Difference between revisions of "Mitochondria function"

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<h3>Defective mitochondria</h3>
 
<h3>Defective mitochondria</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11898607">PMID: 11898607</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/16814712">PMID: 16814712</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11600563">PMID: 11600563</a><br /></div>
 
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<h3>Mutant and damaged  Mitochondrial proteins </h3>
 
<h3>Mutant and damaged  Mitochondrial proteins </h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16365283">PMID: 16365283</a><br /></div>
 
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<h3>Mitochondrial permeability transition pores</h3>
 
<h3>Mitochondrial permeability transition pores</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12729580">PMID: 12729580</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11855853">PMID: 11855853</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11852041">PMID: 11852041</a><br /></div>
 
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<h3>Apoptosis- Inducing  Factor</h3>
 
<h3>Apoptosis- Inducing  Factor</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11279485">PMID: 11279485</a><br /></div>
 
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<h3>Apoptosis</h3>
 
<h3>Apoptosis</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11711427">PMID: 11711427</a><br /></div>
 
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<h3>Repair effectiveness</h3>
 
<h3>Repair effectiveness</h3>
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<div class="links"></div>
 
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<h3>Homoplasy of mutant mtDNA</h3>
 
<h3>Homoplasy of mutant mtDNA</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16354751">PMID: 16354751</a><br /></div>
 
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<h3>Cytochrome c</h3>
 
<h3>Cytochrome c</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/22224850">PMID: 22224850</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/10702305">PMID: 10702305</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11855853">PMID: 11855853</a><br /></div>
 
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<h3>P66</h3>
 
<h3>P66</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16051147">PMID: 16051147</a><br /></div>
 
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<h3>Apoptosoma</h3>
 
<h3>Apoptosoma</h3>
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<h3>Electron transport chain</h3>
 
<h3>Electron transport chain</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11948241">PMID: 11948241</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/10620319">PMID: 10620319</a><br /></div>
 
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<h3>Nuclear DNA damages</h3>
 
<h3>Nuclear DNA damages</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11978482">PMID: 11978482</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11498282">PMID: 11498282</a><br /></div>
 
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<h3>H2O2</h3>
 
<h3>H2O2</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19061483">PMID: 19061483</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/17700625">PMID: 17700625</a><br /></div>
 
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<h3>ATP production</h3>
 
<h3>ATP production</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16814712">PMID: 16814712</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11600563">PMID: 11600563</a><br /></div>
 
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<h3>Organism aging</h3>
 
<h3>Organism aging</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/5046729">PMID: 5046729</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11248228">PMID: 11248228</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/8473911">PMID: 8473911</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/8333254">PMID: 8333254</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/15800038">PMID: 15800038</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/22888430">PMID: 22888430</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/14977532">PMID: 14977532</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/5016631">PMID: 5016631</a><br /></div>
 
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<h3>Cellular senescence</h3>
 
<h3>Cellular senescence</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/15963673">PMID: 15963673</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/12730239">PMID: 12730239</a><br /></div>
 
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<h3>Amino oxidase</h3>
 
<h3>Amino oxidase</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19371079">PMID: 19371079</a><br /></div>
 
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<h3>Mitochondrial DNA</h3>
 
<h3>Mitochondrial DNA</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/17408359">PMID: 17408359</a><br /></div>
 
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<h3>O2</h3>
 
<h3>O2</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19061483">PMID: 19061483</a><br /></div>
 
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<h3>Mutations in mtDNA</h3>
 
<h3>Mutations in mtDNA</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16120266">PMID: 16120266</a><br /></div>
 
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<h3>Sod2</h3>
 
<h3>Sod2</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12126755">PMID: 12126755</a><br /></div>
 
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<h3>H2O2</h3>
 
<h3>H2O2</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19061483">PMID: 19061483</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/17700625">PMID: 17700625</a><br /></div>
 
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<h3>Caspase 3</h3>
 
<h3>Caspase 3</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16469926">PMID: 16469926</a><br /></div>
 
</div>(...)<!--Pop-up for: Mitochondria !Pop-up-->
 
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<h3>Mitochondria</h3>
 
<h3>Mitochondria</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/15734681">PMID: 15734681</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/16860735">PMID: 16860735</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/19427899">PMID: 19427899</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/11248228">PMID: 11248228</a><br /></div>
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</div>(.//.)<h1>Mitochondria function</h1>
 +
 
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<p>Mitochondria are the main sites of biological energy generation in eukaryotes. These organelles are remnants of a bacterial endosymbiont that took up residence inside a host cell over 1,500 million years ago. A wide range of biochemical reactions—such as pyruvate oxidation, the citric acid cycle, electron transport, oxidative phosphorylation and ATP generation—takes place in the mitochondria of aerobic eukaryotes. Mitochondria also have key roles in buffering cytosolic calcium, fatty acid oxidation, haem biosynthesis and the biosynthesis of iron–sulphur (FeS) clusters. </p>
 +
<p>Mitochondrial ROS are known to be important determinants in cell function, participating in many signaling networks and also in a variety of degenerative processes. The primary ROS generated by mitochondria is O2.-, as a result of monoelectronic reduction of O2. The mitochondrial electron transport chain continuously reduces the bulk of O2 consumed to water, a four-electron reduction, but a small quantity of O2.-  is also generated. O2.-, a reasonably reactive ROS, is transformed into more stable H2O2 in mitochondria through the activity of matrix Mn-SOD, as well as Cu,Zn-SOD in the intermembrane space. H2O2 generated in mitochondria has many possible fates. Because H2O2 is relatively stable and membrane-permeative (and transported by aquaporins present in the inner mitochondrial membrane), it can diffuse within the cell and be removed by cytosolic antioxidant systems such as catalase, glutathione peroxidase, and thioredoxin peroxidase. Mitochondrially generated H2O2 can also act as a signaling molecule in the cytosol, affecting multiple networks that control, for example, cell cycle, stress response, energy metabolism, and redox balance. Within mitochondria, many new signaling effects of H2O2 have been uncovered over the past few years, including an important role in the activation of mild mitochondrial uncoupling pathways, which are themselves key regulators of mitochondrial ROS generation. H2O2 can be eliminated by mitochondrial enzymes. Mitochondria are important regulators of cellular redox status and are candidate vascular O2 sensors. Mitochondria-derived activated oxygen species (AOS), like H2O2, can diffuse to the cytoplasm and cause vasodilatation by activating sarcolemmal K+ channels. </p>
 +
<p>Progressive loss of mitochondrial function in several tissues is a common feature of aging. More in general, it has been proposed that mitochondria can be considered as a sort of biological clock for cell timing and aging. According to the hypothesis of Harman and its further extensions, life-long production of reactive oxygen species (ROS) as by-products of oxidative metabolism leads to the accumulation of DNA and protein damages at multiple cellular and tissue levels. This eventually induces the appearance of the aged phenotype, at both cellular and organismal level. Mitochondria play a critical role in aging not only because they are the major source and the most proximal target of reactive oxygen species, but also because they regulate stress response and apoptosis. Recent literature indicates that, in response to stress, a variety of molecules translocate to and localise in mitochondria. These molecules are likely to interact with each other, in order to mediate mitochondria/nucleus cross-talk and to regulate apoptosis. </p>(.//.)<!-- Do not edit!  -->
 
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Revision as of 15:17, 17 June 2015

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Mitochondria function

Mitochondria are the main sites of biological energy generation in eukaryotes. These organelles are remnants of a bacterial endosymbiont that took up residence inside a host cell over 1,500 million years ago. A wide range of biochemical reactions—such as pyruvate oxidation, the citric acid cycle, electron transport, oxidative phosphorylation and ATP generation—takes place in the mitochondria of aerobic eukaryotes. Mitochondria also have key roles in buffering cytosolic calcium, fatty acid oxidation, haem biosynthesis and the biosynthesis of iron–sulphur (FeS) clusters.

Mitochondrial ROS are known to be important determinants in cell function, participating in many signaling networks and also in a variety of degenerative processes. The primary ROS generated by mitochondria is O2.-, as a result of monoelectronic reduction of O2. The mitochondrial electron transport chain continuously reduces the bulk of O2 consumed to water, a four-electron reduction, but a small quantity of O2.- is also generated. O2.-, a reasonably reactive ROS, is transformed into more stable H2O2 in mitochondria through the activity of matrix Mn-SOD, as well as Cu,Zn-SOD in the intermembrane space. H2O2 generated in mitochondria has many possible fates. Because H2O2 is relatively stable and membrane-permeative (and transported by aquaporins present in the inner mitochondrial membrane), it can diffuse within the cell and be removed by cytosolic antioxidant systems such as catalase, glutathione peroxidase, and thioredoxin peroxidase. Mitochondrially generated H2O2 can also act as a signaling molecule in the cytosol, affecting multiple networks that control, for example, cell cycle, stress response, energy metabolism, and redox balance. Within mitochondria, many new signaling effects of H2O2 have been uncovered over the past few years, including an important role in the activation of mild mitochondrial uncoupling pathways, which are themselves key regulators of mitochondrial ROS generation. H2O2 can be eliminated by mitochondrial enzymes. Mitochondria are important regulators of cellular redox status and are candidate vascular O2 sensors. Mitochondria-derived activated oxygen species (AOS), like H2O2, can diffuse to the cytoplasm and cause vasodilatation by activating sarcolemmal K+ channels.

Progressive loss of mitochondrial function in several tissues is a common feature of aging. More in general, it has been proposed that mitochondria can be considered as a sort of biological clock for cell timing and aging. According to the hypothesis of Harman and its further extensions, life-long production of reactive oxygen species (ROS) as by-products of oxidative metabolism leads to the accumulation of DNA and protein damages at multiple cellular and tissue levels. This eventually induces the appearance of the aged phenotype, at both cellular and organismal level. Mitochondria play a critical role in aging not only because they are the major source and the most proximal target of reactive oxygen species, but also because they regulate stress response and apoptosis. Recent literature indicates that, in response to stress, a variety of molecules translocate to and localise in mitochondria. These molecules are likely to interact with each other, in order to mediate mitochondria/nucleus cross-talk and to regulate apoptosis.