Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism
Abstract Astaxanthin is a powerful antioxidant that occurs naturally in a wide variety of living organisms. The aim of this study is to investigate the effect and the mechanism of astaxanthin on reactive oxygen species (ROS)-mediated apoptosis in dopaminergic SH-SY5Y cells. The treatment with DHA hy...
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| Veröffentlicht in: | Brain research 2009-02, Vol.1254, p.18-27 |
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| creator | Liu, Xuebo Shibata, Takahiro Hisaka, Shinsuke Osawa, Toshihiko |
| description | Abstract Astaxanthin is a powerful antioxidant that occurs naturally in a wide variety of living organisms. The aim of this study is to investigate the effect and the mechanism of astaxanthin on reactive oxygen species (ROS)-mediated apoptosis in dopaminergic SH-SY5Y cells. The treatment with DHA hydroperoxide (DHA-OOH) or 6-hydroxydopamine (6-OHDA), either of which is ROS-inducing neurotoxin, led to a significant decrease in viable dopaminergic SH-SY5Y cells by MTT assay, whereas a significant protection was shown while the cells were pretreated with astaxanthin. Moreover, 100 nM astaxanthin pretreatment significantly inhibited apoptosis, mitochondrial abnormalities and intracellular ROS generation occurred in either DHA-OOH- or 6-OHDA-treated cells. The neuroprotective effect of astaxanthin is suggested to be dependent upon its antioxidant potential and mitochondria protection; therefore, it is suggested that astaxanthin may be an effective treatment for oxidative stress-associated neurodegeneration. |
| doi_str_mv | 10.1016/j.brainres.2008.11.076 |
| format | Article |
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The aim of this study is to investigate the effect and the mechanism of astaxanthin on reactive oxygen species (ROS)-mediated apoptosis in dopaminergic SH-SY5Y cells. The treatment with DHA hydroperoxide (DHA-OOH) or 6-hydroxydopamine (6-OHDA), either of which is ROS-inducing neurotoxin, led to a significant decrease in viable dopaminergic SH-SY5Y cells by MTT assay, whereas a significant protection was shown while the cells were pretreated with astaxanthin. Moreover, 100 nM astaxanthin pretreatment significantly inhibited apoptosis, mitochondrial abnormalities and intracellular ROS generation occurred in either DHA-OOH- or 6-OHDA-treated cells. The neuroprotective effect of astaxanthin is suggested to be dependent upon its antioxidant potential and mitochondria protection; therefore, it is suggested that astaxanthin may be an effective treatment for oxidative stress-associated neurodegeneration.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2008.11.076</identifier><identifier>PMID: 19101523</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Antioxidants - pharmacology ; Apoptosis - drug effects ; Astaxanthin ; Blotting, Western ; Cell Line ; Cell Survival - drug effects ; Chromatography, High Pressure Liquid ; Cytochromes c - metabolism ; DNA Fragmentation - drug effects ; Docosahexaenoic Acids - toxicity ; Dopamine - metabolism ; Humans ; Lipid Peroxides - toxicity ; Membrane Potential, Mitochondrial - drug effects ; Microscopy, Fluorescence ; Mitochondria - drug effects ; Mitochondria protection ; Neurology ; Neuronal apoptosis ; Neurons - drug effects ; Neurons - physiology ; Oxidopamine - toxicity ; Parkinson's disease ; Protein Carbonylation - drug effects ; Reactive oxygen specie ; Reactive Oxygen Species - metabolism ; Xanthophylls - pharmacology</subject><ispartof>Brain research, 2009-02, Vol.1254, p.18-27</ispartof><rights>Elsevier B.V.</rights><rights>2008 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c518t-2f19bf1d22e9ef696b22ac3aa89712aa8a630675543090a36a504beba2c816943</citedby><cites>FETCH-LOGICAL-c518t-2f19bf1d22e9ef696b22ac3aa89712aa8a630675543090a36a504beba2c816943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006899308028400$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19101523$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Xuebo</creatorcontrib><creatorcontrib>Shibata, Takahiro</creatorcontrib><creatorcontrib>Hisaka, Shinsuke</creatorcontrib><creatorcontrib>Osawa, Toshihiko</creatorcontrib><title>Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract Astaxanthin is a powerful antioxidant that occurs naturally in a wide variety of living organisms. The aim of this study is to investigate the effect and the mechanism of astaxanthin on reactive oxygen species (ROS)-mediated apoptosis in dopaminergic SH-SY5Y cells. The treatment with DHA hydroperoxide (DHA-OOH) or 6-hydroxydopamine (6-OHDA), either of which is ROS-inducing neurotoxin, led to a significant decrease in viable dopaminergic SH-SY5Y cells by MTT assay, whereas a significant protection was shown while the cells were pretreated with astaxanthin. Moreover, 100 nM astaxanthin pretreatment significantly inhibited apoptosis, mitochondrial abnormalities and intracellular ROS generation occurred in either DHA-OOH- or 6-OHDA-treated cells. The neuroprotective effect of astaxanthin is suggested to be dependent upon its antioxidant potential and mitochondria protection; therefore, it is suggested that astaxanthin may be an effective treatment for oxidative stress-associated neurodegeneration.</description><subject>Antioxidants - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Astaxanthin</subject><subject>Blotting, Western</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Cytochromes c - metabolism</subject><subject>DNA Fragmentation - drug effects</subject><subject>Docosahexaenoic Acids - toxicity</subject><subject>Dopamine - metabolism</subject><subject>Humans</subject><subject>Lipid Peroxides - toxicity</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Microscopy, Fluorescence</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria protection</subject><subject>Neurology</subject><subject>Neuronal apoptosis</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Oxidopamine - toxicity</subject><subject>Parkinson's disease</subject><subject>Protein Carbonylation - drug effects</subject><subject>Reactive oxygen specie</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Xanthophylls - pharmacology</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUsGO0zAUjBCILQu_sMqJW4LtJE5yQaxWC4u0EofCYU_Wi_PSvpLYxXaq9j_4YBxahMSF05OlmXnPM5MkN5zlnHH5bpd3Dsg49LlgrMk5z1ktnyUr3tQik6Jkz5MVY0xmTdsWV8kr73fxWRQte5lc8TaKVKJYJT9vfYAjmLAlk5LZUkfBpw5BBzpgao-nDZrU71ET-mzCniBgn2ocx3kElwZ7JE3hFLlpb_cwkUG3IZ2uH7L1U_X0G-nTA0E6UbB6a03vCLIAboOL0t7ZgOdlE-otGPLT6-TFAKPHN5d5nXz7eP_17iF7_PLp893tY6Yr3oRMDLztBt4LgS0OspWdEKALgKatuYgDZMFkXVVlwVoGhYSKlR12IHTDZVsW18nbs2484seMPqiJ_HIwGLSzV4KJqhCijkB5BmpnvXc4qL2jCdxJcaaWPNRO_clDLXkozlXMIxJvLhvmLpr3l3YJIAI-nAEY_3kgdMpHp42ORrtoi-ot_X_H-38k9EiGNIzf8YR-Z2dnoouKKy8UU-ulFUspWMNEU8ZO_AKAzLgP</recordid><startdate>20090213</startdate><enddate>20090213</enddate><creator>Liu, Xuebo</creator><creator>Shibata, Takahiro</creator><creator>Hisaka, Shinsuke</creator><creator>Osawa, Toshihiko</creator><general>Elsevier 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>7TK</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20090213</creationdate><title>Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism</title><author>Liu, Xuebo ; Shibata, Takahiro ; Hisaka, Shinsuke ; Osawa, Toshihiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c518t-2f19bf1d22e9ef696b22ac3aa89712aa8a630675543090a36a504beba2c816943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Antioxidants - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Astaxanthin</topic><topic>Blotting, Western</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Cytochromes c - metabolism</topic><topic>DNA Fragmentation - drug effects</topic><topic>Docosahexaenoic Acids - toxicity</topic><topic>Dopamine - metabolism</topic><topic>Humans</topic><topic>Lipid Peroxides - toxicity</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Microscopy, Fluorescence</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria protection</topic><topic>Neurology</topic><topic>Neuronal apoptosis</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Oxidopamine - toxicity</topic><topic>Parkinson's disease</topic><topic>Protein Carbonylation - drug effects</topic><topic>Reactive oxygen specie</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Xanthophylls - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Xuebo</creatorcontrib><creatorcontrib>Shibata, Takahiro</creatorcontrib><creatorcontrib>Hisaka, Shinsuke</creatorcontrib><creatorcontrib>Osawa, Toshihiko</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Xuebo</au><au>Shibata, Takahiro</au><au>Hisaka, Shinsuke</au><au>Osawa, Toshihiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2009-02-13</date><risdate>2009</risdate><volume>1254</volume><spage>18</spage><epage>27</epage><pages>18-27</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><abstract>Abstract Astaxanthin is a powerful antioxidant that occurs naturally in a wide variety of living organisms. The aim of this study is to investigate the effect and the mechanism of astaxanthin on reactive oxygen species (ROS)-mediated apoptosis in dopaminergic SH-SY5Y cells. The treatment with DHA hydroperoxide (DHA-OOH) or 6-hydroxydopamine (6-OHDA), either of which is ROS-inducing neurotoxin, led to a significant decrease in viable dopaminergic SH-SY5Y cells by MTT assay, whereas a significant protection was shown while the cells were pretreated with astaxanthin. Moreover, 100 nM astaxanthin pretreatment significantly inhibited apoptosis, mitochondrial abnormalities and intracellular ROS generation occurred in either DHA-OOH- or 6-OHDA-treated cells. The neuroprotective effect of astaxanthin is suggested to be dependent upon its antioxidant potential and mitochondria protection; therefore, it is suggested that astaxanthin may be an effective treatment for oxidative stress-associated neurodegeneration.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>19101523</pmid><doi>10.1016/j.brainres.2008.11.076</doi><tpages>10</tpages></addata></record> |
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| subjects | Antioxidants - pharmacology Apoptosis - drug effects Astaxanthin Blotting, Western Cell Line Cell Survival - drug effects Chromatography, High Pressure Liquid Cytochromes c - metabolism DNA Fragmentation - drug effects Docosahexaenoic Acids - toxicity Dopamine - metabolism Humans Lipid Peroxides - toxicity Membrane Potential, Mitochondrial - drug effects Microscopy, Fluorescence Mitochondria - drug effects Mitochondria protection Neurology Neuronal apoptosis Neurons - drug effects Neurons - physiology Oxidopamine - toxicity Parkinson's disease Protein Carbonylation - drug effects Reactive oxygen specie Reactive Oxygen Species - metabolism Xanthophylls - pharmacology |
| title | Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism |
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