Homocysteine and copper induce cellular apoptosis via caspase activation and nuclear translocation of apoptosis-inducing factor in neuronal cell line SH-SY5Y
Hyperhomocysteinemia has been implicated in dementia and neurodegenerative disease. Physiological homocysteine concentrations did not result in apoptosis in SH-SY5Y cells in the present study. The apoptosis was recognized in millimolar level of homocysteine. However, SH-SY5Y cell death was observed...
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| Veröffentlicht in: | Neuroscience research 2010-08, Vol.67 (4), p.300-306 |
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| creator | Hirashima, Yoshimasa Seshimo, So Fujiki, Yoshika Okabe, Masaaki Nishiyama, Kazuo Matsumoto, Mitsuharu Kanouchi, Hiroaki Oka, Tatsuzo |
| description | Hyperhomocysteinemia has been implicated in dementia and neurodegenerative disease. Physiological homocysteine concentrations did not result in apoptosis in SH-SY5Y cells in the present study. The apoptosis was recognized in millimolar level of homocysteine. However, SH-SY5Y cell death was observed following exposure to micromolar level of homocysteine in combination with copper. Exposure to 250
μM homocysteine and 10
μM CuCl
2 for one day decreased cell viability by 40%. Homocysteine and copper caused apoptosis, because hallmarks of apoptosis were recognized, such as loss of mitochondrial membrane potential, TUNEL-positive cells, release of cytochrome
c from mitochondria, and caspase-3 activation, but not nucleosomal DNA fragmentation. Homocysteine and copper generated the intracellular reactive oxygen species, and homocysteine and copper-induced apoptosis was due to an accumulation of intracellular reactive oxygen species, which was inhibited by catalase. Pan-caspase inhibitor, z-VAD-fmk, could not completely inhibited homocysteine and copper-induced cell death. Homocysteine and copper also caused the nuclear translocation of apoptosis-inducing factor. These results suggested that homocysteine and copper induced not only caspase-dependent apoptosis but also caspase-independent apoptosis-inducing factor related apoptosis. |
| doi_str_mv | 10.1016/j.neures.2010.04.013 |
| format | Article |
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μM homocysteine and 10
μM CuCl
2 for one day decreased cell viability by 40%. Homocysteine and copper caused apoptosis, because hallmarks of apoptosis were recognized, such as loss of mitochondrial membrane potential, TUNEL-positive cells, release of cytochrome
c from mitochondria, and caspase-3 activation, but not nucleosomal DNA fragmentation. Homocysteine and copper generated the intracellular reactive oxygen species, and homocysteine and copper-induced apoptosis was due to an accumulation of intracellular reactive oxygen species, which was inhibited by catalase. Pan-caspase inhibitor, z-VAD-fmk, could not completely inhibited homocysteine and copper-induced cell death. Homocysteine and copper also caused the nuclear translocation of apoptosis-inducing factor. These results suggested that homocysteine and copper induced not only caspase-dependent apoptosis but also caspase-independent apoptosis-inducing factor related apoptosis.</description><identifier>ISSN: 0168-0102</identifier><identifier>EISSN: 1872-8111</identifier><identifier>DOI: 10.1016/j.neures.2010.04.013</identifier><identifier>PMID: 20450942</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Active Transport, Cell Nucleus - drug effects ; Active Transport, Cell Nucleus - physiology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Apoptosis Inducing Factor - physiology ; Apoptosis-inducing factor ; Caspase 3 - drug effects ; Caspase 3 - physiology ; Caspases - metabolism ; Caspases - physiology ; Catalase - pharmacology ; Cell Line, Tumor ; Copper ; Copper - physiology ; Copper - toxicity ; Enzyme Activation - drug effects ; Enzyme Activation - physiology ; Homocysteine ; Homocysteine - physiology ; Homocysteine - toxicity ; Humans ; Hyperhomocysteinemia - enzymology ; Hyperhomocysteinemia - metabolism ; Hyperhomocysteinemia - pathology ; Neurons - drug effects ; Neurons - metabolism ; Reactive oxygen species</subject><ispartof>Neuroscience research, 2010-08, Vol.67 (4), p.300-306</ispartof><rights>2010 Elsevier Ireland Ltd and the Japan Neuroscience Society</rights><rights>Copyright 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-213e255eeba34f228f8ffd9b2306f869e6bfdf988b90ce72e360b920358c4d263</citedby><cites>FETCH-LOGICAL-c483t-213e255eeba34f228f8ffd9b2306f869e6bfdf988b90ce72e360b920358c4d263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0168010210001239$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20450942$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirashima, Yoshimasa</creatorcontrib><creatorcontrib>Seshimo, So</creatorcontrib><creatorcontrib>Fujiki, Yoshika</creatorcontrib><creatorcontrib>Okabe, Masaaki</creatorcontrib><creatorcontrib>Nishiyama, Kazuo</creatorcontrib><creatorcontrib>Matsumoto, Mitsuharu</creatorcontrib><creatorcontrib>Kanouchi, Hiroaki</creatorcontrib><creatorcontrib>Oka, Tatsuzo</creatorcontrib><title>Homocysteine and copper induce cellular apoptosis via caspase activation and nuclear translocation of apoptosis-inducing factor in neuronal cell line SH-SY5Y</title><title>Neuroscience research</title><addtitle>Neurosci Res</addtitle><description>Hyperhomocysteinemia has been implicated in dementia and neurodegenerative disease. Physiological homocysteine concentrations did not result in apoptosis in SH-SY5Y cells in the present study. The apoptosis was recognized in millimolar level of homocysteine. However, SH-SY5Y cell death was observed following exposure to micromolar level of homocysteine in combination with copper. Exposure to 250
μM homocysteine and 10
μM CuCl
2 for one day decreased cell viability by 40%. Homocysteine and copper caused apoptosis, because hallmarks of apoptosis were recognized, such as loss of mitochondrial membrane potential, TUNEL-positive cells, release of cytochrome
c from mitochondria, and caspase-3 activation, but not nucleosomal DNA fragmentation. Homocysteine and copper generated the intracellular reactive oxygen species, and homocysteine and copper-induced apoptosis was due to an accumulation of intracellular reactive oxygen species, which was inhibited by catalase. Pan-caspase inhibitor, z-VAD-fmk, could not completely inhibited homocysteine and copper-induced cell death. Homocysteine and copper also caused the nuclear translocation of apoptosis-inducing factor. These results suggested that homocysteine and copper induced not only caspase-dependent apoptosis but also caspase-independent apoptosis-inducing factor related apoptosis.</description><subject>Active Transport, Cell Nucleus - drug effects</subject><subject>Active Transport, Cell Nucleus - physiology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Apoptosis Inducing Factor - physiology</subject><subject>Apoptosis-inducing factor</subject><subject>Caspase 3 - drug effects</subject><subject>Caspase 3 - physiology</subject><subject>Caspases - metabolism</subject><subject>Caspases - physiology</subject><subject>Catalase - pharmacology</subject><subject>Cell Line, Tumor</subject><subject>Copper</subject><subject>Copper - physiology</subject><subject>Copper - toxicity</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Activation - physiology</subject><subject>Homocysteine</subject><subject>Homocysteine - physiology</subject><subject>Homocysteine - toxicity</subject><subject>Humans</subject><subject>Hyperhomocysteinemia - enzymology</subject><subject>Hyperhomocysteinemia - metabolism</subject><subject>Hyperhomocysteinemia - pathology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Reactive oxygen species</subject><issn>0168-0102</issn><issn>1872-8111</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9q3DAQxkVpaTZp36AU3XryRv_slS6BENJsINBD2kNOQpZHRYtXciR7IQ-Td628TptbehqY-X3zjfQh9IWSNSW0Od-tA0wJ8pqR0iJiTSh_h1ZUblglKaXv0apgsipTdoJOc94RQrgS_CM6YUTURAm2Qs_buI_2KY_gA2ATOmzjMEDCPnSTBWyh76feJGyGOIwx-4wP3mBr8mByEdjRH8zoYzhqw2R7KPCYTMh9tMskuld1ddzrw2_sijbOPnh-RwymP5rhfj7kflvdP9QPn9AHZ_oMn1_qGfr1_frn1ba6-3Fze3V5V1kh-VgxyoHVNUBruHCMSSed61TLOGmcbBQ0reuckrJVxMKGAW9IqxjhtbSiYw0_Q9-WvUOKjxPkUe99nq8xAeKU9aYWNVe12vyf5FxJobgspFhIm2LOCZwekt-b9KQp0XOCeqeXBPWcoCZClwSL7OuLwdTuofsn-htZAS4WAMqHHDwkna2HYKHzCeyou-jfdvgD87-x_Q</recordid><startdate>20100801</startdate><enddate>20100801</enddate><creator>Hirashima, Yoshimasa</creator><creator>Seshimo, So</creator><creator>Fujiki, Yoshika</creator><creator>Okabe, Masaaki</creator><creator>Nishiyama, Kazuo</creator><creator>Matsumoto, Mitsuharu</creator><creator>Kanouchi, Hiroaki</creator><creator>Oka, Tatsuzo</creator><general>Elsevier Ireland Ltd</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>7X8</scope><scope>7TK</scope></search><sort><creationdate>20100801</creationdate><title>Homocysteine and copper induce cellular apoptosis via caspase activation and nuclear translocation of apoptosis-inducing factor in neuronal cell line SH-SY5Y</title><author>Hirashima, Yoshimasa ; Seshimo, So ; Fujiki, Yoshika ; Okabe, Masaaki ; Nishiyama, Kazuo ; Matsumoto, Mitsuharu ; Kanouchi, Hiroaki ; Oka, Tatsuzo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-213e255eeba34f228f8ffd9b2306f869e6bfdf988b90ce72e360b920358c4d263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Active Transport, Cell Nucleus - drug effects</topic><topic>Active Transport, Cell Nucleus - physiology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Apoptosis Inducing Factor - physiology</topic><topic>Apoptosis-inducing factor</topic><topic>Caspase 3 - drug effects</topic><topic>Caspase 3 - physiology</topic><topic>Caspases - metabolism</topic><topic>Caspases - physiology</topic><topic>Catalase - pharmacology</topic><topic>Cell Line, Tumor</topic><topic>Copper</topic><topic>Copper - physiology</topic><topic>Copper - toxicity</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Activation - physiology</topic><topic>Homocysteine</topic><topic>Homocysteine - physiology</topic><topic>Homocysteine - toxicity</topic><topic>Humans</topic><topic>Hyperhomocysteinemia - enzymology</topic><topic>Hyperhomocysteinemia - metabolism</topic><topic>Hyperhomocysteinemia - pathology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Reactive oxygen species</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hirashima, Yoshimasa</creatorcontrib><creatorcontrib>Seshimo, So</creatorcontrib><creatorcontrib>Fujiki, Yoshika</creatorcontrib><creatorcontrib>Okabe, Masaaki</creatorcontrib><creatorcontrib>Nishiyama, Kazuo</creatorcontrib><creatorcontrib>Matsumoto, Mitsuharu</creatorcontrib><creatorcontrib>Kanouchi, Hiroaki</creatorcontrib><creatorcontrib>Oka, Tatsuzo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Neuroscience research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hirashima, Yoshimasa</au><au>Seshimo, So</au><au>Fujiki, Yoshika</au><au>Okabe, Masaaki</au><au>Nishiyama, Kazuo</au><au>Matsumoto, Mitsuharu</au><au>Kanouchi, Hiroaki</au><au>Oka, Tatsuzo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Homocysteine and copper induce cellular apoptosis via caspase activation and nuclear translocation of apoptosis-inducing factor in neuronal cell line SH-SY5Y</atitle><jtitle>Neuroscience research</jtitle><addtitle>Neurosci Res</addtitle><date>2010-08-01</date><risdate>2010</risdate><volume>67</volume><issue>4</issue><spage>300</spage><epage>306</epage><pages>300-306</pages><issn>0168-0102</issn><eissn>1872-8111</eissn><abstract>Hyperhomocysteinemia has been implicated in dementia and neurodegenerative disease. Physiological homocysteine concentrations did not result in apoptosis in SH-SY5Y cells in the present study. The apoptosis was recognized in millimolar level of homocysteine. However, SH-SY5Y cell death was observed following exposure to micromolar level of homocysteine in combination with copper. Exposure to 250
μM homocysteine and 10
μM CuCl
2 for one day decreased cell viability by 40%. Homocysteine and copper caused apoptosis, because hallmarks of apoptosis were recognized, such as loss of mitochondrial membrane potential, TUNEL-positive cells, release of cytochrome
c from mitochondria, and caspase-3 activation, but not nucleosomal DNA fragmentation. Homocysteine and copper generated the intracellular reactive oxygen species, and homocysteine and copper-induced apoptosis was due to an accumulation of intracellular reactive oxygen species, which was inhibited by catalase. Pan-caspase inhibitor, z-VAD-fmk, could not completely inhibited homocysteine and copper-induced cell death. Homocysteine and copper also caused the nuclear translocation of apoptosis-inducing factor. These results suggested that homocysteine and copper induced not only caspase-dependent apoptosis but also caspase-independent apoptosis-inducing factor related apoptosis.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>20450942</pmid><doi>10.1016/j.neures.2010.04.013</doi><tpages>7</tpages></addata></record> |
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| issn | 0168-0102 1872-8111 |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Active Transport, Cell Nucleus - drug effects Active Transport, Cell Nucleus - physiology Apoptosis Apoptosis - drug effects Apoptosis - physiology Apoptosis Inducing Factor - physiology Apoptosis-inducing factor Caspase 3 - drug effects Caspase 3 - physiology Caspases - metabolism Caspases - physiology Catalase - pharmacology Cell Line, Tumor Copper Copper - physiology Copper - toxicity Enzyme Activation - drug effects Enzyme Activation - physiology Homocysteine Homocysteine - physiology Homocysteine - toxicity Humans Hyperhomocysteinemia - enzymology Hyperhomocysteinemia - metabolism Hyperhomocysteinemia - pathology Neurons - drug effects Neurons - metabolism Reactive oxygen species |
| title | Homocysteine and copper induce cellular apoptosis via caspase activation and nuclear translocation of apoptosis-inducing factor in neuronal cell line SH-SY5Y |
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