在大肠杆菌和人类中,CO2保护细胞免受铁-芬顿氧化DNA损伤
Aaron M Fleming1, Justin C Dingman1, Cynthia J Burrows1
1Department of Chemistry, University of Utah, 315 S. 1400 East, Salt Lake City, UT 84112-0850, USA.
bioRxiv : the preprint server for biology
|September 10, 2024
概括
细胞反应产生碳酸盐基离子,而不是基,导致氧化应激. 这导致瓜氧化,这是DNA和RNA损伤的常见途径,由修复酶缓冲.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
背景情况:
- 传统上,基因因与通过芬顿反应的DNA/RNA损伤有关.
- 细胞氧化应激是细胞损伤和疾病的重要因素.
研究的目的:
- 研究在生理条件下负责细胞中氧化损伤的特定基因物种.
- 阐明人类细胞中常见的氧化应激反应途径.
主要方法:
- 代谢组,转录组和核基因组的分析.
- 基于纳米孔的直接RNA对核糖体RNA的测序.
- 氧化性DNA损伤的糖基酶依赖定量PCR (qPCR).
主要成果:
- 碳酸盐基离子,而不是基,是由于二碳酸盐而产生的.
- 过氧化 (H2O2) 诱导的氧化应激总是导致瓜的氧化.
- 氧化性修饰特别针对DNA和RNA中的关氨酸.
结论:
- 在涉及二碳酸盐的细胞氧化应激中,主要的活性物种是碳酸盐基离子.
- 关氨酸氧化是细胞对氧化应激反应的中心途径.
- 基因切除修复酶在减轻氧化损伤和调节基因表达方面发挥作用.
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