2011年2月15日 星期二

Apoptosis and telomeres shortening related to HIV-1 induced oxidative stress in an astrocytoma cell line.[2009](IR92)

Apoptosis and telomeres shortening related to HIV-1 induced oxidative stress in an astrocytoma cell line.[2009](IR92)
Background info (selected by WeiJin Tang (
湯偉晉):
Telomeres (
端粒) serve to maintain the structural integrity of chromosomes (染色體), yet each somatic cell (體細胞) division is associated with a decrease in telomere lengthThe cumulative decrease in telomere length can impose an upper limit for the number of cell divisions that can occur before a cell senesces (衰老).

Source:
Telomere Shortening in Hematopoietic Stem Cell Transplantation: A Potential Mechanism for Late Graft Failure?

Reference:
von Zglinicki T. Oxidative stress shortens telomeres. Trends
Biochem Sci. 2002;27:339-344.

Chronic oxidativestress compromises telomere integrity and accelerates the onset of senescence in human endothelial cells [2004](IR92)

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Apoptosis and telomeres shortening related to HIV-1 induced oxidative stress in an astrocytoma cell line.[2009](IR92)

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(Memo Item created on November 3, 2010 02:57 AM)
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Apoptosis and telomeres shortening related to HIV-1 induced oxidative stress in an astrocytoma cell line.

http://www.ncbi.nlm.nih.gov/pubmed/19463156
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BMC Neurosci. 2009 May 22;10:51.
Apoptosis and telomeres shortening related to HIV-1 induced oxidative stress in an astrocytoma cell line.

Pollicita M, Muscoli C, Sgura A, Biasin A, Granato T, Masuelli L, Mollace V, Tanzarella C, Del Duca C, Rodinò P, Perno CF, Aquaro S.
Department of Experimental Medicine and Biochemical Sciences, University Tor Vergata, Rome, Italy. michela.pollicita@uniroma2.it

Abstract

BACKGROUND: 
Oxidative stress plays a key role in the neuropathogenesis of Human Immunodeficiency Virus-1 (HIV-1) infection causing apoptosis of astroglia cells and neurons. Recent data have shown that oxidative stress is also responsible for the acceleration of human fibroblast telomere shortening in vitro. In the present study we analyzed the potential relations occurring between free radicals formation and telomere length during HIV-1 mediated astroglial death.

RESULTS: 
To this end, U373 human astrocytoma cells have been directly exposed to X4-using HIV-1IIIB strain, for 1, 3 or 5 days and treated (where requested) with N-acetylcysteine (NAC), a cysteine donor involved in the synthesis of glutathione (GSH, a cellular antioxidant) and apoptosis has been evaluated by FACS analysis. Quantitative-FISH (Q-FISH) has been employed for studying the telomere length while intracellular reduced/oxidized glutathione (GSH/GSSG) ratio has been determined by High-Performance Liquid Chromatography (HPLC). Incubation of U373 with HIV-1IIIB led to significant induction of cellular apoptosis that was reduced in the presence of 1 mM NAC. Moreover, NAC improved the GSH/GSSG, a sensitive indicator of oxidative stress, that significantly decreased after HIV-1IIIB exposure in U373. Analysis of telomere length in HIV-1 exposed U373 showed a statistically significant telomere shortening, that was completely reverted in NAC-treated U373.

CONCLUSION: 
Our results support the role of HIV-1-mediated oxidative stress in astrocytic death and the importance of antioxidant compounds in preventing these cellular damages. Moreover, these data indicate that the telomere structure, target for oxidative damage, could be the key sensor of cell apoptosis induced by oxidative stress after HIV infection.

PMID: 19463156 [PubMed - indexed for MEDLINE]PMCID: PMC2694812Free PMC Article
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