Low levels of reactive oxygen species as modulators of cell function
In this paper, we present various arguments supporting the hypothesis that reactive oxygen species (ROS) could be responsible for the modulation of various cellular functions, besides their well known toxic effects. We first review the recent evidence indicating that ROS are able to modulate genome...
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Veröffentlicht in: | Mutation research 1995-02, Vol.316 (3), p.103-122 |
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creator | Remacle, José Raes, Martine Toussaint, Olivier Renard, Patricia Rao, Govind |
description | In this paper, we present various arguments supporting the hypothesis that reactive oxygen species (ROS) could be responsible for the modulation of various cellular functions, besides their well known toxic effects.
We first review the recent evidence indicating that ROS are able to modulate genome expression through specific and precise mechanisms during cell activation. The role of the nitrogen reactive radicals such as nitric oxide is separately analyzed because of its specific role in the nervous and vascular systems. The action of the other ROS on gene activation will then be reviewed by first looking at their possible involvement in the activation of transcription factors like NF-κB. Arguments will then be developed in favor of the implication of the ROS in the cellular effects of PMA, TNF-α and other cytokines on the modulation of the genetic expression. Possible mechanisms will be presented for linking the production of the ROS with cell activation. In a general way we postulate that ROS can play a role of secondary messengers in several cell responses to external stimuli.
In the second part of the paper, we will examine the long term influence of ROS and their possible roles in cellular aging. Different links exist between ROS and aging and the relationship between them is probably indirect. We propose to consider the effect of ROS as one of the multiple challenges that cells have to face, the cell being considered as a global system which must optimize its energy expenditure for carrying out its basic functions such as turnover, differentiated phenotype functions, multiplication, defense and repair processes. This thermodynamic point of view will help to understand the effect of low ROS stresses, among others, on accelerated aging. |
doi_str_mv | 10.1016/0921-8734(95)90004-7 |
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We first review the recent evidence indicating that ROS are able to modulate genome expression through specific and precise mechanisms during cell activation. The role of the nitrogen reactive radicals such as nitric oxide is separately analyzed because of its specific role in the nervous and vascular systems. The action of the other ROS on gene activation will then be reviewed by first looking at their possible involvement in the activation of transcription factors like NF-κB. Arguments will then be developed in favor of the implication of the ROS in the cellular effects of PMA, TNF-α and other cytokines on the modulation of the genetic expression. Possible mechanisms will be presented for linking the production of the ROS with cell activation. In a general way we postulate that ROS can play a role of secondary messengers in several cell responses to external stimuli.
In the second part of the paper, we will examine the long term influence of ROS and their possible roles in cellular aging. Different links exist between ROS and aging and the relationship between them is probably indirect. We propose to consider the effect of ROS as one of the multiple challenges that cells have to face, the cell being considered as a global system which must optimize its energy expenditure for carrying out its basic functions such as turnover, differentiated phenotype functions, multiplication, defense and repair processes. This thermodynamic point of view will help to understand the effect of low ROS stresses, among others, on accelerated aging.</description><identifier>ISSN: 0921-8734</identifier><identifier>ISSN: 0027-5107</identifier><identifier>DOI: 10.1016/0921-8734(95)90004-7</identifier><identifier>PMID: 7862174</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Ageing ; Ageing, cell death ; Animals ; Biological and medical sciences ; Cell activation ; Cell physiology ; Cellular Senescence - physiology ; Cytokine ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - physiology ; Humans ; Molecular and cellular biology ; NF-kappa B - physiology ; NF-κB ; Nitric oxide ; Nitric Oxide - physiology ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Signal Transduction ; Transcription Factor AP-1 - physiology ; Transcriptional Activation ; Tumor Necrosis Factor-alpha - physiology</subject><ispartof>Mutation research, 1995-02, Vol.316 (3), p.103-122</ispartof><rights>1995</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-f2818f8ab5a438c1d98c5ab86804411281a50e8ceb1016d74e606ebf5d758ce93</citedby><cites>FETCH-LOGICAL-c483t-f2818f8ab5a438c1d98c5ab86804411281a50e8ceb1016d74e606ebf5d758ce93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>313,314,780,784,792,27922,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3396357$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7862174$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Remacle, José</creatorcontrib><creatorcontrib>Raes, Martine</creatorcontrib><creatorcontrib>Toussaint, Olivier</creatorcontrib><creatorcontrib>Renard, Patricia</creatorcontrib><creatorcontrib>Rao, Govind</creatorcontrib><title>Low levels of reactive oxygen species as modulators of cell function</title><title>Mutation research</title><addtitle>Mutat Res</addtitle><description>In this paper, we present various arguments supporting the hypothesis that reactive oxygen species (ROS) could be responsible for the modulation of various cellular functions, besides their well known toxic effects.
We first review the recent evidence indicating that ROS are able to modulate genome expression through specific and precise mechanisms during cell activation. The role of the nitrogen reactive radicals such as nitric oxide is separately analyzed because of its specific role in the nervous and vascular systems. The action of the other ROS on gene activation will then be reviewed by first looking at their possible involvement in the activation of transcription factors like NF-κB. Arguments will then be developed in favor of the implication of the ROS in the cellular effects of PMA, TNF-α and other cytokines on the modulation of the genetic expression. Possible mechanisms will be presented for linking the production of the ROS with cell activation. In a general way we postulate that ROS can play a role of secondary messengers in several cell responses to external stimuli.
In the second part of the paper, we will examine the long term influence of ROS and their possible roles in cellular aging. Different links exist between ROS and aging and the relationship between them is probably indirect. We propose to consider the effect of ROS as one of the multiple challenges that cells have to face, the cell being considered as a global system which must optimize its energy expenditure for carrying out its basic functions such as turnover, differentiated phenotype functions, multiplication, defense and repair processes. This thermodynamic point of view will help to understand the effect of low ROS stresses, among others, on accelerated aging.</description><subject>Ageing</subject><subject>Ageing, cell death</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell activation</subject><subject>Cell physiology</subject><subject>Cellular Senescence - physiology</subject><subject>Cytokine</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - physiology</subject><subject>Humans</subject><subject>Molecular and cellular biology</subject><subject>NF-kappa B - physiology</subject><subject>NF-κB</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - physiology</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction</subject><subject>Transcription Factor AP-1 - physiology</subject><subject>Transcriptional Activation</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><issn>0921-8734</issn><issn>0027-5107</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRb0AlVL4A5C8QAgWATt-xNkgofKUKrGBteU4ExSUxsVOCv17nDbqkpWluWeuxgehM0puKKHyluQpTVTG-FUurnNCCE-yAzTdj4_QcQhfhKRMCTJBk0zJlGZ8ih4W7gc3sIYmYFdhD8Z29Rqw-918QovDCmwNAZuAl67sG9M5vwUtNA2u-jbSrj1Bh5VpApyO7wx9PD2-z1-Sxdvz6_x-kViuWJdUqaKqUqYQhjNlaZkrK0yhpCKcUxpTIwgoC8XwpzLjIImEohJlJuI0ZzN0uetdeffdQ-j0sg7DJaYF1wdNpeI5kyqCfAda70LwUOmVr5fGbzQleijXgxk9mNG50FthOotr52N_Xyyh3C-NtmJ-MeYmWNNU3rS2DnuMsVwyMdTc7bAoFdY1eB2ixNZCWXuwnS5d_f8df9XYiFo</recordid><startdate>19950201</startdate><enddate>19950201</enddate><creator>Remacle, José</creator><creator>Raes, Martine</creator><creator>Toussaint, Olivier</creator><creator>Renard, Patricia</creator><creator>Rao, Govind</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>19950201</creationdate><title>Low levels of reactive oxygen species as modulators of cell function</title><author>Remacle, José ; Raes, Martine ; Toussaint, Olivier ; Renard, Patricia ; Rao, Govind</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-f2818f8ab5a438c1d98c5ab86804411281a50e8ceb1016d74e606ebf5d758ce93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Ageing</topic><topic>Ageing, cell death</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell activation</topic><topic>Cell physiology</topic><topic>Cellular Senescence - physiology</topic><topic>Cytokine</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - physiology</topic><topic>Humans</topic><topic>Molecular and cellular biology</topic><topic>NF-kappa B - physiology</topic><topic>NF-κB</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - physiology</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction</topic><topic>Transcription Factor AP-1 - physiology</topic><topic>Transcriptional Activation</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Remacle, José</creatorcontrib><creatorcontrib>Raes, Martine</creatorcontrib><creatorcontrib>Toussaint, Olivier</creatorcontrib><creatorcontrib>Renard, Patricia</creatorcontrib><creatorcontrib>Rao, Govind</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Mutation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Remacle, José</au><au>Raes, Martine</au><au>Toussaint, Olivier</au><au>Renard, Patricia</au><au>Rao, Govind</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Low levels of reactive oxygen species as modulators of cell function</atitle><jtitle>Mutation research</jtitle><addtitle>Mutat Res</addtitle><date>1995-02-01</date><risdate>1995</risdate><volume>316</volume><issue>3</issue><spage>103</spage><epage>122</epage><pages>103-122</pages><issn>0921-8734</issn><issn>0027-5107</issn><abstract>In this paper, we present various arguments supporting the hypothesis that reactive oxygen species (ROS) could be responsible for the modulation of various cellular functions, besides their well known toxic effects.
We first review the recent evidence indicating that ROS are able to modulate genome expression through specific and precise mechanisms during cell activation. The role of the nitrogen reactive radicals such as nitric oxide is separately analyzed because of its specific role in the nervous and vascular systems. The action of the other ROS on gene activation will then be reviewed by first looking at their possible involvement in the activation of transcription factors like NF-κB. Arguments will then be developed in favor of the implication of the ROS in the cellular effects of PMA, TNF-α and other cytokines on the modulation of the genetic expression. Possible mechanisms will be presented for linking the production of the ROS with cell activation. In a general way we postulate that ROS can play a role of secondary messengers in several cell responses to external stimuli.
In the second part of the paper, we will examine the long term influence of ROS and their possible roles in cellular aging. Different links exist between ROS and aging and the relationship between them is probably indirect. We propose to consider the effect of ROS as one of the multiple challenges that cells have to face, the cell being considered as a global system which must optimize its energy expenditure for carrying out its basic functions such as turnover, differentiated phenotype functions, multiplication, defense and repair processes. This thermodynamic point of view will help to understand the effect of low ROS stresses, among others, on accelerated aging.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>7862174</pmid><doi>10.1016/0921-8734(95)90004-7</doi><tpages>20</tpages></addata></record> |
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subjects | Ageing Ageing, cell death Animals Biological and medical sciences Cell activation Cell physiology Cellular Senescence - physiology Cytokine Fundamental and applied biological sciences. Psychology Gene Expression Regulation - physiology Humans Molecular and cellular biology NF-kappa B - physiology NF-κB Nitric oxide Nitric Oxide - physiology Reactive oxygen species Reactive Oxygen Species - metabolism Signal Transduction Transcription Factor AP-1 - physiology Transcriptional Activation Tumor Necrosis Factor-alpha - physiology |
title | Low levels of reactive oxygen species as modulators of cell function |
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