EFFECT OF ORALLY-ADMINISTERED GLUTATHIONE ON GLUTATHIONE LEVELS IN SOME ORGANS OF RATS - ROLE OF SPECIFIC TRANSPORTERS

Citation
F. Favilli et al., EFFECT OF ORALLY-ADMINISTERED GLUTATHIONE ON GLUTATHIONE LEVELS IN SOME ORGANS OF RATS - ROLE OF SPECIFIC TRANSPORTERS, British Journal of Nutrition, 78(2), 1997, pp. 293-300
Citations number
30
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
00071145
Volume
78
Issue
2
Year of publication
1997
Pages
293 - 300
Database
ISI
SICI code
0007-1145(1997)78:2<293:EOOGOG>2.0.ZU;2-5
Abstract
The present study reports data on absorption of orally administered gl utathione (GSH) in rat jejunum and in other organs, and the possible r ole of specific transport systems of GSH and gamma-glutamyltranspeptid ase (EC 2.3.2.1; gamma-GT) activity. GSH levels were measured simultan eously in various organs after oral GSH administration to untreated ra ts and rats treated with L-buthionine sulfoximine (BSO) or acivicin (A T(125)). BSO selectively inhibits GSH intracellular synthesis and AT(1 25) is a specific inhibitor of gamma-GT activity, GSH levels were also measured after oral administration of an equivalent amount of the con stituent amino acids of GSH to untreated and BSO-treated rats. Signifi cant increases in GSH levels were found in jejunum, lung, heart, Liver and brain after oral GSH administration to untreated rats. GSH increa ses were also obtained in all organs, except liver, when GSH was admin istered to rats previously GHS-depleted by treatment with BSO. The ana lysis of all results allowed us to distinguish between the increase in GSH intracellular levels due to intact GSH uptake by specific transpo rters, and that due to GSH degradation by gamma-GT activity and subseq uent absorption of degradation products with intracellular resynthesis of GSH; both these mechanisms seemed to be involved in increasing GSH content in heart after oral GSH administration. Jejunum, lung and bra in took up GSH mostly intact, by specific transport systems, while in liver GSH uptake occurred only by its breakdown by gamma-GT activity f ollowed by intracellular resynthesis.