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Oxidative Stress Response in Telomerase‐Immortalized Fibroblasts from a Centenarian
Author(s) -
MONDELLO CHIARA,
BOTTONE MARIA GRAZIA,
NORIKI SAKON,
SOLDANI CRISTIANA,
PELLICCIARI CARLO,
SCOVASSI ANNA IVANA
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1378.058
Subject(s) - telomerase , apoptosis , oxidative stress , telomere , programmed cell death , microbiology and biotechnology , chemistry , fragmentation (computing) , poly adp ribose polymerase , centenarian , phosphatidylserine , dna damage , biology , biochemistry , dna , genetics , longevity , ecology , polymerase , gene , phospholipid , membrane
It has been reported that cells with ectopic expression of telomerase are more resistant to apoptotic cell death than their normal counterpart. However, controversial results were obtained when the cellular response to oxidative stress was analyzed. The present research was therefore aimed at defining the effect of the oxidative stress induced by tert ‐butylhydroperoxide (tBOOH) and 2‐deoxy‐ d ‐ribose ( d ‐ribose) in human fibroblasts from a centenarian (cen3) and, in parallel, on the same cells after telomerase immortalization (cen3tel cells). By studying different parameters of apoptosis in situ (i.e., chromatin condensation, phosphatidylserine externalization, and DNA fragmentation), we found that both tBOOH and d ‐ribose induce apoptosis to a greater extent in cen3 than in cen3tel cells, suggesting a protective role of telomerase toward apoptotic death. However, monitoring the cell number during treatment with the drugs, we found a decrease in cell number; since this reduction was lower in cen3 fibroblasts compared to cen3tel cells, it is likely that telomerase does not fully protect cells from drug toxicity.