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Glutathione and Crohn's disease,
Colitis, Inflammatory Bowel Disease (IBD)

Glutathione metabolism in Crohn's disease
Iantomasi T, Marraccini P, Favilli F, Vincenzini MT, Ferretti P, Tonelli F. [Biochem Med Metab Biol 1994 Dec;53(2):87-91] A statistically significant decrease of glutathione (GSH) and an increase of GSH disulfide (GSSG) both in healthy and ill ileum of patients with Crohn's disease in comparison with the controls (without this pathology) is demonstrated. However, the lowering of these levels was more remarkable in ill ileum in which high levels of GSSG were detected, too. These alterations may be in part explained by the changes obtained in GSH-related enzyme levels. Finally, considering the results that others and we obtained by studies on GSH oral absorption in rat intestine, an oral therapy of GSH in Crohn's disease is suggested.

Low levels of glutathione in endoscopic biopsies of patients with Crohn's colitis: the role of malnutrition
Miralles-Barrachina O, Savoye G, and others. [Clin Nutr 1999 Oct;18(5):313-7.] "Mucosal glutathione is markedly lower in active Crohn's colitis, even in healthy mucosa; glutathione depletion tends to be more severe in malnourished patients.
Glutathione depletion may be related in part to malnutrition and contribute to a prolonged evolution of disease and could be a target for pharmacological and nutritional support." (Copyright 1999 Harcourt Publishers Ltd.)

Impairment of intestinal glutathione synthesis in patients with inflammatory bowel disease
Sido B, Hack V, and others. [Gut 1998 Apr;42(4):485-92.] " Decreased activity of key enzymes involved in GSH synthesis accompanied by a decreased availability of cyst(e)ine for GSH synthesis contribute to mucosal GSH deficiency in IBD. As the impaired mucosal antioxidative capacity may further promote oxidative damage, GSH deficiency might be a target for therapeutic intervention in IBD [inflammatory bowel disease].

Replenishment of Glutathione Levels Improves Mucosal Function in Experimental Acute Colitis
Esther Ardite, Miguel Sans, Juliá Panés, Francisco J. Romero, Josep M. Piqué, and José C. Fernández-Checa [Liver Unit (EA, JCF-C) and Department of Gastroenterology (MS, JP, JMP), Institut Malalties Digestives, Instituto Investigaciones Biomedicas August Pi I Suñer, Consejo Superior Investigaciones Cientificas, Barcelona, Spain; and Experimental Toxicology and Neurotoxicology Unit (FJR), Department of Physiology, School of Medicine and Dentistry, University of Valencia, Valencia, Spain] Because reactive oxygen species (ROS) have been implicated as mediators of inflammatory bowel disease (IBD), the purpose of the present work was to determine the functional role of mucosal GSH in the trinitrobenzenesulfonic acid in 50% ethanol (TNBS+ethanol)-induced colitis in rats. Accordingly, in vivo administration of NAC attenuates the acute colitis through increased mucosal GSH levels, suggesting that GSH precursors may be of relevance in the acute relapse of IBD.

Glutathione and Malnutrition

In vivo rates of erythrocyte glutathione synthesis in children with severe protein-energy malnutrition
Reid M, Badaloo A, and others. [Am J Physiol Endocrinol Metab 2000 Mar;278(3):E405-12.] "Children with edematous PEM had significantly lower erythrocyte GSH and slower absolute rates of GSH synthesis than children with nonedematous PEM ......These results confirm that GSH deficiency is characteristic of edematous PEM [protein-energy malnutrition] and suggest that this is due to a reduced rate of synthesis secondary to a shortage in cysteine."


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