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Implication of Dietary Iron-Chelating Bioactive Compounds in Molecular Mechanisms of Oxidative Stress-Induced Cell Ageing
One of the prevailing perceptions regarding the ageing of cells and organisms is the intracellular gradual accumulation of oxidatively damaged macromolecules, leading to the decline of cell and organ function (free radical theory of ageing). This chemically undefined material known as "lipofusc...
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| Published in: | Antioxidants 2021-03, Vol.10 (3), p.491 |
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| creator | Barbouti, Alexandra Lagopati, Nefeli Veroutis, Dimitris Goulas, Vlasios Evangelou, Konstantinos Kanavaros, Panagiotis Gorgoulis, Vassilis G Galaris, Dimitrios |
| description | One of the prevailing perceptions regarding the ageing of cells and organisms is the intracellular gradual accumulation of oxidatively damaged macromolecules, leading to the decline of cell and organ function (free radical theory of ageing). This chemically undefined material known as "lipofuscin," "ceroid," or "age pigment" is mainly formed through unregulated and nonspecific oxidative modifications of cellular macromolecules that are induced by highly reactive free radicals. A necessary precondition for reactive free radical generation and lipofuscin formation is the intracellular availability of ferrous iron (Fe
) ("labile iron"), catalyzing the conversion of weak oxidants such as peroxides, to extremely reactive ones like hydroxyl (HO
) or alcoxyl (RO
) radicals. If the oxidized materials remain unrepaired for extended periods of time, they can be further oxidized to generate ultimate over-oxidized products that are unable to be repaired, degraded, or exocytosed by the relevant cellular systems. Additionally, over-oxidized materials might inactivate cellular protection and repair mechanisms, thus allowing for futile cycles of increasingly rapid lipofuscin accumulation. In this review paper, we present evidence that the modulation of the labile iron pool distribution by nutritional or pharmacological means represents a hitherto unappreciated target for hampering lipofuscin accumulation and cellular ageing. |
| doi_str_mv | 10.3390/antiox10030491 |
| format | article |
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) ("labile iron"), catalyzing the conversion of weak oxidants such as peroxides, to extremely reactive ones like hydroxyl (HO
) or alcoxyl (RO
) radicals. If the oxidized materials remain unrepaired for extended periods of time, they can be further oxidized to generate ultimate over-oxidized products that are unable to be repaired, degraded, or exocytosed by the relevant cellular systems. Additionally, over-oxidized materials might inactivate cellular protection and repair mechanisms, thus allowing for futile cycles of increasingly rapid lipofuscin accumulation. In this review paper, we present evidence that the modulation of the labile iron pool distribution by nutritional or pharmacological means represents a hitherto unappreciated target for hampering lipofuscin accumulation and cellular ageing.</description><identifier>ISSN: 2076-3921</identifier><identifier>EISSN: 2076-3921</identifier><identifier>DOI: 10.3390/antiox10030491</identifier><identifier>PMID: 33800975</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>ageing mechanisms ; Aging ; Bioactive compounds ; bioactive dietary compounds ; By products ; cellular senescence ; Cytochrome ; Defense mechanisms ; Enzymes ; Free radicals ; Intracellular ; Iron ; iron-chelating agents ; labile iron ; Lipids ; Macromolecules ; Molecular modelling ; Oxidants ; Oxidation ; Oxidative stress ; Review</subject><ispartof>Antioxidants, 2021-03, Vol.10 (3), p.491</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c484t-e51117667aee016565cc5db2a2c1c4257effd57a1c83a42985d54b37dec1f8ba3</citedby><cites>FETCH-LOGICAL-c484t-e51117667aee016565cc5db2a2c1c4257effd57a1c83a42985d54b37dec1f8ba3</cites><orcidid>0000-0001-6730-359X ; 0000-0001-9001-4112 ; 0000-0001-7527-1559</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2524418050/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2524418050?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,38516,43895,44590,53791,53793,74412,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33800975$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Barbouti, Alexandra</creatorcontrib><creatorcontrib>Lagopati, Nefeli</creatorcontrib><creatorcontrib>Veroutis, Dimitris</creatorcontrib><creatorcontrib>Goulas, Vlasios</creatorcontrib><creatorcontrib>Evangelou, Konstantinos</creatorcontrib><creatorcontrib>Kanavaros, Panagiotis</creatorcontrib><creatorcontrib>Gorgoulis, Vassilis G</creatorcontrib><creatorcontrib>Galaris, Dimitrios</creatorcontrib><title>Implication of Dietary Iron-Chelating Bioactive Compounds in Molecular Mechanisms of Oxidative Stress-Induced Cell Ageing</title><title>Antioxidants</title><addtitle>Antioxidants (Basel)</addtitle><description>One of the prevailing perceptions regarding the ageing of cells and organisms is the intracellular gradual accumulation of oxidatively damaged macromolecules, leading to the decline of cell and organ function (free radical theory of ageing). This chemically undefined material known as "lipofuscin," "ceroid," or "age pigment" is mainly formed through unregulated and nonspecific oxidative modifications of cellular macromolecules that are induced by highly reactive free radicals. A necessary precondition for reactive free radical generation and lipofuscin formation is the intracellular availability of ferrous iron (Fe
) ("labile iron"), catalyzing the conversion of weak oxidants such as peroxides, to extremely reactive ones like hydroxyl (HO
) or alcoxyl (RO
) radicals. If the oxidized materials remain unrepaired for extended periods of time, they can be further oxidized to generate ultimate over-oxidized products that are unable to be repaired, degraded, or exocytosed by the relevant cellular systems. Additionally, over-oxidized materials might inactivate cellular protection and repair mechanisms, thus allowing for futile cycles of increasingly rapid lipofuscin accumulation. In this review paper, we present evidence that the modulation of the labile iron pool distribution by nutritional or pharmacological means represents a hitherto unappreciated target for hampering lipofuscin accumulation and cellular ageing.</description><subject>ageing mechanisms</subject><subject>Aging</subject><subject>Bioactive compounds</subject><subject>bioactive dietary compounds</subject><subject>By products</subject><subject>cellular senescence</subject><subject>Cytochrome</subject><subject>Defense mechanisms</subject><subject>Enzymes</subject><subject>Free radicals</subject><subject>Intracellular</subject><subject>Iron</subject><subject>iron-chelating agents</subject><subject>labile iron</subject><subject>Lipids</subject><subject>Macromolecules</subject><subject>Molecular modelling</subject><subject>Oxidants</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Review</subject><issn>2076-3921</issn><issn>2076-3921</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>COVID</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkk1v1DAQQCMEolXplSOKxIVLih3biX1BKuFrpVY9AGdrYk92vUrsxU6q9t_j7Zaqiy9jeZ6fZkZTFG8puWBMkY_gZxfuKCGMcEVfFKc1aZuKqZq-fHY_Kc5T2pJ8FGWSqNfFCcuRqFacFveraTc6A1nkyzCUXxzOEO_LVQy-6jY45oxfl59dADO7Wyy7MO3C4m0qnS-vw4hmGSGW12g24F2a0t5yc-csPOA_54gpVStvF4O27HAcy8s1Zueb4tUAY8Lzx3hW_P729Vf3o7q6-b7qLq8qwyWfKxSU0rZpWkAktBGNMEbYvobaUMNr0eIwWNECNZIBr5UUVvCetRYNHWQP7KxYHbw2wFbvoptyfzqA0w8PIa41xNmZEbVV2W2ADw02vAGjSMtkT6SUihPRq-z6dHDtln5Ca9DPEcYj6XHGu41eh1udx80k3ws-PApi-LNgmvXkkslDAY9hSboWRIq2VkRm9P1_6DYs0edRZarmnEoiSKYuDpSJIaWIw1MxlOj9kujjJckf3j1v4Qn_txLsL1Cnuig</recordid><startdate>20210321</startdate><enddate>20210321</enddate><creator>Barbouti, Alexandra</creator><creator>Lagopati, Nefeli</creator><creator>Veroutis, Dimitris</creator><creator>Goulas, Vlasios</creator><creator>Evangelou, Konstantinos</creator><creator>Kanavaros, Panagiotis</creator><creator>Gorgoulis, Vassilis G</creator><creator>Galaris, Dimitrios</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QR</scope><scope>7T5</scope><scope>7TO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-6730-359X</orcidid><orcidid>https://orcid.org/0000-0001-9001-4112</orcidid><orcidid>https://orcid.org/0000-0001-7527-1559</orcidid></search><sort><creationdate>20210321</creationdate><title>Implication of Dietary Iron-Chelating Bioactive Compounds in Molecular Mechanisms of Oxidative Stress-Induced Cell Ageing</title><author>Barbouti, Alexandra ; Lagopati, Nefeli ; Veroutis, Dimitris ; Goulas, Vlasios ; Evangelou, Konstantinos ; Kanavaros, Panagiotis ; Gorgoulis, Vassilis G ; Galaris, Dimitrios</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c484t-e51117667aee016565cc5db2a2c1c4257effd57a1c83a42985d54b37dec1f8ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>ageing mechanisms</topic><topic>Aging</topic><topic>Bioactive compounds</topic><topic>bioactive dietary compounds</topic><topic>By products</topic><topic>cellular senescence</topic><topic>Cytochrome</topic><topic>Defense mechanisms</topic><topic>Enzymes</topic><topic>Free radicals</topic><topic>Intracellular</topic><topic>Iron</topic><topic>iron-chelating agents</topic><topic>labile iron</topic><topic>Lipids</topic><topic>Macromolecules</topic><topic>Molecular modelling</topic><topic>Oxidants</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Review</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Barbouti, Alexandra</creatorcontrib><creatorcontrib>Lagopati, Nefeli</creatorcontrib><creatorcontrib>Veroutis, Dimitris</creatorcontrib><creatorcontrib>Goulas, Vlasios</creatorcontrib><creatorcontrib>Evangelou, Konstantinos</creatorcontrib><creatorcontrib>Kanavaros, Panagiotis</creatorcontrib><creatorcontrib>Gorgoulis, Vassilis G</creatorcontrib><creatorcontrib>Galaris, Dimitrios</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest - Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Antioxidants</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Barbouti, Alexandra</au><au>Lagopati, Nefeli</au><au>Veroutis, Dimitris</au><au>Goulas, Vlasios</au><au>Evangelou, Konstantinos</au><au>Kanavaros, Panagiotis</au><au>Gorgoulis, Vassilis G</au><au>Galaris, Dimitrios</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Implication of Dietary Iron-Chelating Bioactive Compounds in Molecular Mechanisms of Oxidative Stress-Induced Cell Ageing</atitle><jtitle>Antioxidants</jtitle><addtitle>Antioxidants (Basel)</addtitle><date>2021-03-21</date><risdate>2021</risdate><volume>10</volume><issue>3</issue><spage>491</spage><pages>491-</pages><issn>2076-3921</issn><eissn>2076-3921</eissn><abstract>One of the prevailing perceptions regarding the ageing of cells and organisms is the intracellular gradual accumulation of oxidatively damaged macromolecules, leading to the decline of cell and organ function (free radical theory of ageing). This chemically undefined material known as "lipofuscin," "ceroid," or "age pigment" is mainly formed through unregulated and nonspecific oxidative modifications of cellular macromolecules that are induced by highly reactive free radicals. A necessary precondition for reactive free radical generation and lipofuscin formation is the intracellular availability of ferrous iron (Fe
) ("labile iron"), catalyzing the conversion of weak oxidants such as peroxides, to extremely reactive ones like hydroxyl (HO
) or alcoxyl (RO
) radicals. If the oxidized materials remain unrepaired for extended periods of time, they can be further oxidized to generate ultimate over-oxidized products that are unable to be repaired, degraded, or exocytosed by the relevant cellular systems. Additionally, over-oxidized materials might inactivate cellular protection and repair mechanisms, thus allowing for futile cycles of increasingly rapid lipofuscin accumulation. In this review paper, we present evidence that the modulation of the labile iron pool distribution by nutritional or pharmacological means represents a hitherto unappreciated target for hampering lipofuscin accumulation and cellular ageing.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>33800975</pmid><doi>10.3390/antiox10030491</doi><orcidid>https://orcid.org/0000-0001-6730-359X</orcidid><orcidid>https://orcid.org/0000-0001-9001-4112</orcidid><orcidid>https://orcid.org/0000-0001-7527-1559</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Antioxidants, 2021-03, Vol.10 (3), p.491 |
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| subjects | ageing mechanisms Aging Bioactive compounds bioactive dietary compounds By products cellular senescence Cytochrome Defense mechanisms Enzymes Free radicals Intracellular Iron iron-chelating agents labile iron Lipids Macromolecules Molecular modelling Oxidants Oxidation Oxidative stress Review |
| title | Implication of Dietary Iron-Chelating Bioactive Compounds in Molecular Mechanisms of Oxidative Stress-Induced Cell Ageing |
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