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.
journal_name
Free Radic Resjournal_title
Free radical researchauthors
Ho HY,Cheng ML,Cheng PF,Chiu DTdoi
10.1080/10715760601184819subject
Has Abstractpub_date
2007-05-01 00:00:00pages
571-9issue
5eissn
1071-5762issn
1029-2470pii
776344234journal_volume
41pub_type
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journal_title:Free radical research
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journal_title:Free radical research
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journal_title:Free radical research
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