Low oxygen tension alleviates oxidative damage and delays cellular senescence in G6PD-deficient cells.
Free Radic Res
; 41(5): 571-9, 2007 May.
Article
en En
| MEDLINE
| ID: mdl-17454140
ABSTRACT
Previous studies have shown that glucose-6-phosphate dehydrogenase (G6PD)-deficient cells are under increased oxidative stress and undergo premature cellular senescence. The present study demonstrates that G6PD-deficient cells cultured under 3% oxygen concentration had an extended replicative lifespan, as compared with those cultured under atmospheric oxygen level. This was accompanied by a reduction in the number of senescence-associated beta-galactosidase (SA-beta-Gal) positive and morphologically senile cells at comparable population doubling levels (PDL). Concomitant with the extension of lifespan was decreased production of reactive oxygen species. Additionally, lifespan extension was paralleled by the greatly abated formation of such oxidative damage markers as 8-hydroxy-deoxyguanosine (8-OHdG) as well as the oxidized and cross-linked proteins. Moreover, the mitochondrial mass increased, but the mitochondrial membrane potential DeltaPsim decreased in cells upon serial propagation. These changes were inhibited by lowering the oxygen tension. Our findings provide additional support to the notion that oxidative damage contributes to replicative senescence of G6PD-deficient cells and reduction of oxidative damage by lowering oxygen tension can delay the onset of cellular senescence.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Oxígeno
/
Senescencia Celular
/
Estrés Oxidativo
/
Potencial de la Membrana Mitocondrial
/
Fibroblastos
/
Glucosafosfato Deshidrogenasa
/
Deficiencia de Glucosafosfato Deshidrogenasa
Límite:
Humans
Idioma:
En
Revista:
Free Radic Res
Asunto de la revista:
BIOQUIMICA
Año:
2007
Tipo del documento:
Article
País de afiliación:
Taiwán