Oxygen-induced pulmonary injury in gamma-glutamyl transpeptidase-deficient mice

We used mice with a targeted disruption in g-glutamyl transpeptidase (GGT-deficient mice) to study the role of glutathione (GSH) in protection against oxygen-induced lung injury. These mice had reduced levels of lung GSH and restricted ability to synthesize GSH because of low levels of cysteine. Whe...

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Bibliographic Details
Published in:Lung 2001, Vol.179 (5), p.319-330
Main Authors: Barrios, R, Shi, Z Z, Kala, S V, Wiseman, A L, Welty, S E, Kala, G, Bahler, A A, Ou, C N, Lieberman, M W
Format: Article
Language:English
Subjects:
Acetylcysteine - pharmacology
Animals
Cysteine - metabolism
gamma-Glutamyltransferase - deficiency
Glutamate-Cysteine Ligase - metabolism
Glutathione - physiology
Hyperoxia - etiology
Hyperoxia - metabolism
Lung - metabolism
Lung Injury
Mice
RNA - genetics
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Summary:We used mice with a targeted disruption in g-glutamyl transpeptidase (GGT-deficient mice) to study the role of glutathione (GSH) in protection against oxygen-induced lung injury. These mice had reduced levels of lung GSH and restricted ability to synthesize GSH because of low levels of cysteine. When GGT-deficient mice were exposed to 80% oxygen, they developed diffuse pulmonary injury and died within eight days. Ten of 12 wild-type mice were alive after 18 days. Administration of N-acetylcysteine (NAC) to GGT-deficient mice corrected GSH values and prevented the development of severe pulmonary injury and death. Oxygen exposure induced an increase in lung GSH levels in both wild-type and GGT-deficient mice, but induced levels in the mutant mice were
ISSN:0341-2040
DOI:10.1007/s004080000071