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Age-Related Loss of the DNA Repair Response Following Exposure to Oxidative Stress
Young (4- to 6-month-old) and aged (24- to 28-month-old) mice were exposed to 2-nitropropane (2-NP), a DNA oxidizing agent, and the ability to induce DNA polymerase β (β-pol) and AP endonuclease (APE) was determined. In contrast to the inducibility of these gene products in response to oxidative dam...
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| Published in: | The journals of gerontology. Series A, Biological sciences and medical sciences Biological sciences and medical sciences, 2006-05, Vol.61 (5), p.427-434 |
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| Main Authors: | , , , , , |
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| Language: | English |
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| cited_by | cdi_FETCH-LOGICAL-c467t-23da268b804c6d9d9fd6810ecc05f333d20351d2106363340c274a9711077e323 |
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| cites | cdi_FETCH-LOGICAL-c467t-23da268b804c6d9d9fd6810ecc05f333d20351d2106363340c274a9711077e323 |
| container_end_page | 434 |
| container_issue | 5 |
| container_start_page | 427 |
| container_title | The journals of gerontology. Series A, Biological sciences and medical sciences |
| container_volume | 61 |
| creator | Cabelof, Diane C. Raffoul, Julian J. Ge, Yubin Van Remmen, Holly Matherly, Larry H. Heydari, Ahmad R. |
| description | Young (4- to 6-month-old) and aged (24- to 28-month-old) mice were exposed to 2-nitropropane (2-NP), a DNA oxidizing agent, and the ability to induce DNA polymerase β (β-pol) and AP endonuclease (APE) was determined. In contrast to the inducibility of these gene products in response to oxidative damage in young mice, aged mice showed a lack of inducibility of β-pol and APE. APE protein level and endonuclease activity were both reduced 40% (p |
| doi_str_mv | 10.1093/gerona/61.5.427 |
| format | article |
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In contrast to the inducibility of these gene products in response to oxidative damage in young mice, aged mice showed a lack of inducibility of β-pol and APE. APE protein level and endonuclease activity were both reduced 40% (p <.01) in response to 2-NP. Accordingly, the accumulation of DNA repair intermediates in response to 2-NP differed with age. Young animals accumulated 3′OH-containing DNA strand breaks, whereas the aged animals did not. A role for p53 in the difference in DNA damage response with age is suggested by the observation that the accumulation of p53 protein in response to DNA damage in young animals was absent in the aged animals. Our results are consistent with a reduced ability to process DNA damage with age.</description><identifier>ISSN: 1079-5006</identifier><identifier>EISSN: 1758-535X</identifier><identifier>DOI: 10.1093/gerona/61.5.427</identifier><identifier>PMID: 16720738</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Age ; Age Factors ; Aging - physiology ; Analysis of Variance ; Animals ; Blotting, Western ; Disease Models, Animal ; DNA Damage ; DNA repair ; DNA Repair - drug effects ; DNA Repair - physiology ; DNA-(Apurinic or Apyrimidinic Site) Lyase - drug effects ; DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism ; Genomics ; Male ; Mice ; Mice, Inbred Strains ; Mutation ; Nitroparaffins - pharmacology ; Oxidative Stress ; Probability ; Propane - analogs & derivatives ; Propane - pharmacology ; Reference Values ; Reverse Transcriptase Polymerase Chain Reaction ; Risk Factors ; Rodents</subject><ispartof>The journals of gerontology. Series A, Biological sciences and medical sciences, 2006-05, Vol.61 (5), p.427-434</ispartof><rights>Copyright Gerontological Society of America, Incorporated May 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-23da268b804c6d9d9fd6810ecc05f333d20351d2106363340c274a9711077e323</citedby><cites>FETCH-LOGICAL-c467t-23da268b804c6d9d9fd6810ecc05f333d20351d2106363340c274a9711077e323</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/16720738$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cabelof, Diane C.</creatorcontrib><creatorcontrib>Raffoul, Julian J.</creatorcontrib><creatorcontrib>Ge, Yubin</creatorcontrib><creatorcontrib>Van Remmen, Holly</creatorcontrib><creatorcontrib>Matherly, Larry H.</creatorcontrib><creatorcontrib>Heydari, Ahmad R.</creatorcontrib><title>Age-Related Loss of the DNA Repair Response Following Exposure to Oxidative Stress</title><title>The journals of gerontology. Series A, Biological sciences and medical sciences</title><addtitle>J Gerontol A Biol Sci Med Sci</addtitle><description>Young (4- to 6-month-old) and aged (24- to 28-month-old) mice were exposed to 2-nitropropane (2-NP), a DNA oxidizing agent, and the ability to induce DNA polymerase β (β-pol) and AP endonuclease (APE) was determined. In contrast to the inducibility of these gene products in response to oxidative damage in young mice, aged mice showed a lack of inducibility of β-pol and APE. APE protein level and endonuclease activity were both reduced 40% (p <.01) in response to 2-NP. Accordingly, the accumulation of DNA repair intermediates in response to 2-NP differed with age. Young animals accumulated 3′OH-containing DNA strand breaks, whereas the aged animals did not. A role for p53 in the difference in DNA damage response with age is suggested by the observation that the accumulation of p53 protein in response to DNA damage in young animals was absent in the aged animals. Our results are consistent with a reduced ability to process DNA damage with age.</description><subject>Age</subject><subject>Age Factors</subject><subject>Aging - physiology</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Blotting, Western</subject><subject>Disease Models, Animal</subject><subject>DNA Damage</subject><subject>DNA repair</subject><subject>DNA Repair - drug effects</subject><subject>DNA Repair - physiology</subject><subject>DNA-(Apurinic or Apyrimidinic Site) Lyase - drug effects</subject><subject>DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism</subject><subject>Genomics</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mutation</subject><subject>Nitroparaffins - pharmacology</subject><subject>Oxidative Stress</subject><subject>Probability</subject><subject>Propane - analogs & derivatives</subject><subject>Propane - pharmacology</subject><subject>Reference Values</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Risk Factors</subject><subject>Rodents</subject><issn>1079-5006</issn><issn>1758-535X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNpdkEtP3DAQgK2qqLx65lZZPfSW3bEd28lxxaMgViAtrYq4WCaeLIFsnNpJWf49RrsqEnOZkeab0cxHyBGDCYNSTJcYfGenik3kJOf6E9ljWhaZFPL2c6pBl5kEULtkP8ZHeAvJv5BdpjQHLYo9spgtMVtgawd0dO5jpL6mwwPSk6sZXWBvm5BS7H0XkZ75tvXPTbekp-vexzEgHTy9XjfODs0_pDdDwBgPyU5t24hft_mA_D47_XV8ns2vf14cz-ZZlSs9ZFw4y1VxX0BeKVe6snaqYIBVBbIWQjgOQjLHGSihhMih4jq3pWbpK42CiwPyY7O3D_7viHEwqyZW2La2Qz9GowoAnrgEfv8APvoxdOk2w6FQDFheJmi6gaqQLASsTR-alQ0vhoF5c202ro1iRprkOk18264d71fo3vmt3ARkG6CJA67_9214MkoLLc357Z25-XPFLhcnuZHiFbvmiCQ</recordid><startdate>20060501</startdate><enddate>20060501</enddate><creator>Cabelof, Diane C.</creator><creator>Raffoul, Julian J.</creator><creator>Ge, Yubin</creator><creator>Van Remmen, Holly</creator><creator>Matherly, Larry H.</creator><creator>Heydari, Ahmad R.</creator><general>Oxford University Press</general><scope>BSCLL</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20060501</creationdate><title>Age-Related Loss of the DNA Repair Response Following Exposure to Oxidative Stress</title><author>Cabelof, Diane C. ; Raffoul, Julian J. ; Ge, Yubin ; Van Remmen, Holly ; Matherly, Larry H. ; Heydari, Ahmad R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c467t-23da268b804c6d9d9fd6810ecc05f333d20351d2106363340c274a9711077e323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Age</topic><topic>Age Factors</topic><topic>Aging - physiology</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Blotting, Western</topic><topic>Disease Models, Animal</topic><topic>DNA Damage</topic><topic>DNA repair</topic><topic>DNA Repair - drug effects</topic><topic>DNA Repair - physiology</topic><topic>DNA-(Apurinic or Apyrimidinic Site) Lyase - drug effects</topic><topic>DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism</topic><topic>Genomics</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mutation</topic><topic>Nitroparaffins - pharmacology</topic><topic>Oxidative Stress</topic><topic>Probability</topic><topic>Propane - analogs & derivatives</topic><topic>Propane - pharmacology</topic><topic>Reference Values</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Risk Factors</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cabelof, Diane C.</creatorcontrib><creatorcontrib>Raffoul, Julian J.</creatorcontrib><creatorcontrib>Ge, Yubin</creatorcontrib><creatorcontrib>Van Remmen, Holly</creatorcontrib><creatorcontrib>Matherly, Larry H.</creatorcontrib><creatorcontrib>Heydari, Ahmad R.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>The journals of gerontology. 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Series A, Biological sciences and medical sciences</jtitle><addtitle>J Gerontol A Biol Sci Med Sci</addtitle><date>2006-05-01</date><risdate>2006</risdate><volume>61</volume><issue>5</issue><spage>427</spage><epage>434</epage><pages>427-434</pages><issn>1079-5006</issn><eissn>1758-535X</eissn><abstract>Young (4- to 6-month-old) and aged (24- to 28-month-old) mice were exposed to 2-nitropropane (2-NP), a DNA oxidizing agent, and the ability to induce DNA polymerase β (β-pol) and AP endonuclease (APE) was determined. In contrast to the inducibility of these gene products in response to oxidative damage in young mice, aged mice showed a lack of inducibility of β-pol and APE. APE protein level and endonuclease activity were both reduced 40% (p <.01) in response to 2-NP. Accordingly, the accumulation of DNA repair intermediates in response to 2-NP differed with age. Young animals accumulated 3′OH-containing DNA strand breaks, whereas the aged animals did not. A role for p53 in the difference in DNA damage response with age is suggested by the observation that the accumulation of p53 protein in response to DNA damage in young animals was absent in the aged animals. Our results are consistent with a reduced ability to process DNA damage with age.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>16720738</pmid><doi>10.1093/gerona/61.5.427</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1079-5006 |
| ispartof | The journals of gerontology. Series A, Biological sciences and medical sciences, 2006-05, Vol.61 (5), p.427-434 |
| issn | 1079-5006 1758-535X |
| language | eng |
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| source | Oxford Journals Online |
| subjects | Age Age Factors Aging - physiology Analysis of Variance Animals Blotting, Western Disease Models, Animal DNA Damage DNA repair DNA Repair - drug effects DNA Repair - physiology DNA-(Apurinic or Apyrimidinic Site) Lyase - drug effects DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism Genomics Male Mice Mice, Inbred Strains Mutation Nitroparaffins - pharmacology Oxidative Stress Probability Propane - analogs & derivatives Propane - pharmacology Reference Values Reverse Transcriptase Polymerase Chain Reaction Risk Factors Rodents |
| title | Age-Related Loss of the DNA Repair Response Following Exposure to Oxidative Stress |
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