Dincer Yildiz, Erzin Yusuf, Himmetoglu Solen, Gunes Kezban Nur, Bal Kadir, Akcay Tülay
Department of Biochemistry, Istanbul University, Dere Sok., Umut Ap No 21/44, Sahrayi Cedid, Erenkoy, Istanbul, Turkey.
Dig Dis Sci. 2007 Jul;52(7):1636-41. doi: 10.1007/s10620-006-9386-8. Epub 2007 Mar 29.
Chronic inflammation may contribute to cancer risk through the accumulation of specific products as a result of DNA damage. Endogenous antioxidant enzymes prevent the formation of these harmful products. Oxidative DNA damage and endogenous antioxidant defense were determined in patients with inflammatory bowel disease (IBD). Plasma levels of 8-hydroxydeoxyguanosine (8-OHdG) and nitric oxide (NO) and plasma activities of glutathione peroxidase (G-Px) and superoxide dismutase (SOD) were determined in patients with IBD by ELISA and spectrophotometric assay, respectively. Plasma levels of 8-OHdG, SOD, and G-Px activity were found to be increased in the patient group compared to the control group (P < 0.02, P < 0.001, and P < 0.001, respectively), whereas NO was unchanged. 8-OHdG level was found to be weakly correlated with age, NO, and SOD. The results show increased DNA damage in patients with IBD. This may explain the increased risk of developing colon cancer in these patients.
慢性炎症可能通过DNA损伤导致特定产物的积累从而增加癌症风险。内源性抗氧化酶可阻止这些有害产物的形成。本研究测定了炎症性肠病（IBD）患者的氧化DNA损伤和内源性抗氧化防御能力。分别采用ELISA法和分光光度法测定了IBD患者血浆中8-羟基脱氧鸟苷（8-OHdG）和一氧化氮（NO）的水平以及谷胱甘肽过氧化物酶（G-Px）和超氧化物歧化酶（SOD）的活性。与对照组相比，患者组血浆8-OHdG、SOD水平及G-Px活性均升高（P分别<0.02、<0.001和<0.001），而NO水平无变化。发现8-OHdG水平与年龄、NO和SOD呈弱相关。结果表明IBD患者的DNA损伤增加。这可能解释了这些患者患结肠癌风险增加的原因。
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