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由2,3,7,8-四二二子-p-素诱导的氧化应激对DNA损伤的影响

Chao Wang¹, Xiaoxin Liu², Junqiu Zhai³

¹Guangdong Provincial Laboratory of Chemistry and Fine Chemical Engineering Jieyang Center, Jieyang 515200, China; Guangdong Provincial Key Laboratory of Water Quality Improvement and Ecological Restoration for Watersheds, School of Ecology, Environment and Resources, Guangdong University of Technology, Guangzhou 510006, China.

Journal of hazardous materials

|May 3, 2024

概括

2,3,7,8-四二二氧化 (TCDD) 通过增加活性氧物种 (ROS) 和降低抗氧化防御能力,导致DNA损伤. 这种持久性有机污染物 (POP) 引发氧化应激,通过基切除修复途径导致DNA损伤.

科学领域:

环境毒理学环境毒理学
分子生物学分子生物学
生物化学生物化学

背景情况:

2,3,7,8-四二二氧化 (TCDD) 是一种有毒的持久性有机污染物 (POP).
氧化应激是已知的DNA损伤机制,但其在TCDD毒性中的作用尚未完全理解.
了解TCDD的基因毒性对于公共卫生和环境安全至关重要.

研究的目的:

调查氧化应激在TCDD诱导的DNA损伤中的作用.
确定TCDD在AP地点引起DNA损伤的特定机制.
为了阐明涉及TCDD毒性影响的细胞通路.

主要方法:

同时监测反应性氧物种 (ROS) 生产和AP位点DNA损伤.
测定超氧化物脱酶 (SOD) 和酶 (CAT) 活动.
转录组测序以分析基因表达变化.

主要成果:

TCDD削弱了SOD和CAT活动,增加了ROS (O2.-和NO) 产量.
增加的ROS导致了AP现场的DNA损伤.
基切除修复 (BER) 途径基因的升级和ROS的抑制减少了DNA损伤.
在MAPK,cAMP和与氧化压力相关的乳腺癌途径中,TCDD上调调基因.

结论:

通过破坏抗氧化防御,TCDD主要通过氧化应激诱导DNA损伤.
基切除修复通路被激活,以应对TCDD诱导的DNA损伤.
MAPK,cAMP和乳腺癌途径与TCDD的氧化应激中介毒性有关.

关键词:

造成的DNA损伤是DNA损伤.氧化应激是一种氧化应激.对于TCDDD来说,这是一个很大的问题.转录组分析转录组分析

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