Induction of enlarged intestinal lymphoid aggregates during acute glutathione depletion in a murine model

Citation
Tr. Koch et al., Induction of enlarged intestinal lymphoid aggregates during acute glutathione depletion in a murine model, DIG DIS SCI, 45(11), 2000, pp. 2115-2121
Citations number
30
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
DIGESTIVE DISEASES AND SCIENCES
ISSN journal
01632116 → ACNP
Volume
45
Issue
11
Year of publication
2000
Pages
2115 - 2121
Database
ISI
SICI code
0163-2116(200011)45:11<2115:IOEILA>2.0.ZU;2-0
Abstract
Glutathione is a nonenzymatic antioxidant synthesized by most animal cells and is depleted in inflammatory bowel disease. The effects of glutathione d epletion on intestinal histology and inhibitory neurochemicals was examined in a mouse model. Glutathione depletion in A/J mice involved inhibition of gamma -glutamylcysteine synthetase using L-buthionine-(S,R)sulfoximine (BS O) for 10 days. Ileum and colon were obtained from saline-control mice, BSO -treated mice, and BSO-treated mice receiving ascorbate or glutathione mono ethylester. Glutathione, lipid peroxides, and nicotineamide adenine dinucle otide phosphate diaphorase activity were measured by colorimetric assays. V asoactive intestinal peptide was measured by radioimmunoassay, Glutathione depletion induced enlargement of mucosal-submucosal lymphoid aggregates wit hout germinal centers in ileum and colon. These aggregates were prevented b y supplementation with glutathione monoethylester but not ascorbate. Tissue levels of inhibitory neurochemicals were unchanged. Depletion of glutathio ne appears to induce enlarged lymphoid aggregates by recruitment of lymphoc ytes from the peripheral circulation. A component of the inflammation that develops in inflammatory bowel disease could be related to depletion of tis sue levels of glutathione.