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Wagner, G.* ; Stettmaier, K. ; Bors, W. ; Sies, H.* ; Wagner, E.M.* ; Reuter, A.* ; Weiher, H.*

Enhanced Gamma-Glutamyl Transpeptidase Expression and Superoxide Production in Mpv17-/- Glomerulosclerosis Mice.

Biol. Chem. 382, 1019-1025 (2001)
DOI PMC
Open Access Gold möglich sobald Verlagsversion bei der ZB eingereicht worden ist.
Recently, gamma-glutamyl transpeptidase, which initiates cleavage of extracellular glutathione, has been shown to promote oxidative damage to cells. Here we examined a murine disease model of glomerulosclerosis, involving loss of the Mpv17 gene coding for a peroxisomal protein. In Mpv17-/- cells, enzyme activity and mRNA expression (examined by quantitative RT-PCR) of membrane-bound gamma-glutamyl transpeptidase were increased, while plasma glutathione peroxidase and superoxide dismutase levels were lowered. Superoxide anion production in these cells was increased as documented by electron spin resonance spectroscopy. In the presence of Mn(III)tetrakis(4-benzoic acid)porphyrin, the activities of gamma-glutamyl transpeptidase and plasma glutathione peroxidase were unchanged, suggesting a relationship between enzyme expression and the amount of reactive oxygen species. Inhibition of gamma-glutamyl transpeptidase by acivicin reverted the lowered plasma glutathione peroxidase and superoxide dismutase activities, indicating reciprocal control of gene expression for these enzymes.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Gene expression Glomerulopathy Glutathione cycle Reactive oxygen Transgenic mice
Sprache englisch
Veröffentlichungsjahr 2001
HGF-Berichtsjahr 0
ISSN (print) / ISBN 1431-6730
e-ISSN 1437-4315
Zeitschrift Biological Chemistry
Quellenangaben Band: 382, Heft: 7, Seiten: 1019-1025 Artikelnummer: , Supplement: ,
Verlag de Gruyter
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Radiation Biology (ISB)
POF Topic(s)
Forschungsfeld(er)
Radiation Sciences
PSP-Element(e) FE 70232
PubMed ID 11530932
DOI 10.1515/BC.2001.128
Erfassungsdatum 2001-12-31
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