Document Detail

Adaptive responses to the stress induced by hyperthermia or hydrogen peroxide in human fibroblasts.
MedLine Citation:
PMID:  12709575     Owner:  NLM     Status:  MEDLINE    
Perturbation of oxidant/antioxidant cellular balance, induced by cellular metabolism and by exogenous sources, causes deleterious effects to proteins, lipids, and nucleic acids, leading to a condition named "oxidative stress" that is involved in several diseases, such as cancer, ischemia-reperfusion injury, and neurodegenerative disorders. Among the exogenous agents, both H(2)O(2) and hyperthermia have been implicated in oxidative stress promotion linked with the activation of apoptotic or necrotic mechanisms of cell death. The goal of this work was to better understand the involvement of some stress-related proteins in adaptive responses mounted by human fibroblasts versus the oxidative stress differently induced by 42 degrees C hyperthermia or H(2)O(2.) The research was developed, switching off inducible nitric oxide synthase (iNOS) expression through antisense oligonucleotide transfection by studying the possible coregulation in the expression of HSP32 (also named HO-1), HSP70, and iNOS and their involvement in the induction of DNA damage. Several biochemical parameters, such as cell viability (MTT assay), cell membrane integrity (lactate dehydrogenase release), reactive oxygen species formation, glutathione levels, immunocytochemistry analysis of iNOS, HSP70, and HO-1 levels, genomic DNA fragmentation (HALO/COMET assay), and transmembrane mitochondrial potential (deltaPsi) were examined. Cells were collected immediately at the end of the stress-inducing treatment. The results, confirming the pleiotropic function of i-NOS, indicate that: (i). HO-1/HSP32, HSP70, and iNOS are finely tuned in their expression to contribute all together, in human fibroblasts, in ameliorating the resistance to oxidative stress damage; (ii). ROS exposure, at least in hyperthermia, in human fibroblasts contributes to growth arrest more than to apoptosis activation; and (iii). mitochondrial dysfunction, in presence of iNOS inhibition seems to be clearly involved in apoptotic cell death of human fibroblasts after H(2)O(2) treatment, but not after hyperthermia.
S Grasso; C Scifo; V Cardile; R Gulino; M Renis
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Experimental biology and medicine (Maywood, N.J.)     Volume:  228     ISSN:  1535-3702     ISO Abbreviation:  Exp. Biol. Med. (Maywood)     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-04-23     Completed Date:  2003-06-12     Revised Date:  2011-10-27    
Medline Journal Info:
Nlm Unique ID:  100973463     Medline TA:  Exp Biol Med (Maywood)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  491-8     Citation Subset:  IM    
Department of Biological Chemistry, Catania 95125, Italy.
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MeSH Terms
Antioxidants / metabolism
Cell Death / physiology
Cell Survival / physiology
Cells, Cultured
Comet Assay
DNA Damage
Fibroblasts / cytology,  metabolism*
Glutathione / metabolism
HSP70 Heat-Shock Proteins / metabolism
Heme Oxygenase (Decyclizing) / metabolism*
Heme Oxygenase-1
Hot Temperature*
Hydrogen Peroxide / metabolism*
Membrane Proteins
Mitochondria / metabolism
Nitric Oxide Synthase / genetics,  metabolism*
Nitric Oxide Synthase Type II
Oligonucleotides, Antisense / genetics,  metabolism
Oxidants / metabolism*
Oxidative Stress*
Reactive Oxygen Species / metabolism
Reg. No./Substance:
0/Antioxidants; 0/HSP70 Heat-Shock Proteins; 0/Membrane Proteins; 0/Oligonucleotides, Antisense; 0/Oxidants; 0/Reactive Oxygen Species; 70-18-8/Glutathione; 7722-84-1/Hydrogen Peroxide; EC protein, human; EC Oxide Synthase; EC Oxide Synthase Type II; EC protein, human; EC Oxygenase (Decyclizing); EC Oxygenase-1

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