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Science Forum Index » Life Extension Forum » Chronic treatment with N-acetyl-cystein delays...
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| rs1000b at (no spam) yahoo.com... |
 Posted: Sun May 11, 2008 12:01 pm |
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Mech Ageing Dev. 2008 May;129(5):261-70. Epub 2008 Jan 20.
Chronic treatment with N-acetyl-cystein delays cellular senescence in
endothelial cells isolated from a subgroup of atherosclerotic
patients.
Voghel G, Thorin-Trescases N, Farhat N, Mamarbachi AM, Villeneuve L,
Fortier A, Perrault LP, Carrier M, Thorin E.
Department of Surgery, Research Center, Montreal Heart Institute,
Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada.
Endothelial senescence may contribute to the pathogenesis of age-
related vascular disorders. Furthermore, chronic exposure to risk
factors for cardiovascular disease (CVD) accelerates the effects of
chronological aging by generating stress-dependent damages, including
oxidative stress, therefore promoting stress-induced premature
senescence. Our objective was to determine whether a chronic treatment
with an antioxidant (N-acetyl-cystein, NAC) could delay senescence of
endothelial cells (EC) isolated and cultured from arterial segments of
patients with severe coronary artery disease. If EC were considered as
one population (n=26), chronic NAC treatment slightly shortened
telomere attrition rate associated with senescence but did not
significantly delay the onset of endothelial senescence. However, in a
subgroup of NAC-treated EC (n=15) cellular senescence was
significantly delayed, NAC decreased lipid peroxidation (HNE),
activated the catalytic subunit of telomerase (hTERT) and inhibited
telomere attrition. In contrast, in another subgroup of EC (n=11)
characterized by initial short telomeres, no effect of NAC on HNE and
high levels of DNA damages, the antioxidant was not beneficial on
senescence, suggesting an irreversible stress-dependent damage. In
conclusion, chronic exposure to NAC can delay senescence of diseased
EC via hTERT activation and transient telomere stabilization, unless
oxidative stress-associated cell damage has become irreversible.
PMID: 18302967 [PubMed - in process] |
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