Reactive species and DNA damage in chronic inflammation: reconciling chemical mechanisms and biological fates.
Reactive species and DNA damage in chronic inflammation: reconciling chemical mechanisms and biological fates.
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DOI：
10.1002/ijc.25815
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发表时间：
2011-05-01
影响因子：
6.4
通讯作者：
Dedon, Peter C.
中科院分区：
文献类型：
--
作者：
Lonkar, Pallavi;Dedon, Peter C.
关键词：
长期以来，慢性炎症一直被认为是许多人类癌症的危险因素。炎症和癌症之间的一种机制联系涉及由浸润炎症部位的巨噬细胞和嗜中性粒细胞产生一氧化氮、超氧化物和其他活性氧和氮物质。虽然病理学上高水平的这些活性物质会对生物分子（包括DNA）造成损伤，但较低水平的一氧化氮在细胞信号传导和凋亡中起着重要的生理作用。这就提出了由炎症化学介质介导的炎症诱导的生理和病理途径失衡的问题。在病理学水平上，核酸持续的损伤代表了化学反应的全谱，并可能在致癌作用中起重要作用。这表明DNA损伤产物可以作为临床可及的隔室（如血液和尿液）中炎症和氧化应激的生物标志物。然而，最近的研究的生物转化的DNA损伤产物排泄前指出，在我们的理解的DNA病变的生物命运的弱点，从而在使用DNA病变作为生物标志物的限制。这篇评论将解决这些和其他问题周围炎症介导的DNA损伤的道路上的癌症。
Chronic inflammation has long been recognized as a risk factor for many human cancers. One mechanistic link between inflammation and cancer involves the generation of nitric oxide, superoxide and other reactive oxygen and nitrogen species by macrophages and neutrophils that infiltrate sites of inflammation. While pathologically high levels of these reactive species cause damage to biological molecules, including DNA, nitric oxide at lower levels plays important physiological roles in cell signaling and apoptosis. This raises the question of inflammation-induced imbalances in physiological and pathological pathways mediated by chemical mediators of inflammation. At pathological levels, the damage sustained by nucleic acids represents the full spectrum of chemistries and likely plays an important role in carcinogenesis. This suggests that DNA damage products could serve as biomarkers of inflammation and oxidative stress in clinically accessible compartments such as blood and urine. However, recent studies of the biotransformation of DNA damage products prior to excretion point to a weakness in our understanding of the biological fates of the DNA lesions and thus to a limitation in the use of DNA lesions as biomarkers. This review will address these and other issues surrounding inflammation-mediated DNA damage on the road to cancer.
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影响因子：
2.4
作者：
Cooke MS;Henderson PT;Evans MD
通讯作者：
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DOI：
10.1016/s0027-5107(99)00009-3
发表时间：
1999-03-08
影响因子：
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作者：
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