Difference between revisions of "Free radicals effects"

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<h3>Oxidative modification of proteins </h3>
 
<h3>Oxidative modification of proteins </h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/14661084">PMID: 14661084</a><br /></div>
 
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<h3>Carbonylation</h3>
 
<h3>Carbonylation</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12727143">PMID: 12727143</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/16796807">PMID: 16796807</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/15088069">PMID: 15088069</a><br /></div>
 
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<h3>Free radicals  (• O2-, • OH, H2O2, ONOO-, NO2Cl)</h3>
 
<h3>Free radicals  (• O2-, • OH, H2O2, ONOO-, NO2Cl)</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/7915779">PMID: 7915779</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11773609">PMID: 11773609</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/12008112">PMID: 12008112</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/16978905">PMID: 16978905</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11773609">PMID: 11773609</a><br /></div>
 
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<h3>Heavy metals</h3>
 
<h3>Heavy metals</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16430879">PMID: 16430879</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11741035">PMID: 11741035</a><br /></div>
 
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<h3>Release of inflammatory mediators and toxins</h3>
 
<h3>Release of inflammatory mediators and toxins</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/8221019">PMID: 8221019</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/8471159">PMID: 8471159</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/6928666">PMID: 6928666</a><br /></div>
 
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<h3>Regulation of  proliferation  and apoptosis</h3>
 
<h3>Regulation of  proliferation  and apoptosis</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/7750801">PMID: 7750801</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11976182">PMID: 11976182</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/10687951">PMID: 10687951</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/10230803">PMID: 10230803</a><br /></div>
 
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<h3>Replication</h3>
 
<h3>Replication</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12429704">PMID: 12429704</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11100718">PMID: 11100718</a><br /></div>
 
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<h3>Glycoxidation</h3>
 
<h3>Glycoxidation</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/7519659">PMID: 7519659</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/14661084">PMID: 14661084</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/8626637">PMID: 8626637</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/10866821">PMID: 10866821</a><br /></div>
 
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<h3>Epoxides</h3>
 
<h3>Epoxides</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/15748653">PMID: 15748653</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/21861450">PMID: 21861450</a><br /></div>
 
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<h3>Inflammatory  Reactions</h3>
 
<h3>Inflammatory  Reactions</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/8862535">PMID: 8862535</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/6282132">PMID: 6282132</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/8221019">PMID: 8221019</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/8471159">PMID: 8471159</a><br /></div>
 
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<h3>Generalized inflammation</h3>
 
<h3>Generalized inflammation</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/17218425">PMID: 17218425</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/15230345">PMID: 15230345</a><br /></div>
 
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<h3>Membrane lipids  Peroxidation</h3>
 
<h3>Membrane lipids  Peroxidation</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/17068300">PMID: 17068300</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/1654835">PMID: 1654835</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/19500666">PMID: 19500666</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/21861450">PMID: 21861450</a><br /></div>
 
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<h3>Ionizing radiation</h3>
 
<h3>Ionizing radiation</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/7905906">PMID: 7905906</a><br /></div>
 
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<h3>Sulfur oxidation</h3>
 
<h3>Sulfur oxidation</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/1847917">PMID: 1847917</a><br /></div>
 
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<h3>Bactericidal action</h3>
 
<h3>Bactericidal action</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/7981786">PMID: 7981786</a><br /></div>
 
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<h3>Mitochondrial vicious cycle</h3>
 
<h3>Mitochondrial vicious cycle</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16841200">PMID: 16841200</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11050436">PMID: 11050436</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/17997255">PMID: 17997255</a><br /></div>
 
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<h3>Mutagenesis</h3>
 
<h3>Mutagenesis</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12832285">PMID: 12832285</a><br /></div>
 
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<h3>Protein aggregates</h3>
 
<h3>Protein aggregates</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/7519659">PMID: 7519659</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/12942175">PMID: 12942175</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11348660">PMID: 11348660</a><br /></div>
 
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<h3>Transcription</h3>
 
<h3>Transcription</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11713193">PMID: 11713193</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/15546503">PMID: 15546503</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/15343279">PMID: 15343279</a><br /></div>
 
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<h3>Oxidation of bases</h3>
 
<h3>Oxidation of bases</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12086677">PMID: 12086677</a><br /></div>
 
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<h3>Glycation</h3>
 
<h3>Glycation</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11795527">PMID: 11795527</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/8674901">PMID: 8674901</a><br /></div>
 
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<h3>Malonaldehide</h3>
 
<h3>Malonaldehide</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16737718">PMID: 16737718</a><br /></div>
 
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<h3>Endoperoxide</h3>
 
<h3>Endoperoxide</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/17349930">PMID: 17349930</a><br /></div>
 
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<h3>DNA damage</h3>
 
<h3>DNA damage</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12031895">PMID: 12031895</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/3065826">PMID: 3065826</a><br /></div>
 
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<h3>Stress-signaling</h3>
 
<h3>Stress-signaling</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11076791">PMID: 11076791</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/10924854">PMID: 10924854</a><br /></div>
 
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<h3>Crosslinks</h3>
 
<h3>Crosslinks</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/8168645">PMID: 8168645</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/10866821">PMID: 10866821</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/1855674">PMID: 1855674</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/8582666">PMID: 8582666</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/15795165">PMID: 15795165</a><br /></div>
 
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<h3>Reduced antioxidant level</h3>
 
<h3>Reduced antioxidant level</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16978905">PMID: 16978905</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/12361782">PMID: 12361782</a><br /></div>
 
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<h3>External stress factors</h3>
 
<h3>External stress factors</h3>
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</div>(.//.)<h1>Free radicals effects</h1>
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<p>The presence of free radicals in biological materials was discovered less than 50 years ago. The most relevant radicals in biological regulation are superoxide and NO. The superoxide anion is formed by the univalent reduction of triplet-state molecular oxygen (3 O2). This process is mediated by enzymes such as NAD(P)H oxidases and xanthine oxidase or nonenzymically by redoxreactive compounds such as the semi-ubiquinone compound of the mitochondrial electron transport chain. SODs convert superoxide enzymically into hydrogen peroxide. In biological tissues superoxide can also be converted nonenzymically into the nonradical species hydrogen peroxide and singlet oxygen (1 O2). In the presence of reduced transition metals (e.g., ferrous or cuprous ions), hydrogen peroxide can be converted into the highly reactive hydroxyl radical (•OH). The NO radical (NO•) is produced in higher organisms by the oxidation of one of the terminal guanidonitrogen atoms of L-arginine. This process is catalyzed by the enzyme NOS. Depending on the microenvironment, NO can be converted to various other reactive nitrogen species (RNS) such as nitrosonium cation (NO+), nitroxyl anion (NO ̶ ) or peroxynitrite (ONOO ̶ ).</p>
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<p>At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish “redox homeostasis.” Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively.</p>
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<p>Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. Free radicals and other reactive species have been implicated in the pathology of over 100 human diseases. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases.</p>
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Latest revision as of 09:26, 2 August 2015

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Free radicals effects

The presence of free radicals in biological materials was discovered less than 50 years ago. The most relevant radicals in biological regulation are superoxide and NO. The superoxide anion is formed by the univalent reduction of triplet-state molecular oxygen (3 O2). This process is mediated by enzymes such as NAD(P)H oxidases and xanthine oxidase or nonenzymically by redoxreactive compounds such as the semi-ubiquinone compound of the mitochondrial electron transport chain. SODs convert superoxide enzymically into hydrogen peroxide. In biological tissues superoxide can also be converted nonenzymically into the nonradical species hydrogen peroxide and singlet oxygen (1 O2). In the presence of reduced transition metals (e.g., ferrous or cuprous ions), hydrogen peroxide can be converted into the highly reactive hydroxyl radical (•OH). The NO radical (NO•) is produced in higher organisms by the oxidation of one of the terminal guanidonitrogen atoms of L-arginine. This process is catalyzed by the enzyme NOS. Depending on the microenvironment, NO can be converted to various other reactive nitrogen species (RNS) such as nitrosonium cation (NO+), nitroxyl anion (NO ̶ ) or peroxynitrite (ONOO ̶ ).

At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish “redox homeostasis.” Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively.

Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. Free radicals and other reactive species have been implicated in the pathology of over 100 human diseases. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases.