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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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BACKGROUND AND AIMS: 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. RESULTS: Using ultrasensitive and specific detection methods for the analysis of human tissues, cells, and urine, etheno-DNA adduct levels were found to be significantly elevated in the affected organs of subjects with chronic pancreatitis, ulcerative colitis, and Crohn's disease. Patients with alcohol-related liver diseases showed excess hepatic DNA damage progressively increasing from hepatitis, fatty liver, to liver cirrhosis. Ethenodeoxyadenosine excreted after DNA repair in urine of hepatitis B virus-related chronic hepatitis and liver cirrhosis patients was increased up to 90-fold. Putative mechanisms that may control DNA damage in inflamed tissues including impaired or imbalanced DNA repair pathways are reviewed. CONCLUSION: Persistent oxidativeitrosative stress and excess LPO are induced by inflammatory processes in a self-perpetuating process and cause progressive accumulation of DNA damage in target organs. Together with deregulation of cell homeostasis, the resulting genetic changes act as driving force in chronic inflammation-associated human disease pathogenesis. Thus steady-state levels of DNA damage caused by ROS, RNS, and LPO end products provide promising molecular signatures for risk prediction and potential targets and biomarkers for preventive measures.
机译：背景与目的：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。结果：使用超灵敏和特异性检测方法对人体组织，细胞和尿液进行分析，发现慢性胰腺炎，溃疡性结肠炎和克罗恩病患者的受影响器官中的乙烯-DNA加合物水平显着升高。患有酒精相关性肝病的患者表现出过量的肝DNA损伤，从肝炎，脂肪肝到肝硬化逐渐增加。 DNA修复后，乙型肝炎病毒相关的慢性肝炎和肝硬化患者尿液中的乙氧基脱氧腺苷增加至90倍。审查了可能控制发炎的组织中DNA损伤（包括受损或失衡的DNA修复途径）的机制。结论：持续的氧化/亚硝化应激和过量的LPO是由炎症过程在自我延续过程中诱导的，并导致靶器官中DNA损伤的逐步积累。与细胞稳态的失调一起，导致的遗传变化成为慢性炎症相关人类疾病发病机理的驱动力。因此，由ROS，RNS和LPO最终产物引起的DNA损伤的稳态水平为风险预测和潜在目标提供了有希望的分子特征，并为预防措施提供了生物标记。

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