Age related distribution of 4-hydroxy 2-nonenal immunoreactivity in human retina.
Identifieur interne : 000393 ( Main/Exploration ); précédent : 000392; suivant : 000394Age related distribution of 4-hydroxy 2-nonenal immunoreactivity in human retina.
Auteurs : Tapas C. Nag [Inde] ; Pankaj Kumar [Inde] ; Shashi Wadhwa [Inde]Source :
- Experimental eye research [ 1096-0007 ] ; 2017.
Descripteurs français
- KwdFr :
- Adulte (MeSH), Adulte d'âge moyen (MeSH), Aldéhydes (métabolisme), Cellules photoréceptrices en cône de la rétine (métabolisme), Femelle (MeSH), Humains (MeSH), Immunohistochimie (MeSH), Mâle (MeSH), Répartition par âge (MeSH), Rétine (métabolisme), Segment externe de cellule photoréceptrice rétinienne (métabolisme), Sujet âgé (MeSH), Sujet âgé de 80 ans ou plus (MeSH), Vieillissement (immunologie).
- MESH :
English descriptors
- KwdEn :
- Adult (MeSH), Age Distribution (MeSH), Aged (MeSH), Aged, 80 and over (MeSH), Aging (immunology), Aldehydes (metabolism), Female (MeSH), Humans (MeSH), Immunohistochemistry (MeSH), Male (MeSH), Middle Aged (MeSH), Retina (metabolism), Retinal Cone Photoreceptor Cells (metabolism), Retinal Photoreceptor Cell Outer Segment (metabolism).
- MESH :
- chemical , metabolism : Aldehydes.
- immunology : Aging.
- metabolism : Retina, Retinal Cone Photoreceptor Cells, Retinal Photoreceptor Cell Outer Segment.
- Adult, Age Distribution, Aged, Aged, 80 and over, Female, Humans, Immunohistochemistry, Male, Middle Aged.
Abstract
The retina is prone to be damaged by oxidative stress (OS), owing to its constant exposure to light, high rate of oxygen consumption and high membrane lipid content. Lipid peroxidation in aging human retina has been shown by biochemical means. However, information on the cellular sites of OS and antioxidant responses in aging human retina remains limited. Here, we show distribution of immunoreactivity (IR) to a marker of lipid peroxidation (4-hydroxy 2-nonenal [HNE] and antioxidant enzymes involved in counteracting lipid peroxidation (glutathione S-transferase-π1 and glutarexoxin-1) in donor human retinas at different ages (35-91 years; N = 24). Initially, HNE-IR was present in few macular cone outer segments (COS, sixth decade). With aging, IR appeared in many COS and peaked at ninth decade (14 vs 62 per 3850 μm2 area between 6 and 9 decade; p < 0.001) in the parafovea then seen elsewhere (perifoveal, mid-peripheral and nasal). IR was seen in the parafovea of all retinas, whereas it was present in 8/24 of perifoveal and 6/24 of mid-peripheral retinas, indicating that the parafovea is susceptible to undergo lipid peroxidation. Foveolar COS were immunonegative until 81 years, which developed IR later (>83 years). IR to glutathione S-transferase-π1 was moderate until eight decade and then showed a decrease in photoreceptor cells between ninth and tenth decade, while glutaredoxin-1 maintained a steady expression with aging. Damaged COS were present in aged retinas, and inner segments and photoreceptor nuclei also showed some degree of alterations. Although there was increased lipid peroxidation with aging, cone death was minimal in those retinas. The two antioxidant enzymes studied here, may play a role in protecting photoreceptors against OS with advanced aging.
DOI: 10.1016/j.exer.2017.09.014
PubMed: 28986146
Affiliations:
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Electronic address: tapas_nag@yahoo.com.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029</wicri:regionArea><wicri:noRegion>New Delhi 110029</wicri:noRegion></affiliation></author><author><name sortKey="Kumar, Pankaj" sort="Kumar, Pankaj" uniqKey="Kumar P" first="Pankaj" last="Kumar">Pankaj Kumar</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029</wicri:regionArea><wicri:noRegion>New Delhi 110029</wicri:noRegion></affiliation></author><author><name sortKey="Wadhwa, Shashi" sort="Wadhwa, Shashi" uniqKey="Wadhwa S" first="Shashi" last="Wadhwa">Shashi Wadhwa</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029</wicri:regionArea><wicri:noRegion>New Delhi 110029</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28986146</idno><idno type="pmid">28986146</idno><idno type="doi">10.1016/j.exer.2017.09.014</idno><idno type="wicri:Area/Main/Corpus">000305</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000305</idno><idno type="wicri:Area/Main/Curation">000305</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000305</idno><idno type="wicri:Area/Main/Exploration">000305</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Age related distribution of 4-hydroxy 2-nonenal immunoreactivity in human retina.</title><author><name sortKey="Nag, Tapas C" sort="Nag, Tapas C" uniqKey="Nag T" first="Tapas C" last="Nag">Tapas C. Nag</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India. Electronic address: tapas_nag@yahoo.com.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029</wicri:regionArea><wicri:noRegion>New Delhi 110029</wicri:noRegion></affiliation></author><author><name sortKey="Kumar, Pankaj" sort="Kumar, Pankaj" uniqKey="Kumar P" first="Pankaj" last="Kumar">Pankaj Kumar</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029</wicri:regionArea><wicri:noRegion>New Delhi 110029</wicri:noRegion></affiliation></author><author><name sortKey="Wadhwa, Shashi" sort="Wadhwa, Shashi" uniqKey="Wadhwa S" first="Shashi" last="Wadhwa">Shashi Wadhwa</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029</wicri:regionArea><wicri:noRegion>New Delhi 110029</wicri:noRegion></affiliation></author></analytic><series><title level="j">Experimental eye research</title><idno type="eISSN">1096-0007</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult (MeSH)</term><term>Age Distribution (MeSH)</term><term>Aged (MeSH)</term><term>Aged, 80 and over (MeSH)</term><term>Aging (immunology)</term><term>Aldehydes (metabolism)</term><term>Female (MeSH)</term><term>Humans (MeSH)</term><term>Immunohistochemistry (MeSH)</term><term>Male (MeSH)</term><term>Middle Aged (MeSH)</term><term>Retina (metabolism)</term><term>Retinal Cone Photoreceptor Cells (metabolism)</term><term>Retinal Photoreceptor Cell Outer Segment (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte (MeSH)</term><term>Adulte d'âge moyen (MeSH)</term><term>Aldéhydes (métabolisme)</term><term>Cellules photoréceptrices en cône de la rétine (métabolisme)</term><term>Femelle (MeSH)</term><term>Humains (MeSH)</term><term>Immunohistochimie (MeSH)</term><term>Mâle (MeSH)</term><term>Répartition par âge (MeSH)</term><term>Rétine (métabolisme)</term><term>Segment externe de cellule photoréceptrice rétinienne (métabolisme)</term><term>Sujet âgé (MeSH)</term><term>Sujet âgé de 80 ans ou plus (MeSH)</term><term>Vieillissement (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Aldehydes</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Vieillissement</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Aging</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Retina</term><term>Retinal Cone Photoreceptor Cells</term><term>Retinal Photoreceptor Cell Outer Segment</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Aldéhydes</term><term>Cellules photoréceptrices en cône de la rétine</term><term>Rétine</term><term>Segment externe de cellule photoréceptrice rétinienne</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Age Distribution</term><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>Male</term><term>Middle Aged</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Adulte d'âge moyen</term><term>Femelle</term><term>Humains</term><term>Immunohistochimie</term><term>Mâle</term><term>Répartition par âge</term><term>Sujet âgé</term><term>Sujet âgé de 80 ans ou plus</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The retina is prone to be damaged by oxidative stress (OS), owing to its constant exposure to light, high rate of oxygen consumption and high membrane lipid content. Lipid peroxidation in aging human retina has been shown by biochemical means. However, information on the cellular sites of OS and antioxidant responses in aging human retina remains limited. Here, we show distribution of immunoreactivity (IR) to a marker of lipid peroxidation (4-hydroxy 2-nonenal [HNE] and antioxidant enzymes involved in counteracting lipid peroxidation (glutathione S-transferase-π1 and glutarexoxin-1) in donor human retinas at different ages (35-91 years; N = 24). Initially, HNE-IR was present in few macular cone outer segments (COS, sixth decade). With aging, IR appeared in many COS and peaked at ninth decade (14 vs 62 per 3850 μm<sup>2</sup> area between 6 and 9 decade; p < 0.001) in the parafovea then seen elsewhere (perifoveal, mid-peripheral and nasal). IR was seen in the parafovea of all retinas, whereas it was present in 8/24 of perifoveal and 6/24 of mid-peripheral retinas, indicating that the parafovea is susceptible to undergo lipid peroxidation. Foveolar COS were immunonegative until 81 years, which developed IR later (>83 years). IR to glutathione S-transferase-π1 was moderate until eight decade and then showed a decrease in photoreceptor cells between ninth and tenth decade, while glutaredoxin-1 maintained a steady expression with aging. Damaged COS were present in aged retinas, and inner segments and photoreceptor nuclei also showed some degree of alterations. Although there was increased lipid peroxidation with aging, cone death was minimal in those retinas. The two antioxidant enzymes studied here, may play a role in protecting photoreceptors against OS with advanced aging.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28986146</PMID><DateCompleted><Year>2017</Year><Month>12</Month><Day>01</Day></DateCompleted><DateRevised><Year>2017</Year><Month>12</Month><Day>12</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0007</ISSN><JournalIssue CitedMedium="Internet"><Volume>165</Volume><PubDate><Year>2017</Year><Month>12</Month></PubDate></JournalIssue><Title>Experimental eye research</Title><ISOAbbreviation>Exp Eye Res</ISOAbbreviation></Journal><ArticleTitle>Age related distribution of 4-hydroxy 2-nonenal immunoreactivity in human retina.</ArticleTitle><Pagination><MedlinePgn>125-135</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0014-4835(17)30362-7</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.exer.2017.09.014</ELocationID><Abstract><AbstractText>The retina is prone to be damaged by oxidative stress (OS), owing to its constant exposure to light, high rate of oxygen consumption and high membrane lipid content. Lipid peroxidation in aging human retina has been shown by biochemical means. However, information on the cellular sites of OS and antioxidant responses in aging human retina remains limited. Here, we show distribution of immunoreactivity (IR) to a marker of lipid peroxidation (4-hydroxy 2-nonenal [HNE] and antioxidant enzymes involved in counteracting lipid peroxidation (glutathione S-transferase-π1 and glutarexoxin-1) in donor human retinas at different ages (35-91 years; N = 24). Initially, HNE-IR was present in few macular cone outer segments (COS, sixth decade). With aging, IR appeared in many COS and peaked at ninth decade (14 vs 62 per 3850 μm<sup>2</sup> area between 6 and 9 decade; p < 0.001) in the parafovea then seen elsewhere (perifoveal, mid-peripheral and nasal). IR was seen in the parafovea of all retinas, whereas it was present in 8/24 of perifoveal and 6/24 of mid-peripheral retinas, indicating that the parafovea is susceptible to undergo lipid peroxidation. Foveolar COS were immunonegative until 81 years, which developed IR later (>83 years). IR to glutathione S-transferase-π1 was moderate until eight decade and then showed a decrease in photoreceptor cells between ninth and tenth decade, while glutaredoxin-1 maintained a steady expression with aging. Damaged COS were present in aged retinas, and inner segments and photoreceptor nuclei also showed some degree of alterations. Although there was increased lipid peroxidation with aging, cone death was minimal in those retinas. The two antioxidant enzymes studied here, may play a role in protecting photoreceptors against OS with advanced aging.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nag</LastName><ForeName>Tapas C</ForeName><Initials>TC</Initials><AffiliationInfo><Affiliation>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India. Electronic address: tapas_nag@yahoo.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kumar</LastName><ForeName>Pankaj</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wadhwa</LastName><ForeName>Shashi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Anatomy, Neurobiology Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>10</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Exp Eye Res</MedlineTA><NlmUniqueID>0370707</NlmUniqueID><ISSNLinking>0014-4835</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000447">Aldehydes</NameOfSubstance></Chemical><Chemical><RegistryNumber>K1CVM13F96</RegistryNumber><NameOfSubstance UI="C027576">4-hydroxy-2-nonenal</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017677" MajorTopicYN="N">Age Distribution</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000447" MajorTopicYN="N">Aldehydes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012160" MajorTopicYN="N">Retina</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017949" MajorTopicYN="N">Retinal Cone Photoreceptor Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055214" MajorTopicYN="N">Retinal Photoreceptor Cell Outer Segment</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">4-Hydroxy 2-nonenal</Keyword><Keyword MajorTopicYN="Y">Glutaredoxin-1</Keyword><Keyword MajorTopicYN="Y">Lipid peroxidation</Keyword><Keyword MajorTopicYN="Y">Macula</Keyword><Keyword MajorTopicYN="Y">Photoreceptor cells</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>05</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>08</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>09</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>10</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>10</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28986146</ArticleId><ArticleId IdType="pii">S0014-4835(17)30362-7</ArticleId><ArticleId IdType="doi">10.1016/j.exer.2017.09.014</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Nag, Tapas C" sort="Nag, Tapas C" uniqKey="Nag T" first="Tapas C" last="Nag">Tapas C. Nag</name></noRegion><name sortKey="Kumar, Pankaj" sort="Kumar, Pankaj" uniqKey="Kumar P" first="Pankaj" last="Kumar">Pankaj Kumar</name><name sortKey="Wadhwa, Shashi" sort="Wadhwa, Shashi" uniqKey="Wadhwa S" first="Shashi" last="Wadhwa">Shashi Wadhwa</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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