Oxidative stress and brain aging: is zinc the link?
Zn(2+) dyshomeostasis has been strongly linked to neuronal injury in many neurological conditions. Toxic accumulation of intracellular free Zn(2+) ([Zn(2+)](i)) may result from either flux of the cation through glutamate receptor-associated channels, voltage-sensitive calcium channels, or Zn(2+)-sen...
Gespeichert in:
| Veröffentlicht in: | Biogerontology (Dordrecht) 2006-10, Vol.7 (5-6), p.307-314 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 314 |
|---|---|
| container_issue | 5-6 |
| container_start_page | 307 |
| container_title | Biogerontology (Dordrecht) |
| container_volume | 7 |
| creator | Frazzini, V Rockabrand, E Mocchegiani, E Sensi, S L |
| description | Zn(2+) dyshomeostasis has been strongly linked to neuronal injury in many neurological conditions. Toxic accumulation of intracellular free Zn(2+) ([Zn(2+)](i)) may result from either flux of the cation through glutamate receptor-associated channels, voltage-sensitive calcium channels, or Zn(2+)-sensitive membrane transporters. Injurious [Zn(2+)](i) rises can also result from release of the cation from intracellular sites such as metallothioneins (MTs) and mitochondria. Chronic inflammation and oxidative stress are hallmarks of aging. Zn(2+) homeostasis is affected by oxidative stress, which is a potent trigger for detrimental Zn(2+) release from MTs. Interestingly, Zn(2+) itself is a strong inducer of oxidative stress by promoting mitochondrial and extra-mitochondrial production of reactive oxygen species. In this review, we examine how Zn(2+) dyshomeostasis and oxidative stress might act synergistically to promote aging-related neurodegeneration. |
| doi_str_mv | 10.1007/s10522-006-9045-7 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_20249973</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20249973</sourcerecordid><originalsourceid>FETCH-LOGICAL-c390t-a2f50a902e24fb62e9d0bb3d2cb183d3b196b6ef3658aa15f95dcc2ff18b29253</originalsourceid><addsrcrecordid>eNp9kE1LAzEQhoMoVqs_wIsED-JlNZlsko0XkeIXFHrRc0h2k5q63a3Jrqi_3i0tCB48zRye92XmQeiEkktKiLxKlHCAjBCRKZLzTO6gA8oly4QUxe6ws0JlXIIaocOUFoRQAYLvoxGVBArF4ACx2WeoTBc-HE5ddClh01TYRhMabOahmV_jkPB3aErcvTpch-bt5gjteVMnd7ydY_Ryf_c8ecyms4enye00K5kiXWbAc2IUAQe5twKcqoi1rILS0oJVzFIlrHCeCV4YQ7lXvCpL8J4WFhRwNkbnm95VbN97lzq9DKl0dW0a1_ZJA4FcKckG8OJfkDKlhjtyAQN69gddtH1shje05EBBCLqG6AYqY5tSdF6vYlia-KUp0WvzemNeD-b12ryWQ-Z0W9zbpat-E1vV7AeHjnwI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>752126612</pqid></control><display><type>article</type><title>Oxidative stress and brain aging: is zinc the link?</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Frazzini, V ; Rockabrand, E ; Mocchegiani, E ; Sensi, S L</creator><creatorcontrib>Frazzini, V ; Rockabrand, E ; Mocchegiani, E ; Sensi, S L</creatorcontrib><description>Zn(2+) dyshomeostasis has been strongly linked to neuronal injury in many neurological conditions. Toxic accumulation of intracellular free Zn(2+) ([Zn(2+)](i)) may result from either flux of the cation through glutamate receptor-associated channels, voltage-sensitive calcium channels, or Zn(2+)-sensitive membrane transporters. Injurious [Zn(2+)](i) rises can also result from release of the cation from intracellular sites such as metallothioneins (MTs) and mitochondria. Chronic inflammation and oxidative stress are hallmarks of aging. Zn(2+) homeostasis is affected by oxidative stress, which is a potent trigger for detrimental Zn(2+) release from MTs. Interestingly, Zn(2+) itself is a strong inducer of oxidative stress by promoting mitochondrial and extra-mitochondrial production of reactive oxygen species. In this review, we examine how Zn(2+) dyshomeostasis and oxidative stress might act synergistically to promote aging-related neurodegeneration.</description><identifier>ISSN: 1389-5729</identifier><identifier>EISSN: 1573-6768</identifier><identifier>DOI: 10.1007/s10522-006-9045-7</identifier><identifier>PMID: 17028932</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Aging ; Aging - metabolism ; Aging - pathology ; Animals ; Antioxidants ; Apoptosis ; Brain - metabolism ; Brain - pathology ; Cation Transport Proteins - metabolism ; Homeostasis ; Humans ; Metallothionein - metabolism ; Mitochondria - metabolism ; Nerve Degeneration ; Oxidative Stress ; Reactive Oxygen Species - metabolism ; Zinc - metabolism</subject><ispartof>Biogerontology (Dordrecht), 2006-10, Vol.7 (5-6), p.307-314</ispartof><rights>Springer Science+Business Media, Inc. 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-a2f50a902e24fb62e9d0bb3d2cb183d3b196b6ef3658aa15f95dcc2ff18b29253</citedby><cites>FETCH-LOGICAL-c390t-a2f50a902e24fb62e9d0bb3d2cb183d3b196b6ef3658aa15f95dcc2ff18b29253</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17028932$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frazzini, V</creatorcontrib><creatorcontrib>Rockabrand, E</creatorcontrib><creatorcontrib>Mocchegiani, E</creatorcontrib><creatorcontrib>Sensi, S L</creatorcontrib><title>Oxidative stress and brain aging: is zinc the link?</title><title>Biogerontology (Dordrecht)</title><addtitle>Biogerontology</addtitle><description>Zn(2+) dyshomeostasis has been strongly linked to neuronal injury in many neurological conditions. Toxic accumulation of intracellular free Zn(2+) ([Zn(2+)](i)) may result from either flux of the cation through glutamate receptor-associated channels, voltage-sensitive calcium channels, or Zn(2+)-sensitive membrane transporters. Injurious [Zn(2+)](i) rises can also result from release of the cation from intracellular sites such as metallothioneins (MTs) and mitochondria. Chronic inflammation and oxidative stress are hallmarks of aging. Zn(2+) homeostasis is affected by oxidative stress, which is a potent trigger for detrimental Zn(2+) release from MTs. Interestingly, Zn(2+) itself is a strong inducer of oxidative stress by promoting mitochondrial and extra-mitochondrial production of reactive oxygen species. In this review, we examine how Zn(2+) dyshomeostasis and oxidative stress might act synergistically to promote aging-related neurodegeneration.</description><subject>Aging</subject><subject>Aging - metabolism</subject><subject>Aging - pathology</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Cation Transport Proteins - metabolism</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Metallothionein - metabolism</subject><subject>Mitochondria - metabolism</subject><subject>Nerve Degeneration</subject><subject>Oxidative Stress</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Zinc - metabolism</subject><issn>1389-5729</issn><issn>1573-6768</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kE1LAzEQhoMoVqs_wIsED-JlNZlsko0XkeIXFHrRc0h2k5q63a3Jrqi_3i0tCB48zRye92XmQeiEkktKiLxKlHCAjBCRKZLzTO6gA8oly4QUxe6ws0JlXIIaocOUFoRQAYLvoxGVBArF4ACx2WeoTBc-HE5ddClh01TYRhMabOahmV_jkPB3aErcvTpch-bt5gjteVMnd7ydY_Ryf_c8ecyms4enye00K5kiXWbAc2IUAQe5twKcqoi1rILS0oJVzFIlrHCeCV4YQ7lXvCpL8J4WFhRwNkbnm95VbN97lzq9DKl0dW0a1_ZJA4FcKckG8OJfkDKlhjtyAQN69gddtH1shje05EBBCLqG6AYqY5tSdF6vYlia-KUp0WvzemNeD-b12ryWQ-Z0W9zbpat-E1vV7AeHjnwI</recordid><startdate>20061001</startdate><enddate>20061001</enddate><creator>Frazzini, V</creator><creator>Rockabrand, E</creator><creator>Mocchegiani, E</creator><creator>Sensi, S L</creator><general>Springer Nature B.V</general><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>0-V</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88J</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2R</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20061001</creationdate><title>Oxidative stress and brain aging: is zinc the link?</title><author>Frazzini, V ; Rockabrand, E ; Mocchegiani, E ; Sensi, S L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-a2f50a902e24fb62e9d0bb3d2cb183d3b196b6ef3658aa15f95dcc2ff18b29253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Aging</topic><topic>Aging - metabolism</topic><topic>Aging - pathology</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Cation Transport Proteins - metabolism</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Metallothionein - metabolism</topic><topic>Mitochondria - metabolism</topic><topic>Nerve Degeneration</topic><topic>Oxidative Stress</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Zinc - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Frazzini, V</creatorcontrib><creatorcontrib>Rockabrand, E</creatorcontrib><creatorcontrib>Mocchegiani, E</creatorcontrib><creatorcontrib>Sensi, S L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Social Science Premium Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Social Science Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Biogerontology (Dordrecht)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Frazzini, V</au><au>Rockabrand, E</au><au>Mocchegiani, E</au><au>Sensi, S L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress and brain aging: is zinc the link?</atitle><jtitle>Biogerontology (Dordrecht)</jtitle><addtitle>Biogerontology</addtitle><date>2006-10-01</date><risdate>2006</risdate><volume>7</volume><issue>5-6</issue><spage>307</spage><epage>314</epage><pages>307-314</pages><issn>1389-5729</issn><eissn>1573-6768</eissn><abstract>Zn(2+) dyshomeostasis has been strongly linked to neuronal injury in many neurological conditions. Toxic accumulation of intracellular free Zn(2+) ([Zn(2+)](i)) may result from either flux of the cation through glutamate receptor-associated channels, voltage-sensitive calcium channels, or Zn(2+)-sensitive membrane transporters. Injurious [Zn(2+)](i) rises can also result from release of the cation from intracellular sites such as metallothioneins (MTs) and mitochondria. Chronic inflammation and oxidative stress are hallmarks of aging. Zn(2+) homeostasis is affected by oxidative stress, which is a potent trigger for detrimental Zn(2+) release from MTs. Interestingly, Zn(2+) itself is a strong inducer of oxidative stress by promoting mitochondrial and extra-mitochondrial production of reactive oxygen species. In this review, we examine how Zn(2+) dyshomeostasis and oxidative stress might act synergistically to promote aging-related neurodegeneration.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>17028932</pmid><doi>10.1007/s10522-006-9045-7</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1389-5729 |
| ispartof | Biogerontology (Dordrecht), 2006-10, Vol.7 (5-6), p.307-314 |
| issn | 1389-5729 1573-6768 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_20249973 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Aging Aging - metabolism Aging - pathology Animals Antioxidants Apoptosis Brain - metabolism Brain - pathology Cation Transport Proteins - metabolism Homeostasis Humans Metallothionein - metabolism Mitochondria - metabolism Nerve Degeneration Oxidative Stress Reactive Oxygen Species - metabolism Zinc - metabolism |
| title | Oxidative stress and brain aging: is zinc the link? |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-18T21%3A17%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Oxidative%20stress%20and%20brain%20aging:%20is%20zinc%20the%20link?&rft.jtitle=Biogerontology%20(Dordrecht)&rft.au=Frazzini,%20V&rft.date=2006-10-01&rft.volume=7&rft.issue=5-6&rft.spage=307&rft.epage=314&rft.pages=307-314&rft.issn=1389-5729&rft.eissn=1573-6768&rft_id=info:doi/10.1007/s10522-006-9045-7&rft_dat=%3Cproquest_cross%3E20249973%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=752126612&rft_id=info:pmid/17028932&rfr_iscdi=true |