Abstract

Oxidative stress plays an important role in IBD because chronic intestinal inflammation is associated with the overproduction of reactive oxygen species (ROS) leading to oxidative stress, which has been implicated in IBD. Many lines of evidence suggest that IBD is associated with an imbalance between ROS and antioxidant activity which generates oxidative stress as the result of either ROS overproduction or a decrease in antioxidant activity. Our study was to evaluate the influence of oxidative stress and antioxidants on the course of the disease and treatment of IBD patients. Our results show that an increase of LOOH levels positively correlates with an increase in MDA levels; therefore, MDA may be a marker indicating lipid peroxidation. Also, being the decomposition product of oxidation processes, MDA may be applied as a useful biomarker for identifying the effect of endogenous oxidative stress in Crohn's disease patients. The anti-inflammatory efficacy of AZA drugs may be the result of a reduction of the amount of lipid peroxides in the intestinal mucosa cells in CD patients and facilitate mucosal healing.

Highlights

  • Inflammatory bowel diseases (IBDs) mainly include Crohn’s disease (CD) and ulcerative colitis (UC)

  • A group of 20 individuals comprised patients diagnosed with ulcerative colitis, K51 according to the ICD-10 classification (UC)

  • Table 1shows the results of Cu, Zn, Na, CAT, GSH + GSSG, MDA, LOOH, and Cp levels among CD and UC patients and control individuals, which we compare against Table 2 showing the results of the correlation of age, duration, C-reactive protein (CRP), WBC, RBC Cu, Zn, Na, CAT, GSH + GSSG, MDA, LOOH, and Cp among CD and UC patients and control individuals (Pearson correlation coefficient)

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Summary

Introduction

Inflammatory bowel diseases (IBDs) mainly include Crohn’s disease (CD) and ulcerative colitis (UC). Both conditions constitute a chronic and relapsing disorder of the gastrointestinal tract (GI), associated with an exacerbated intestinal immune response to harmless stimulus, leading to an upregulation of proinflammatory mediators, which may trigger the onset and perpetuation of IBD [1,2,3]. In UC, inflammation involves only the superficial layers of the intestinal mucosa and is localized to regions of the gut most highly colonized by bacteria, at the rectum and moving proximally along the large bowel [4]. Oxidative stress in IBD patients with increased ROS levels and decreased antioxidant levels in the inflamed mucosa, could contribute to chronic tissue damage [5].

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