Glutathione Metabolism in Crohn′s Disease

Iantomasi, Teresa; Marraccini, Patrizia; Favilli, Franco; Vincenzini, Massimo; Ferretti, Patrizia; Tonelli, Francesco

doi:10.1006/bmmb.1994.1062

Cited by 56 publications

(42 citation statements)

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“…Previously, studies performed by Kruidenier et al 31 and Iantomasi et al, 32 addressed this issue describing a significant increase in GPx activity in inflamed intestinal CD mucosa compared to controls. Differences in methodologies used in these studies, however, do not allow accurate comparisons with the present study.…”

Section: 30mentioning

confidence: 98%

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Does active Crohn's disease have decreased intestinal antioxidant capacity?

Pinto

Lopes

Bastos

et al. 2013

Journal of Crohn's and Colitis

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Background and aims: Oxidative stress is presumed to play an important role in Crohn's disease (CD) pathogenesis. Nevertheless, the evaluation of the intestinal antioxidant capacity through the analysis of glutathione peroxidase activity in CD remains to be determined. Methods: 20 CD outpatients and 16 volunteers going through colonic cancer screening were enrolled. Colonoscopy with biopsies was performed in all individuals. Samples from inflamed and non-inflamed mucosa were taken when there was CD endoscopic activity. Spectrophotometric assays were performed to measure tissue glutathione peroxidase (GPx) activity, and total (GSH T ) and oxidized (GSSG) glutathione in all samples. Demographics and clinical characteristics were collected from clinical charts. Results: Inflamed CD mucosa presented reduced GPx activity compared to non-inflamed CD mucosa (42.94 mU/mg protein vs 79.62 mU/mg protein, P b 0.05) and control mucosa (42.94 mU/mg protein vs 95.08 mU/mg protein, P b 0.001). GSH T concentration was reduced in inflamed mucosa when compared to non-inflamed CD mucosa (0.78 μmol/g vs 1.98 μmol/g, P b 0.01) and the control group (0.78 μmol/g vs 2.11 μmol/g, P b 0.001). A significant correlation was detected between GPx activity and GSSG (r = −0.599), disease duration (r = 0.546), and thiopurine treatment (r = −0.480) in non-inflamed CD mucosa. A v a i l a b l e o n l i n e a t w w w . s c i e n c e d i r e c t . c o m ScienceDirectJournal of Crohn's and Colitis (2013) 7, e358-e366Downloaded from https://academic.oup.com/ecco-jcc/article-abstract/7/9/e358/426937 by guest on 07 June 2019Conclusion: Our findings suggest that reduced GPx activity is present in inflamed CD mucosa. In addition, endoscopic activity, disease duration and thiopurine therapy could be associated with mucosal decreased antioxidant activity.

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Section: 30mentioning

confidence: 98%

“…32 Possibly, this result may be associated with the efflux mechanism of intracellular GSSG. The ability to export GSSG can be an important factor in the cell sensitivity to oxidative stress.…”

mentioning

confidence: 99%

Does active Crohn's disease have decreased intestinal antioxidant capacity?

Pinto

Lopes

Bastos

et al. 2013

Journal of Crohn's and Colitis

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“…IECs also participate in modulating local immune function [33]. Proximity to luminal contents predestines the IEC to play the role of mediator: processing and presenting luminal antigens to the mucosal immune system and transforming and detoxifying xenobiotic agents (especially under conditions of stress such as inflammation, cell damage, or infection) [34,35]. ROS, generated as a consequence of these activities, play a causative role in IBD symptoms, regulate intestinal inflammation, and increase susceptibility to injury in the absence of normal oxidative defense mechanisms.…”

Section: Oxidative Stress In Inflammatory Bowel Diseasementioning

confidence: 99%

Clinical implications of oxidative stress and antioxidant therapy

Dryden

Deaciuc²,

Arteel³

et al. 2005

Curr Gastroenterol Rep

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Oxidative stress occurs when there is an imbalance between generation of reactive oxygen species and inadequate antioxidant defense systems. Oxidative stress can cause cell damage either directly or through altering signaling pathways. Oxidative stress is a unifying mechanism of injury in many types of disease processes, including gastrointestinal diseases. For example, in alcoholic liver disease, reactive oxygen species have been detected through direct spin-trapping techniques and through indirect markers, such as products of lipid peroxidation. A host of antioxidants have protected against liver injury in animal models of alcoholic liver disease. Similarly, in inflammatory bowel disease, oxidative stress has been postulated to play a role in disease initiation and progression, and antioxidant therapy, such as green tea polyphenols and gene therapy with superoxide dismutase, has a markedly attenuated disease. Downregulation of specific detoxification genes may play a role in the pathogenesis of inflammatory bowel disease, especially in ulcerative colitis. Oxidative stress is postulated to play a sustaining role in acute and chronic pancreatitis. Antioxidant supplementation has been used with some success in the treatment of chronic pancreatitis. This review covers recent findings related to oxidative stress in liver disease, inflammatory bowel disease, and pancreatitis.

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“…In clinical IBD, oxidative stress compromises GSH status-GSH concentration is lower in the plasma and colon [18,19]; GSSG concentration and GPx activity are relatively increased in colon mucosa [5,20,21]; GST activity is decreased in the small intestine [20] and colon mucosa [5]. Piglets consuming a low protein diet cannot maintain GSH concentration or synthesis following a systemic inflammatory stress [22].…”

Section: ]mentioning

confidence: 99%