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首页> 外文期刊>Langenbeck's Archives of Surgery >Chronic inflammation and oxidative stress in the genesis and perpetuation of cancer: role of lipid peroxidation, DNA damage, and repair
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Chronic inflammation and oxidative stress in the genesis and perpetuation of cancer: role of lipid peroxidation, DNA damage, and repair

机译:癌症的起源和永存中的慢性炎症和氧化应激:脂质过氧化,DNA损伤和修复的作用

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摘要

Chronic inflammation, induced by biological, chemical, and physical factors, was associated with increased risk of human cancer at various sites. Chronic inflammatory processes induce oxidativeitrosative stress and lipid peroxidation (LPO), thereby generating excess reactive oxygen species (ROS), reactive nitrogen species (RNS), and DNA-reactive aldehydes. Miscoding etheno- and propano-modified DNA bases are generated inter alia by reaction of DNA with these major LPO products. Steady-state levels of LPO-derived (etheno-) DNA adducts in organs affected by persistent inflammatory processes were investigated as potential lead markers for assessing progression of inflammatory cancer-prone diseases.
机译:由生物,化学和物理因素引起的慢性炎症与在各个部位罹患人类癌症的风险增加相关。慢性炎症过程会引起氧化/亚硝化应激和脂质过氧化(LPO),从而产生过量的活性氧(ROS),活性氮(RNS)和DNA反应性醛。编码错误的乙烯和丙酸修饰的DNA碱基尤其是通过DNA与这些主要LPO产物的反应而产生。研究了受持续性炎症过程影响的器官中LPO衍生的(etheno-)DNA加合物的稳态水平,作为评估易发炎症性疾病进展的潜在先导标记。

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