Hydrogen Sulfide Scavenges the Cytotoxic Lipid Oxidation Product 4-HNE
Highly reactive α,β-unsaturated aldehydes like 4-hydroxy-2-nonenal (4-HNE), generated from oxidation of polyunsaturated fatty acids, can bind to proteins, polynucleotides and exert cytotoxicity. 4-HNE is known to react readily with thiol and amino groups on free or bound amino acids. Recently, hydro...
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| Veröffentlicht in: | Neurotoxicity research 2010-04, Vol.17 (3), p.249-256 |
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| creator | Schreier, Sabine M. Muellner, Markus K. Steinkellner, Hannes Hermann, Marcela Esterbauer, Harald Exner, Markus Gmeiner, Bernhard M. K. Kapiotis, Stylianos Laggner, Hilde |
| description | Highly reactive α,β-unsaturated aldehydes like 4-hydroxy-2-nonenal (4-HNE), generated from oxidation of polyunsaturated fatty acids, can bind to proteins, polynucleotides and exert cytotoxicity. 4-HNE is known to react readily with thiol and amino groups on free or bound amino acids. Recently, hydrogen sulfide (H
2
S) has been identified as an endogenous vascular gasotransmitter and neuromodulator which can reach up to 160 μmol/l in the brain. Markedly higher 4-HNE concentrations were reported in the brain of patients suffering from Alzheimer’s disease. Assuming that the low molecular thiol H
2
S may react with 4-HNE, we have tested the ability of H
2
S to counteract the cytotoxic and protein-modifying activity of 4-HNE. The results show that H
2
S at physiologically relevant concentrations could effectively protect neuronal cells (SH-SY5Y) from the cytotoxic action of 4-HNE. The HNE-modification of cellular proteins was also inhibited in presence of H
2
S. These data suggest that H
2
S may be an important protective factor against carbonyl stress by inactivating/modulating the action of highly reactive α,β-unsaturated aldehydes like 4-HNE in the brain. |
| doi_str_mv | 10.1007/s12640-009-9099-9 |
| format | Article |
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2
S) has been identified as an endogenous vascular gasotransmitter and neuromodulator which can reach up to 160 μmol/l in the brain. Markedly higher 4-HNE concentrations were reported in the brain of patients suffering from Alzheimer’s disease. Assuming that the low molecular thiol H
2
S may react with 4-HNE, we have tested the ability of H
2
S to counteract the cytotoxic and protein-modifying activity of 4-HNE. The results show that H
2
S at physiologically relevant concentrations could effectively protect neuronal cells (SH-SY5Y) from the cytotoxic action of 4-HNE. The HNE-modification of cellular proteins was also inhibited in presence of H
2
S. These data suggest that H
2
S may be an important protective factor against carbonyl stress by inactivating/modulating the action of highly reactive α,β-unsaturated aldehydes like 4-HNE in the brain.</description><identifier>ISSN: 1029-8428</identifier><identifier>EISSN: 1476-3524</identifier><identifier>DOI: 10.1007/s12640-009-9099-9</identifier><identifier>PMID: 19680736</identifier><language>eng</language><publisher>New York: Springer-Verlag</publisher><subject>Air Pollutants - pharmacology ; Aldehydes - metabolism ; Aldehydes - pharmacology ; Analysis of Variance ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Line, Tumor ; Cell Survival - drug effects ; Dose-Response Relationship, Drug ; Drug Interactions ; Electrophoretic Mobility Shift Assay - methods ; Humans ; Hydrogen Sulfide - pharmacology ; Lipid Peroxidation - drug effects ; Neurobiology ; Neuroblastoma - pathology ; Neurochemistry ; Neurology ; Neurosciences ; Pharmacology/Toxicology</subject><ispartof>Neurotoxicity research, 2010-04, Vol.17 (3), p.249-256</ispartof><rights>Springer Science+Business Media, LLC 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-p183t-3bd59240fb5b6fdb503b3dff5968da722dfe0b5268487ffb3b0bb8ac174b10623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12640-009-9099-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12640-009-9099-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27913,27914,41477,42546,51308</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19680736$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schreier, Sabine M.</creatorcontrib><creatorcontrib>Muellner, Markus K.</creatorcontrib><creatorcontrib>Steinkellner, Hannes</creatorcontrib><creatorcontrib>Hermann, Marcela</creatorcontrib><creatorcontrib>Esterbauer, Harald</creatorcontrib><creatorcontrib>Exner, Markus</creatorcontrib><creatorcontrib>Gmeiner, Bernhard M. K.</creatorcontrib><creatorcontrib>Kapiotis, Stylianos</creatorcontrib><creatorcontrib>Laggner, Hilde</creatorcontrib><title>Hydrogen Sulfide Scavenges the Cytotoxic Lipid Oxidation Product 4-HNE</title><title>Neurotoxicity research</title><addtitle>Neurotox Res</addtitle><addtitle>Neurotox Res</addtitle><description>Highly reactive α,β-unsaturated aldehydes like 4-hydroxy-2-nonenal (4-HNE), generated from oxidation of polyunsaturated fatty acids, can bind to proteins, polynucleotides and exert cytotoxicity. 4-HNE is known to react readily with thiol and amino groups on free or bound amino acids. Recently, hydrogen sulfide (H
2
S) has been identified as an endogenous vascular gasotransmitter and neuromodulator which can reach up to 160 μmol/l in the brain. Markedly higher 4-HNE concentrations were reported in the brain of patients suffering from Alzheimer’s disease. Assuming that the low molecular thiol H
2
S may react with 4-HNE, we have tested the ability of H
2
S to counteract the cytotoxic and protein-modifying activity of 4-HNE. The results show that H
2
S at physiologically relevant concentrations could effectively protect neuronal cells (SH-SY5Y) from the cytotoxic action of 4-HNE. The HNE-modification of cellular proteins was also inhibited in presence of H
2
S. These data suggest that H
2
S may be an important protective factor against carbonyl stress by inactivating/modulating the action of highly reactive α,β-unsaturated aldehydes like 4-HNE in the brain.</description><subject>Air Pollutants - pharmacology</subject><subject>Aldehydes - metabolism</subject><subject>Aldehydes - pharmacology</subject><subject>Analysis of Variance</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Interactions</subject><subject>Electrophoretic Mobility Shift Assay - methods</subject><subject>Humans</subject><subject>Hydrogen Sulfide - pharmacology</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Neurobiology</subject><subject>Neuroblastoma - pathology</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Pharmacology/Toxicology</subject><issn>1029-8428</issn><issn>1476-3524</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kE1PwzAMhiMEYmPwA7ig3jgVnI8m7RFNG0OaGNLgHDVNMjJ1TWlatP17Mm1cbEt-ZPl9ELrH8IQBxHPAhDNIAYq0gCKWCzTGTPCUZoRdxhlIkeaM5CN0E8IWgOCMi2s0wgXPQVA-RvPFQXd-Y5pkPdTWaZOsq_LXNBsTkv7bJNND73u_d1WydK3TyWrvdNk73yQfnddD1ScsXbzPbtGVLetg7s59gr7ms8_pIl2uXt-mL8u0xTntU6p0VhAGVmWKW60yoIpqa7P4jy4FIdoaUBnhOcuFtYoqUCovKyyYwsAJnaDH09228z-DCb3cuVCZui4b44cgBcsKIQgTkXw4k4PaGS3bzu3K7iD_o0eAnIAQVzFvJ7d-6Jr4vcQgj37lya-MfuXRryzoHwVQaqQ</recordid><startdate>20100401</startdate><enddate>20100401</enddate><creator>Schreier, Sabine M.</creator><creator>Muellner, Markus K.</creator><creator>Steinkellner, Hannes</creator><creator>Hermann, Marcela</creator><creator>Esterbauer, Harald</creator><creator>Exner, Markus</creator><creator>Gmeiner, Bernhard M. K.</creator><creator>Kapiotis, Stylianos</creator><creator>Laggner, Hilde</creator><general>Springer-Verlag</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20100401</creationdate><title>Hydrogen Sulfide Scavenges the Cytotoxic Lipid Oxidation Product 4-HNE</title><author>Schreier, Sabine M. ; Muellner, Markus K. ; Steinkellner, Hannes ; Hermann, Marcela ; Esterbauer, Harald ; Exner, Markus ; Gmeiner, Bernhard M. K. ; Kapiotis, Stylianos ; Laggner, Hilde</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p183t-3bd59240fb5b6fdb503b3dff5968da722dfe0b5268487ffb3b0bb8ac174b10623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Air Pollutants - pharmacology</topic><topic>Aldehydes - metabolism</topic><topic>Aldehydes - pharmacology</topic><topic>Analysis of Variance</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Interactions</topic><topic>Electrophoretic Mobility Shift Assay - methods</topic><topic>Humans</topic><topic>Hydrogen Sulfide - pharmacology</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Neurobiology</topic><topic>Neuroblastoma - pathology</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Pharmacology/Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schreier, Sabine M.</creatorcontrib><creatorcontrib>Muellner, Markus K.</creatorcontrib><creatorcontrib>Steinkellner, Hannes</creatorcontrib><creatorcontrib>Hermann, Marcela</creatorcontrib><creatorcontrib>Esterbauer, Harald</creatorcontrib><creatorcontrib>Exner, Markus</creatorcontrib><creatorcontrib>Gmeiner, Bernhard M. K.</creatorcontrib><creatorcontrib>Kapiotis, Stylianos</creatorcontrib><creatorcontrib>Laggner, Hilde</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Neurotoxicity research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schreier, Sabine M.</au><au>Muellner, Markus K.</au><au>Steinkellner, Hannes</au><au>Hermann, Marcela</au><au>Esterbauer, Harald</au><au>Exner, Markus</au><au>Gmeiner, Bernhard M. K.</au><au>Kapiotis, Stylianos</au><au>Laggner, Hilde</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hydrogen Sulfide Scavenges the Cytotoxic Lipid Oxidation Product 4-HNE</atitle><jtitle>Neurotoxicity research</jtitle><stitle>Neurotox Res</stitle><addtitle>Neurotox Res</addtitle><date>2010-04-01</date><risdate>2010</risdate><volume>17</volume><issue>3</issue><spage>249</spage><epage>256</epage><pages>249-256</pages><issn>1029-8428</issn><eissn>1476-3524</eissn><abstract>Highly reactive α,β-unsaturated aldehydes like 4-hydroxy-2-nonenal (4-HNE), generated from oxidation of polyunsaturated fatty acids, can bind to proteins, polynucleotides and exert cytotoxicity. 4-HNE is known to react readily with thiol and amino groups on free or bound amino acids. Recently, hydrogen sulfide (H
2
S) has been identified as an endogenous vascular gasotransmitter and neuromodulator which can reach up to 160 μmol/l in the brain. Markedly higher 4-HNE concentrations were reported in the brain of patients suffering from Alzheimer’s disease. Assuming that the low molecular thiol H
2
S may react with 4-HNE, we have tested the ability of H
2
S to counteract the cytotoxic and protein-modifying activity of 4-HNE. The results show that H
2
S at physiologically relevant concentrations could effectively protect neuronal cells (SH-SY5Y) from the cytotoxic action of 4-HNE. The HNE-modification of cellular proteins was also inhibited in presence of H
2
S. These data suggest that H
2
S may be an important protective factor against carbonyl stress by inactivating/modulating the action of highly reactive α,β-unsaturated aldehydes like 4-HNE in the brain.</abstract><cop>New York</cop><pub>Springer-Verlag</pub><pmid>19680736</pmid><doi>10.1007/s12640-009-9099-9</doi><tpages>8</tpages></addata></record> |
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| subjects | Air Pollutants - pharmacology Aldehydes - metabolism Aldehydes - pharmacology Analysis of Variance Biomedical and Life Sciences Biomedicine Cell Biology Cell Line, Tumor Cell Survival - drug effects Dose-Response Relationship, Drug Drug Interactions Electrophoretic Mobility Shift Assay - methods Humans Hydrogen Sulfide - pharmacology Lipid Peroxidation - drug effects Neurobiology Neuroblastoma - pathology Neurochemistry Neurology Neurosciences Pharmacology/Toxicology |
| title | Hydrogen Sulfide Scavenges the Cytotoxic Lipid Oxidation Product 4-HNE |
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