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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