Glutathione efflux associated with a low gamma-glutamyl transpeptidase activity in human melanoma cells.

Détails

ID Serval
serval:BIB_68EFD339F70F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Glutathione efflux associated with a low gamma-glutamyl transpeptidase activity in human melanoma cells.
Périodique
British Journal of Dermatology
Auteur⸱e⸱s
Benathan M.
ISSN
0007-0963
Statut éditorial
Publié
Date de publication
11/1997
Peer-reviewed
Oui
Volume
137
Numéro
5
Pages
721-727
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't - Publication Status: ppublish
Résumé
The cellular concentration of reduced glutathione (GSH) modulates the sensitivity of human melanoma cells to alkylating drugs in vitro. To investigate whether the membrane-associated enzyme gamma-glutamyl transpeptidase (gamma-GTP) involved in GSH breakdown was expressed in melanoma cells, the enzymatic activity of gamma-GTP as well as the secretion of GSH were measured in human melanoma cells from four different cell lines (Me8, JUSO, GLL19, Swift). All the cells showed low gamma-GTP activities (0-1 mU/mg protein) and released GSH in culture supernatants at significant rates. After incubation for 24 h in growth medium containing 0.1 mmol/L cystine, the levels of GSH in supernatants ranged from 56 to 111 nmol GSH/mg protein. The GSH metabolism of melanoma cells was also evaluated by measuring the levels of the melanogenesis intermediate 5-S-cysteinyldopa under different experimental conditions. The results of these experiments suggest that melanoma cells have a low ability to metabolize the tripeptide GSH, which appears to be responsible for GSH secretion and accumulation in culture supernatants.
Mots-clé
Cell Division, Cysteinyldopa, Fibroblasts, Glutathione, Humans, Melanoma, Monophenol Monooxygenase, Skin, Skin Neoplasms, Tumor Cells, Cultured, gamma-Glutamyltransferase
Pubmed
Web of science
Création de la notice
28/01/2008 8:20
Dernière modification de la notice
20/08/2019 14:24
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