World J Gastroenterol. 2010 Feb 14;16(6):663-72. doi: 10.3748/wjg.v16.i6.663.
The carcinogenic potential of iron in colorectal cancer (CRC) is not fully understood. Iron is able to undergo reduction and oxidation, making it important in many physiological processes. This inherent redox property of iron, however, also renders it toxic when it is present in excess. Iron-mediated generation of reactive oxygen species via the Fenton reaction, if uncontrolled, may lead to cell damage as a result of lipid peroxidation and oxidative DNA and protein damage. This may promote carcinogenesis through increased genomic instability, chromosomal rearrangements as well as mutations of proto-oncogenes and tumour suppressor genes. Carcinogenesis is also affected by inflammation which is exacerbated by iron. Population studies indicate an association between high dietary iron intake and CRC risk. In this editorial, we examine the link between iron-induced oxidative stress and inflammation on the pathogenesis of CRC.
铁在结直肠癌（CRC）中的致癌潜力尚未完全阐明。铁能够进行还原和氧化，使其在许多生理过程中发挥重要作用。然而，铁的这种固有氧化还原特性使其在过量存在时也具有毒性。铁通过 Fenton 反应介导的活性氧生成，如果不受控制，可能会导致脂质过氧化、氧化 DNA 和蛋白质损伤，从而导致细胞损伤。这可能会通过增加基因组不稳定性、染色体重排以及原癌基因和肿瘤抑制基因的突变，促进癌变。癌变也受到炎症的影响，而铁会加剧炎症。人群研究表明，高膳食铁摄入与 CRC 风险之间存在关联。在这篇社论中，我们研究了铁诱导的氧化应激和炎症与 CRC 发病机制之间的联系。
