DIFFERENTIAL ROLE OF CATALASE AND GLUTATHIONE-PEROXIDASE IN CULTURED HUMAN FIBROBLASTS UNDER EXPOSURE OF H2O2 OR ULTRAVIOLET-B LIGHT

Citation
H. Masaki et al., DIFFERENTIAL ROLE OF CATALASE AND GLUTATHIONE-PEROXIDASE IN CULTURED HUMAN FIBROBLASTS UNDER EXPOSURE OF H2O2 OR ULTRAVIOLET-B LIGHT, Archives of dermatological research, 290(3), 1998, pp. 113-118
Citations number
32
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
0340-3696
Volume
290
Issue
3
Year of publication
1998
Pages
113 - 118
Database
ISI
SICI code
0340-3696(1998)290:3<113:DROCAG>2.0.ZU;2-2
Abstract
The purpose of this study was to elucidate the differential contributi on of catalase and glutathione peroxidase (GSH-Px) to H2O2 scavenging in cultured human dermal fibroblasts. Responses of the cells in terms of both enzyme activities were examined by using two sorts of inhibito rs, 3-amino-1H-1,2,4-triazole (AT) for catalase and DL-buthionine-[S, R]-sulfoximine (BSO) for GSH-Px, under exposure to H2O2 or ultraviolet (UV) B radiation. AT treatment resulted in a decrease in H2O2 scaveng ing activity, while BSO treatment did not affect H2O2 scavenging. When fibroblasts were exposed to a low concentration of H2O2 (100 mu M). A T treatment resulted in a significant decrease in cell survival, but B SO treatment did not affect survival. At higher concentrations of H2O2 ranging from 500 mu M to 1 mM, BSO-treated fibroblasts showed reduced survival. In addition, AT treatment was much more cytotoxic in the pr esence of UVB than BSO treatment. The intracellular levels of H2O2 in fibroblasts treated with AT or BSO were also determined. BSO-treated c ells showed similar H2O2 levels to control cells, but the intracellula r H2O2 levels of AT-treated fibroblasts were 1.4-fold higher than foun d in control cells. These results with human dermal fibroblasts indica te that catalase acts as a primary defence against oxidative stress fr om exogenous or endogenous H2O2 at low concentrations. In contrast, GS H-Px helps protect the cell from damage during exposure to high concen trations of H2O2.