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Changes in reactive oxygen species begin early during replicative aging of Saccharomyces cerevisiae cells
Increased reactive oxygen species (ROS) are a feature of aging cells, but little is known about when ROS generation begins as cells age. Here we show how ROS change in Saccharomyces cerevisiae cells throughout their early replicative life span using the fluorescent ROS indicator dihydroethidium (DHE...
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Published in: | Free radical biology & medicine 2011-04, Vol.50 (8), p.963-970 |
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creator | Lam, Yuen T. Aung-Htut, May T. Lim, Yu L. Yang, Hongyuan Dawes, Ian W. |
description | Increased reactive oxygen species (ROS) are a feature of aging cells, but little is known about when ROS generation begins as cells age. Here we show how ROS change in
Saccharomyces cerevisiae cells throughout their early replicative life span using the fluorescent ROS indicator dihydroethidium (DHE), which has some specificity for the superoxide anion. Cells in a particular age range were heterogeneous with respect to their ROS burden. Surprisingly, some cells as young as 5–7 generations acquired a greatly increased level of ROS detected by DHE relative to virgin cells. By 12 generations 50% of cells had a substantial ROS burden despite being only halfway through their life span. In contrast to the wild type, cells of a
sir2 mutant had lower levels of ROS reacting with DHE. Daughters from older mothers had low ROS levels, and this asymmetric distribution of ROS was
SIR2-independent. Mitochondrial fragmentation also began to occur in cells after 4 generations and increased markedly as cells aged. Daughter cells regenerated normal tubular mitochondria despite the fragmentation of mitochondria in the mother cells, whereas daughters of the
sir2 mutant had fragmented mitochondria at all ages. |
doi_str_mv | 10.1016/j.freeradbiomed.2011.01.013 |
format | article |
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Saccharomyces cerevisiae cells throughout their early replicative life span using the fluorescent ROS indicator dihydroethidium (DHE), which has some specificity for the superoxide anion. Cells in a particular age range were heterogeneous with respect to their ROS burden. Surprisingly, some cells as young as 5–7 generations acquired a greatly increased level of ROS detected by DHE relative to virgin cells. By 12 generations 50% of cells had a substantial ROS burden despite being only halfway through their life span. In contrast to the wild type, cells of a
sir2 mutant had lower levels of ROS reacting with DHE. Daughters from older mothers had low ROS levels, and this asymmetric distribution of ROS was
SIR2-independent. Mitochondrial fragmentation also began to occur in cells after 4 generations and increased markedly as cells aged. Daughter cells regenerated normal tubular mitochondria despite the fragmentation of mitochondria in the mother cells, whereas daughters of the
sir2 mutant had fragmented mitochondria at all ages.</description><identifier>ISSN: 0891-5849</identifier><identifier>EISSN: 1873-4596</identifier><identifier>DOI: 10.1016/j.freeradbiomed.2011.01.013</identifier><identifier>PMID: 21255640</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Cell aging ; Cell Division ; daughters ; Flow Cytometry ; fluorescence ; Free radicals ; longevity ; Microscopy, Fluorescence ; mitochondria ; Mitochondrial morphology ; mothers ; mutants ; Oxidative stress ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae - cytology ; Saccharomyces cerevisiae - metabolism ; Saccharomyces cerevisiae - physiology ; SIR2 ; Superoxide anion ; Yeast</subject><ispartof>Free radical biology & medicine, 2011-04, Vol.50 (8), p.963-970</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-498f291b2ae3a3103082d71f2a191f442f44eef6d6c25611915975fd2abec0763</citedby><cites>FETCH-LOGICAL-c438t-498f291b2ae3a3103082d71f2a191f442f44eef6d6c25611915975fd2abec0763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21255640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lam, Yuen T.</creatorcontrib><creatorcontrib>Aung-Htut, May T.</creatorcontrib><creatorcontrib>Lim, Yu L.</creatorcontrib><creatorcontrib>Yang, Hongyuan</creatorcontrib><creatorcontrib>Dawes, Ian W.</creatorcontrib><title>Changes in reactive oxygen species begin early during replicative aging of Saccharomyces cerevisiae cells</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>Increased reactive oxygen species (ROS) are a feature of aging cells, but little is known about when ROS generation begins as cells age. Here we show how ROS change in
Saccharomyces cerevisiae cells throughout their early replicative life span using the fluorescent ROS indicator dihydroethidium (DHE), which has some specificity for the superoxide anion. Cells in a particular age range were heterogeneous with respect to their ROS burden. Surprisingly, some cells as young as 5–7 generations acquired a greatly increased level of ROS detected by DHE relative to virgin cells. By 12 generations 50% of cells had a substantial ROS burden despite being only halfway through their life span. In contrast to the wild type, cells of a
sir2 mutant had lower levels of ROS reacting with DHE. Daughters from older mothers had low ROS levels, and this asymmetric distribution of ROS was
SIR2-independent. Mitochondrial fragmentation also began to occur in cells after 4 generations and increased markedly as cells aged. Daughter cells regenerated normal tubular mitochondria despite the fragmentation of mitochondria in the mother cells, whereas daughters of the
sir2 mutant had fragmented mitochondria at all ages.</description><subject>Cell aging</subject><subject>Cell Division</subject><subject>daughters</subject><subject>Flow Cytometry</subject><subject>fluorescence</subject><subject>Free radicals</subject><subject>longevity</subject><subject>Microscopy, Fluorescence</subject><subject>mitochondria</subject><subject>Mitochondrial morphology</subject><subject>mothers</subject><subject>mutants</subject><subject>Oxidative stress</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Saccharomyces cerevisiae</subject><subject>Saccharomyces cerevisiae - cytology</subject><subject>Saccharomyces cerevisiae - metabolism</subject><subject>Saccharomyces cerevisiae - physiology</subject><subject>SIR2</subject><subject>Superoxide anion</subject><subject>Yeast</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqNkU1vEzEQhi1ERdPCX4CVOHDa4O_1ihOK2oJUiUPbszXrHW8dbdbBTqLm3-Nt2gMnkMbyaOZ5xyO_hHxmdMko01_XS58QE_RdiBvsl5wytqRziDdkwUwjaqla_ZYsqGlZrYxsz8lFzmtKqVTCvCPnnHGltKQLElaPMA2YqzBVCcHtwgGr-HQccKryFl0orQ6H0kVI47Hq9ylMQ0G3Y3DwTMMwV6Kv7sC5R0hxc3RF5TDhIeQAWNJxzO_JmYcx44eX-5I8XF_dr37Ut79ufq6-39ZOCrOrZWs8b1nHAQUIRgU1vG-Y58Ba5qXk5SB63WvHlWalqNpG-Z5Dh442WlySL6e52xR_7zHv7CbkeQOYMO6zbZmhkgvW_JM0ZX7DtaGF_HYiXYo5J_R2m8IG0tEyamdT7Nr-ZYqdTbF0DlHUH1_e2Xdz71X76kIBPp0AD9HCkEK2D3dlgqJFriUzhbg6EVh-7hAw2VysmRz2IaHb2T6G_1rlD6eorxA</recordid><startdate>20110415</startdate><enddate>20110415</enddate><creator>Lam, Yuen T.</creator><creator>Aung-Htut, May T.</creator><creator>Lim, Yu L.</creator><creator>Yang, Hongyuan</creator><creator>Dawes, Ian W.</creator><general>Elsevier Inc</general><scope>FBQ</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>7X8</scope><scope>M7N</scope></search><sort><creationdate>20110415</creationdate><title>Changes in reactive oxygen species begin early during replicative aging of Saccharomyces cerevisiae cells</title><author>Lam, Yuen T. ; Aung-Htut, May T. ; Lim, Yu L. ; Yang, Hongyuan ; Dawes, Ian W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-498f291b2ae3a3103082d71f2a191f442f44eef6d6c25611915975fd2abec0763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Cell aging</topic><topic>Cell Division</topic><topic>daughters</topic><topic>Flow Cytometry</topic><topic>fluorescence</topic><topic>Free radicals</topic><topic>longevity</topic><topic>Microscopy, Fluorescence</topic><topic>mitochondria</topic><topic>Mitochondrial morphology</topic><topic>mothers</topic><topic>mutants</topic><topic>Oxidative stress</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Saccharomyces cerevisiae</topic><topic>Saccharomyces cerevisiae - cytology</topic><topic>Saccharomyces cerevisiae - metabolism</topic><topic>Saccharomyces cerevisiae - physiology</topic><topic>SIR2</topic><topic>Superoxide anion</topic><topic>Yeast</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lam, Yuen T.</creatorcontrib><creatorcontrib>Aung-Htut, May T.</creatorcontrib><creatorcontrib>Lim, Yu L.</creatorcontrib><creatorcontrib>Yang, Hongyuan</creatorcontrib><creatorcontrib>Dawes, Ian W.</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lam, Yuen T.</au><au>Aung-Htut, May T.</au><au>Lim, Yu L.</au><au>Yang, Hongyuan</au><au>Dawes, Ian W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in reactive oxygen species begin early during replicative aging of Saccharomyces cerevisiae cells</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>2011-04-15</date><risdate>2011</risdate><volume>50</volume><issue>8</issue><spage>963</spage><epage>970</epage><pages>963-970</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><abstract>Increased reactive oxygen species (ROS) are a feature of aging cells, but little is known about when ROS generation begins as cells age. Here we show how ROS change in
Saccharomyces cerevisiae cells throughout their early replicative life span using the fluorescent ROS indicator dihydroethidium (DHE), which has some specificity for the superoxide anion. Cells in a particular age range were heterogeneous with respect to their ROS burden. Surprisingly, some cells as young as 5–7 generations acquired a greatly increased level of ROS detected by DHE relative to virgin cells. By 12 generations 50% of cells had a substantial ROS burden despite being only halfway through their life span. In contrast to the wild type, cells of a
sir2 mutant had lower levels of ROS reacting with DHE. Daughters from older mothers had low ROS levels, and this asymmetric distribution of ROS was
SIR2-independent. Mitochondrial fragmentation also began to occur in cells after 4 generations and increased markedly as cells aged. Daughter cells regenerated normal tubular mitochondria despite the fragmentation of mitochondria in the mother cells, whereas daughters of the
sir2 mutant had fragmented mitochondria at all ages.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>21255640</pmid><doi>10.1016/j.freeradbiomed.2011.01.013</doi><tpages>8</tpages></addata></record> |
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subjects | Cell aging Cell Division daughters Flow Cytometry fluorescence Free radicals longevity Microscopy, Fluorescence mitochondria Mitochondrial morphology mothers mutants Oxidative stress Reactive oxygen species Reactive Oxygen Species - metabolism Saccharomyces cerevisiae Saccharomyces cerevisiae - cytology Saccharomyces cerevisiae - metabolism Saccharomyces cerevisiae - physiology SIR2 Superoxide anion Yeast |
title | Changes in reactive oxygen species begin early during replicative aging of Saccharomyces cerevisiae cells |
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