- 在HPRT1和TP53基因中,损伤频率增加.
结论:
- T-2毒素对人类皮肤纤维细胞 (Hs68细胞) 具有基因毒性作用.
- 该机制涉及nDNA损伤,包括链断裂和性性部位.
- 炎症和DNA修复基因的改变表达有助于有毒效应.
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