The sulfite molecule enhances homocysteine toxicity in SH-SY5Y cells
Homocysteine (hcy) is an amino acid that contains sulfur species. In healthy individuals, plasma hcy levels are low. The aim of this study was to investigate the potential neurotoxic effects of hcy and sulfite (sft) molecules alone and in their combination, and also to identify the relationship of t...
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| Veröffentlicht in: | Molecular biology reports 2019-08, Vol.46 (4), p.4017-4025 |
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| description | Homocysteine (hcy) is an amino acid that contains sulfur species. In healthy individuals, plasma hcy levels are low. The aim of this study was to investigate the potential neurotoxic effects of hcy and sulfite (sft) molecules alone and in their combination, and also to identify the relationship of these substances on oxidative stress. SH-SY5Y cells were used as an invitro neurodegenerative disease model. The SH-SY5Y cells were treated with various concentrations of hcy alone, sft alone (final concentrations in the well were 10–250 µM and 0.1–5 mM, respectively) and a combination of both (hcy + sft). Their cytotoxicity and genotoxic effects were investigated using the XTT test and Comet assay and, their impact on oxidative stress was examined using total antioxidant–oxidant status (TAS-TOS) kits. The highest toxic doses of hcy and sft were found to be 250 μM and 5 mM, respectively, but the maximum toxic effect was observed for hcy + sft (p |
| doi_str_mv | 10.1007/s11033-019-04850-3 |
| format | Article |
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In healthy individuals, plasma hcy levels are low. The aim of this study was to investigate the potential neurotoxic effects of hcy and sulfite (sft) molecules alone and in their combination, and also to identify the relationship of these substances on oxidative stress. SH-SY5Y cells were used as an invitro neurodegenerative disease model. The SH-SY5Y cells were treated with various concentrations of hcy alone, sft alone (final concentrations in the well were 10–250 µM and 0.1–5 mM, respectively) and a combination of both (hcy + sft). Their cytotoxicity and genotoxic effects were investigated using the XTT test and Comet assay and, their impact on oxidative stress was examined using total antioxidant–oxidant status (TAS-TOS) kits. The highest toxic doses of hcy and sft were found to be 250 μM and 5 mM, respectively, but the maximum toxic effect was observed for hcy + sft (p < 0.001). In addition, an increase in DNA damage was evident in all groups, but maximal damage was inflicted using in hcy + sft (p < 0.001). The oxidative stress index was significantly increased in hcy + sft (p < 0.05). Determining the increase in sft and hcy levels may contribute to delaying the occurrence of diseases before symptoms of neurodegenerative disease appear.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-019-04850-3</identifier><identifier>PMID: 31079315</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Amino acids ; Amino Acids, Sulfur - metabolism ; Animal Anatomy ; Animal Biochemistry ; Antioxidants ; Antioxidants - metabolism ; Biomedical and Life Sciences ; Cell Line, Tumor ; Comet Assay ; Cytotoxicity ; disease models ; DNA damage ; DNA Damage - drug effects ; Genotoxicity ; Histology ; Homocysteine ; Homocysteine - metabolism ; Homocysteine - toxicity ; Humans ; Life Sciences ; Lipid Peroxidation - drug effects ; Morphology ; mutagens ; Neurodegenerative diseases ; Neurodegenerative Diseases - metabolism ; Neurotoxicity ; Original Article ; Oxidative stress ; Oxidative Stress - drug effects ; Sulfite ; Sulfite Oxidase - metabolism ; sulfites ; Sulfites - metabolism ; Sulfites - toxicity ; Sulfur</subject><ispartof>Molecular biology reports, 2019-08, Vol.46 (4), p.4017-4025</ispartof><rights>Springer Nature B.V. 2019</rights><rights>Molecular Biology Reports is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-b1e0dc9ef7c2b3bb5695a82dfdf262528ee803099bd633615c3c86cdc7398d63</citedby><cites>FETCH-LOGICAL-c408t-b1e0dc9ef7c2b3bb5695a82dfdf262528ee803099bd633615c3c86cdc7398d63</cites><orcidid>0000-0002-9924-5176</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-019-04850-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-019-04850-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31079315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gundogdu, Gulsah</creatorcontrib><creatorcontrib>Dodurga, Yavuz</creatorcontrib><creatorcontrib>Kucukatay, Vural</creatorcontrib><title>The sulfite molecule enhances homocysteine toxicity in SH-SY5Y cells</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Homocysteine (hcy) is an amino acid that contains sulfur species. In healthy individuals, plasma hcy levels are low. The aim of this study was to investigate the potential neurotoxic effects of hcy and sulfite (sft) molecules alone and in their combination, and also to identify the relationship of these substances on oxidative stress. SH-SY5Y cells were used as an invitro neurodegenerative disease model. The SH-SY5Y cells were treated with various concentrations of hcy alone, sft alone (final concentrations in the well were 10–250 µM and 0.1–5 mM, respectively) and a combination of both (hcy + sft). Their cytotoxicity and genotoxic effects were investigated using the XTT test and Comet assay and, their impact on oxidative stress was examined using total antioxidant–oxidant status (TAS-TOS) kits. The highest toxic doses of hcy and sft were found to be 250 μM and 5 mM, respectively, but the maximum toxic effect was observed for hcy + sft (p < 0.001). In addition, an increase in DNA damage was evident in all groups, but maximal damage was inflicted using in hcy + sft (p < 0.001). The oxidative stress index was significantly increased in hcy + sft (p < 0.05). Determining the increase in sft and hcy levels may contribute to delaying the occurrence of diseases before symptoms of neurodegenerative disease appear.</description><subject>Amino acids</subject><subject>Amino Acids, Sulfur - metabolism</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Line, Tumor</subject><subject>Comet Assay</subject><subject>Cytotoxicity</subject><subject>disease models</subject><subject>DNA damage</subject><subject>DNA Damage - drug effects</subject><subject>Genotoxicity</subject><subject>Histology</subject><subject>Homocysteine</subject><subject>Homocysteine - metabolism</subject><subject>Homocysteine - toxicity</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Morphology</subject><subject>mutagens</subject><subject>Neurodegenerative diseases</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurotoxicity</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Sulfite</subject><subject>Sulfite Oxidase - metabolism</subject><subject>sulfites</subject><subject>Sulfites - metabolism</subject><subject>Sulfites - toxicity</subject><subject>Sulfur</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</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>eNp9kE1LxDAQhoMoun78AQ9S8OIlOpNp2uYofoPgwb14Cm06dSv90KYF998b3VXBg6fAzDNvXh4hDhFOESA984hAJAGNhDjTIGlDzFCnJGOTZptiBgQowwZ3xK73LwAQY6q3xQ4hpIZQz8TlfMGRn5qqHjlq-4bd1HDE3SLvHPto0be9W_qR646jsX-vXT0uo7qLHm_l45N-ihw3jd8XW1XeeD5Yv3tifn01v7iV9w83dxfn99LFkI2yQIbSGa5SpwoqCp0YnWeqrMpKJUqrjDkLlY0pyoQoQe3IZYkrXUomC6M9cbKKfR36t4n9aNvafxbIO-4nbxWBRoMm1gE9_oO-9NPQhXJWKUVIRmsMlFpRbui9H7iyr0Pd5sPSIthPxXal2AbF9kuxpXB0tI6eipbLn5NvpwGgFeDDqnvm4ffvf2I_AL8khT8</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Gundogdu, Gulsah</creator><creator>Dodurga, Yavuz</creator><creator>Kucukatay, Vural</creator><general>Springer Netherlands</general><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>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-9924-5176</orcidid></search><sort><creationdate>20190801</creationdate><title>The sulfite molecule enhances homocysteine toxicity in SH-SY5Y cells</title><author>Gundogdu, Gulsah ; Dodurga, Yavuz ; Kucukatay, Vural</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-b1e0dc9ef7c2b3bb5695a82dfdf262528ee803099bd633615c3c86cdc7398d63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Amino acids</topic><topic>Amino Acids, Sulfur - metabolism</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Antioxidants</topic><topic>Antioxidants - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Line, Tumor</topic><topic>Comet Assay</topic><topic>Cytotoxicity</topic><topic>disease models</topic><topic>DNA damage</topic><topic>DNA Damage - drug effects</topic><topic>Genotoxicity</topic><topic>Histology</topic><topic>Homocysteine</topic><topic>Homocysteine - metabolism</topic><topic>Homocysteine - toxicity</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Morphology</topic><topic>mutagens</topic><topic>Neurodegenerative diseases</topic><topic>Neurodegenerative Diseases - metabolism</topic><topic>Neurotoxicity</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Sulfite</topic><topic>Sulfite Oxidase - metabolism</topic><topic>sulfites</topic><topic>Sulfites - metabolism</topic><topic>Sulfites - toxicity</topic><topic>Sulfur</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gundogdu, Gulsah</creatorcontrib><creatorcontrib>Dodurga, Yavuz</creatorcontrib><creatorcontrib>Kucukatay, Vural</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 Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>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>Engineering Research Database</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gundogdu, Gulsah</au><au>Dodurga, Yavuz</au><au>Kucukatay, Vural</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The sulfite molecule enhances homocysteine toxicity in SH-SY5Y cells</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>46</volume><issue>4</issue><spage>4017</spage><epage>4025</epage><pages>4017-4025</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Homocysteine (hcy) is an amino acid that contains sulfur species. In healthy individuals, plasma hcy levels are low. The aim of this study was to investigate the potential neurotoxic effects of hcy and sulfite (sft) molecules alone and in their combination, and also to identify the relationship of these substances on oxidative stress. SH-SY5Y cells were used as an invitro neurodegenerative disease model. The SH-SY5Y cells were treated with various concentrations of hcy alone, sft alone (final concentrations in the well were 10–250 µM and 0.1–5 mM, respectively) and a combination of both (hcy + sft). Their cytotoxicity and genotoxic effects were investigated using the XTT test and Comet assay and, their impact on oxidative stress was examined using total antioxidant–oxidant status (TAS-TOS) kits. The highest toxic doses of hcy and sft were found to be 250 μM and 5 mM, respectively, but the maximum toxic effect was observed for hcy + sft (p < 0.001). In addition, an increase in DNA damage was evident in all groups, but maximal damage was inflicted using in hcy + sft (p < 0.001). The oxidative stress index was significantly increased in hcy + sft (p < 0.05). Determining the increase in sft and hcy levels may contribute to delaying the occurrence of diseases before symptoms of neurodegenerative disease appear.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>31079315</pmid><doi>10.1007/s11033-019-04850-3</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-9924-5176</orcidid></addata></record> |
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| subjects | Amino acids Amino Acids, Sulfur - metabolism Animal Anatomy Animal Biochemistry Antioxidants Antioxidants - metabolism Biomedical and Life Sciences Cell Line, Tumor Comet Assay Cytotoxicity disease models DNA damage DNA Damage - drug effects Genotoxicity Histology Homocysteine Homocysteine - metabolism Homocysteine - toxicity Humans Life Sciences Lipid Peroxidation - drug effects Morphology mutagens Neurodegenerative diseases Neurodegenerative Diseases - metabolism Neurotoxicity Original Article Oxidative stress Oxidative Stress - drug effects Sulfite Sulfite Oxidase - metabolism sulfites Sulfites - metabolism Sulfites - toxicity Sulfur |
| title | The sulfite molecule enhances homocysteine toxicity in SH-SY5Y cells |
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