Abstract
Background. The pathogenesis of inflammatory bowel disease is due, in part, to enhanced free-radical
production and reduced antioxidant potential in mucosa cells.
Aim. We evaluated in a rat model of trinitrobenzensulphonic acid (TNBS) colitis to see
whether parenteral administration of glutathione is able to improve mucosal oxidative
damage at onset (study A) and during chronic phases of colitis (study B).
Methods. In study A, the rats were injected with a single dose of glutathione (200 mg/kg,
i.p.) or saline (0,2 ml, i.p.) 1 h before colitis induction and killed 1 h later.
In study B, rats with induced colitis were treated with daily injection of glutathione
(50 mg/kg, i.p.) or saline (0,2 ml, i.p.), and killed at 1, 2, 4 and 8 weeks. We evaluated
on mucosal samples the macroscopic and histological damage and the oxidative stress
assessed by the mucosal levels of lipoperoxides, malonyldialdehyde, glutathione and
cysteine.
Results. In study A, colitis induction caused a significant increase to the total histological
score (p<0.05), lipoperoxide and malonyldialdehyde levels (p<0.001), but did not affect glutathione and cysteine content. Glutathione pre-treatment
decreased both total histological score (p<0.05) and lipoperoxide and malonyldialdehyde values (p<0.001). In study B, the extensive macroscopic and histological colonic damage induced
by TNBS was accompanied by a reduction of glutathione and cysteine mucosal levels
(p<0.01) and increased lipid peroxidation. Glutathione supplementation significantly
improved colonic damage (p<0.01), restored glutathione and cysteine levels, and decreased, and even, if not
totally, abolished lipid peroxidation (p<0.001).
Conclusion. This paper further supports the pathogenic role of the imbalance in oxidant/antioxidant
content in inducing mucosal colonic damage.
Keywords
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Article info
Publication history
Accepted:
May 19,
2003
Received:
March 11,
2003
Identification
Copyright
© 2003 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Inc. All rights reserved.