Gastroenterology Department, Hospital Universitari I Politècnic La Fe, Boulevard Sud, 46026 Valencia, Spain.
Biochem Soc Trans. 2011 Aug;39(4):1102-6. doi: 10.1042/BST0391102.
There is increasing interest in oxidative stress being a potential aetiological factor and/or a triggering factor in Crohn's disease, rather than a concomitant occurrence during the pathogenesis of the disease. Recent research has shown that the immune mononuclear cells of Crohn's disease patients are induced to produce hydrogen peroxide (H2O2). Similarly, the regulation of antioxidant enzymes during disease in these cells has been unravelled, showing that SOD (superoxide dismutase) activity and GPx (glutathione peroxidase) activity is increased during active disease and returns to normal in remission phases. However, catalase remains constantly inhibited which supports the idea that catalase is not a redox-sensitive enzyme, but a regulator of cellular processes. ROS (reactive oxygen species) can be produced under the stimulus of different cytokines such as TNFα (tumour necrosis factor α). It has been shown in different experimental models that they are also able to regulate apoptosis and other cellular processes. The status of oxidative stress elements in Crohn's disease and their possible implications in regulating cellular processes are reviewed in the present paper.
人们越来越关注氧化应激可能是克罗恩病的病因和/或触发因素，而不是疾病发病过程中的伴随事件。最近的研究表明，克罗恩病患者的免疫单核细胞被诱导产生过氧化氢（H2O2）。同样，对这些细胞在疾病过程中抗氧化酶的调节也有了揭示，表明超氧化物歧化酶（SOD）活性和谷胱甘肽过氧化物酶（GPx）活性在活动期增加，在缓解期恢复正常。然而，过氧化氢酶一直保持抑制，这支持了过氧化氢酶不是一种氧化还原敏感酶，而是细胞过程调节剂的观点。ROS（活性氧）可以在不同的细胞因子如 TNFα（肿瘤坏死因子 α）的刺激下产生。在不同的实验模型中已经表明，它们还能够调节细胞凋亡和其他细胞过程。本文综述了克罗恩病中氧化应激元素的状态及其在调节细胞过程中的可能意义。
