Sirt3 mediates reduction of oxidative damage and prevention of age-related hearing loss under caloric restriction
Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common age-related disorder associated with oxidative stress. Here, we report that CR reduces oxidative DNA damage in multiple tissues and prevents AH...
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| Vydané v: | Cell Ročník 143; číslo 5; s. 802 |
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| Hlavní autori: | , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
24.11.2010
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| Predmet: | |
| ISSN: | 1097-4172, 1097-4172 |
| On-line prístup: | Zistit podrobnosti o prístupe |
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| Abstract | Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common age-related disorder associated with oxidative stress. Here, we report that CR reduces oxidative DNA damage in multiple tissues and prevents AHL in wild-type mice but fails to modify these phenotypes in mice lacking the mitochondrial deacetylase Sirt3, a member of the sirtuin family. In response to CR, Sirt3 directly deacetylates and activates mitochondrial isocitrate dehydrogenase 2 (Idh2), leading to increased NADPH levels and an increased ratio of reduced-to-oxidized glutathione in mitochondria. In cultured cells, overexpression of Sirt3 and/or Idh2 increases NADPH levels and protects from oxidative stress-induced cell death. Therefore, our findings identify Sirt3 as an essential player in enhancing the mitochondrial glutathione antioxidant defense system during CR and suggest that Sirt3-dependent mitochondrial adaptations may be a central mechanism of aging retardation in mammals. |
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| AbstractList | Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common age-related disorder associated with oxidative stress. Here, we report that CR reduces oxidative DNA damage in multiple tissues and prevents AHL in wild-type mice but fails to modify these phenotypes in mice lacking the mitochondrial deacetylase Sirt3, a member of the sirtuin family. In response to CR, Sirt3 directly deacetylates and activates mitochondrial isocitrate dehydrogenase 2 (Idh2), leading to increased NADPH levels and an increased ratio of reduced-to-oxidized glutathione in mitochondria. In cultured cells, overexpression of Sirt3 and/or Idh2 increases NADPH levels and protects from oxidative stress-induced cell death. Therefore, our findings identify Sirt3 as an essential player in enhancing the mitochondrial glutathione antioxidant defense system during CR and suggest that Sirt3-dependent mitochondrial adaptations may be a central mechanism of aging retardation in mammals.Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common age-related disorder associated with oxidative stress. Here, we report that CR reduces oxidative DNA damage in multiple tissues and prevents AHL in wild-type mice but fails to modify these phenotypes in mice lacking the mitochondrial deacetylase Sirt3, a member of the sirtuin family. In response to CR, Sirt3 directly deacetylates and activates mitochondrial isocitrate dehydrogenase 2 (Idh2), leading to increased NADPH levels and an increased ratio of reduced-to-oxidized glutathione in mitochondria. In cultured cells, overexpression of Sirt3 and/or Idh2 increases NADPH levels and protects from oxidative stress-induced cell death. Therefore, our findings identify Sirt3 as an essential player in enhancing the mitochondrial glutathione antioxidant defense system during CR and suggest that Sirt3-dependent mitochondrial adaptations may be a central mechanism of aging retardation in mammals. Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common age-related disorder associated with oxidative stress. Here, we report that CR reduces oxidative DNA damage in multiple tissues and prevents AHL in wild-type mice but fails to modify these phenotypes in mice lacking the mitochondrial deacetylase Sirt3, a member of the sirtuin family. In response to CR, Sirt3 directly deacetylates and activates mitochondrial isocitrate dehydrogenase 2 (Idh2), leading to increased NADPH levels and an increased ratio of reduced-to-oxidized glutathione in mitochondria. In cultured cells, overexpression of Sirt3 and/or Idh2 increases NADPH levels and protects from oxidative stress-induced cell death. Therefore, our findings identify Sirt3 as an essential player in enhancing the mitochondrial glutathione antioxidant defense system during CR and suggest that Sirt3-dependent mitochondrial adaptations may be a central mechanism of aging retardation in mammals. |
| Author | Vann, James M Tanokura, Masaru Leeuwenburgh, Christiaan Someya, Shinichi Yu, Wei Xu, Jinze Hallows, William C Denu, John M Prolla, Tomas A |
| Author_xml | – sequence: 1 givenname: Shinichi surname: Someya fullname: Someya, Shinichi organization: Departments of Genetics and Medical Genetics, University of Wisconsin, Madison, 53706, USA – sequence: 2 givenname: Wei surname: Yu fullname: Yu, Wei – sequence: 3 givenname: William C surname: Hallows fullname: Hallows, William C – sequence: 4 givenname: Jinze surname: Xu fullname: Xu, Jinze – sequence: 5 givenname: James M surname: Vann fullname: Vann, James M – sequence: 6 givenname: Christiaan surname: Leeuwenburgh fullname: Leeuwenburgh, Christiaan – sequence: 7 givenname: Masaru surname: Tanokura fullname: Tanokura, Masaru – sequence: 8 givenname: John M surname: Denu fullname: Denu, John M – sequence: 9 givenname: Tomas A surname: Prolla fullname: Prolla, Tomas A |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21094524$$D View this record in MEDLINE/PubMed |
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| References | 21111225 - Cell. 2010 Nov 24;143(5):667-8. doi: 10.1016/j.cell.2010.11.009. 22374145 - Nat Rev Mol Cell Biol. 2012 Feb 29;13(4):207. doi: 10.1038/nrm3308. |
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| Snippet | Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common... |
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| SubjectTerms | Aging - metabolism Animals Antioxidants - metabolism Caloric Restriction DNA Damage Female Glutathione - metabolism Hearing Loss - prevention & control Isocitrate Dehydrogenase - metabolism Male Mice Mice, Inbred C57BL Mitochondria - metabolism Oxidative Stress Sirtuin 3 - genetics Sirtuin 3 - metabolism |
| Title | Sirt3 mediates reduction of oxidative damage and prevention of age-related hearing loss under caloric restriction |
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