Fluoxetine (Prozac) interaction with the mitochondrial voltage-dependent anion channel and protection against apoptotic cell death
Fluoxetine (Prozac) is a potent antidepressant compound inhibiting serotonin reuptake, but also Na +, K + and Ca 2+ channels and reported to both trigger and prevent apoptosis. Recently, fluoxetine was found to increase the voltage sensitivity of the mitochondrial voltage-dependent anion channel (VD...
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| Veröffentlicht in: | FEBS letters 2005-09, Vol.579 (22), p.5105-5110 |
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| creator | Nahon, Edna Israelson, Adrian Abu-Hamad, Salah Shoshan-Barmatz, Varda |
| description | Fluoxetine (Prozac) is a potent antidepressant compound inhibiting serotonin reuptake, but also Na
+, K
+ and Ca
2+ channels and reported to both trigger and prevent apoptosis. Recently, fluoxetine was found to increase the voltage sensitivity of the mitochondrial voltage-dependent anion channel (VDAC). VDAC which functions in transporting metabolites across the mitochondria also plays a crucial role in apoptosis.
Here, we demonstrate that fluoxetine interacted with VDAC and decreased its conductance. Fluoxetine inhibited the opening of the mitochondrial permeability transition pore, the release of cytochrome
c, and protected against staurosporine-induced apoptotic cell death. These findings may explain some of the reported fluoxetine side effects. |
| doi_str_mv | 10.1016/j.febslet.2005.08.020 |
| format | Article |
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+, K
+ and Ca
2+ channels and reported to both trigger and prevent apoptosis. Recently, fluoxetine was found to increase the voltage sensitivity of the mitochondrial voltage-dependent anion channel (VDAC). VDAC which functions in transporting metabolites across the mitochondria also plays a crucial role in apoptosis.
Here, we demonstrate that fluoxetine interacted with VDAC and decreased its conductance. Fluoxetine inhibited the opening of the mitochondrial permeability transition pore, the release of cytochrome
c, and protected against staurosporine-induced apoptotic cell death. These findings may explain some of the reported fluoxetine side effects.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/j.febslet.2005.08.020</identifier><identifier>PMID: 16139271</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>Animals ; Apoptosis ; Apoptosis - physiology ; Cell Line ; Cytochrome c ; Cytochromes c - metabolism ; Enzyme Inhibitors - metabolism ; Fluoxetine ; Fluoxetine - metabolism ; Humans ; Mitochondria, Liver - metabolism ; Permeability transition pore ; Porins - metabolism ; Prozac ; PTP ; Rats ; Serotonin Uptake Inhibitors - metabolism ; staurosporine ; Staurosporine - metabolism ; STS ; VDAC ; Voltage-dependent anion channel ; Voltage-Dependent Anion Channels</subject><ispartof>FEBS letters, 2005-09, Vol.579 (22), p.5105-5110</ispartof><rights>2005</rights><rights>FEBS Letters 579 (2005) 1873-3468 © 2015 Federation of European Biochemical Societies</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4283-b3ceb1335db1d6d74d3b6195167569b333b59be6dbf07ac2ad709f302689f07b3</citedby><cites>FETCH-LOGICAL-c4283-b3ceb1335db1d6d74d3b6195167569b333b59be6dbf07ac2ad709f302689f07b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.febslet.2005.08.020$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.febslet.2005.08.020$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,1417,1433,3550,27924,27925,45574,45575,45995,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16139271$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nahon, Edna</creatorcontrib><creatorcontrib>Israelson, Adrian</creatorcontrib><creatorcontrib>Abu-Hamad, Salah</creatorcontrib><creatorcontrib>Shoshan-Barmatz, Varda</creatorcontrib><title>Fluoxetine (Prozac) interaction with the mitochondrial voltage-dependent anion channel and protection against apoptotic cell death</title><title>FEBS letters</title><addtitle>FEBS Lett</addtitle><description>Fluoxetine (Prozac) is a potent antidepressant compound inhibiting serotonin reuptake, but also Na
+, K
+ and Ca
2+ channels and reported to both trigger and prevent apoptosis. Recently, fluoxetine was found to increase the voltage sensitivity of the mitochondrial voltage-dependent anion channel (VDAC). VDAC which functions in transporting metabolites across the mitochondria also plays a crucial role in apoptosis.
Here, we demonstrate that fluoxetine interacted with VDAC and decreased its conductance. Fluoxetine inhibited the opening of the mitochondrial permeability transition pore, the release of cytochrome
c, and protected against staurosporine-induced apoptotic cell death. These findings may explain some of the reported fluoxetine side effects.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Cell Line</subject><subject>Cytochrome c</subject><subject>Cytochromes c - metabolism</subject><subject>Enzyme Inhibitors - metabolism</subject><subject>Fluoxetine</subject><subject>Fluoxetine - metabolism</subject><subject>Humans</subject><subject>Mitochondria, Liver - metabolism</subject><subject>Permeability transition pore</subject><subject>Porins - metabolism</subject><subject>Prozac</subject><subject>PTP</subject><subject>Rats</subject><subject>Serotonin Uptake Inhibitors - metabolism</subject><subject>staurosporine</subject><subject>Staurosporine - metabolism</subject><subject>STS</subject><subject>VDAC</subject><subject>Voltage-dependent anion channel</subject><subject>Voltage-Dependent Anion Channels</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhi0EokvhJ4B8QnBIsON1Yp9QqboUqRJIwNnyx6TxKmuH2NtSjvxyHGUljnCyxnrmndEzCL2kpKaEtu_2dQ8mjZDrhhBeE1GThjxCGyo6VrFtKx6jDSF0W_FOsjP0LKU9KbWg8ik6oy1lsunoBv3ejcf4E7IPgN98meMvbd9iHzLM2mYfA773ecB5AHzwOdohBjd7PeK7OGZ9C5WDCYKDkLEOC24HHQKMpXJ4mmOGNUXfah9SgaY45Zi9xRbGETvQeXiOnvR6TPDi9J6j77urb5fX1c3nj58uL24qu20EqwyzYChj3BnqWtdtHTMtlZy2HW-lYYwZLg20zvSk07bRriOyZ6RphSw_hp2j12tu2evHEVJWB5-WNXSAeEyqFVwKIngB-QraOaY0Q6-m2R_0_KAoUYt8tVcn-WqRr4hQRX7pe3UacDQHcH-7TrYLcL0C936Eh_9LVburD83X5ZLLIQknRErJStT7NQqKsTsPs0rWQ7Dg_FycKxf9P7b9A_eRsLE</recordid><startdate>20050912</startdate><enddate>20050912</enddate><creator>Nahon, Edna</creator><creator>Israelson, Adrian</creator><creator>Abu-Hamad, Salah</creator><creator>Shoshan-Barmatz, Varda</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><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></search><sort><creationdate>20050912</creationdate><title>Fluoxetine (Prozac) interaction with the mitochondrial voltage-dependent anion channel and protection against apoptotic cell death</title><author>Nahon, Edna ; Israelson, Adrian ; Abu-Hamad, Salah ; Shoshan-Barmatz, Varda</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4283-b3ceb1335db1d6d74d3b6195167569b333b59be6dbf07ac2ad709f302689f07b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Cell Line</topic><topic>Cytochrome c</topic><topic>Cytochromes c - metabolism</topic><topic>Enzyme Inhibitors - metabolism</topic><topic>Fluoxetine</topic><topic>Fluoxetine - metabolism</topic><topic>Humans</topic><topic>Mitochondria, Liver - metabolism</topic><topic>Permeability transition pore</topic><topic>Porins - metabolism</topic><topic>Prozac</topic><topic>PTP</topic><topic>Rats</topic><topic>Serotonin Uptake Inhibitors - metabolism</topic><topic>staurosporine</topic><topic>Staurosporine - metabolism</topic><topic>STS</topic><topic>VDAC</topic><topic>Voltage-dependent anion channel</topic><topic>Voltage-Dependent Anion Channels</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nahon, Edna</creatorcontrib><creatorcontrib>Israelson, Adrian</creatorcontrib><creatorcontrib>Abu-Hamad, Salah</creatorcontrib><creatorcontrib>Shoshan-Barmatz, Varda</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nahon, Edna</au><au>Israelson, Adrian</au><au>Abu-Hamad, Salah</au><au>Shoshan-Barmatz, Varda</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fluoxetine (Prozac) interaction with the mitochondrial voltage-dependent anion channel and protection against apoptotic cell death</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>2005-09-12</date><risdate>2005</risdate><volume>579</volume><issue>22</issue><spage>5105</spage><epage>5110</epage><pages>5105-5110</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>Fluoxetine (Prozac) is a potent antidepressant compound inhibiting serotonin reuptake, but also Na
+, K
+ and Ca
2+ channels and reported to both trigger and prevent apoptosis. Recently, fluoxetine was found to increase the voltage sensitivity of the mitochondrial voltage-dependent anion channel (VDAC). VDAC which functions in transporting metabolites across the mitochondria also plays a crucial role in apoptosis.
Here, we demonstrate that fluoxetine interacted with VDAC and decreased its conductance. Fluoxetine inhibited the opening of the mitochondrial permeability transition pore, the release of cytochrome
c, and protected against staurosporine-induced apoptotic cell death. These findings may explain some of the reported fluoxetine side effects.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>16139271</pmid><doi>10.1016/j.febslet.2005.08.020</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Access via Wiley Online Library; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); Alma/SFX Local Collection |
| subjects | Animals Apoptosis Apoptosis - physiology Cell Line Cytochrome c Cytochromes c - metabolism Enzyme Inhibitors - metabolism Fluoxetine Fluoxetine - metabolism Humans Mitochondria, Liver - metabolism Permeability transition pore Porins - metabolism Prozac PTP Rats Serotonin Uptake Inhibitors - metabolism staurosporine Staurosporine - metabolism STS VDAC Voltage-dependent anion channel Voltage-Dependent Anion Channels |
| title | Fluoxetine (Prozac) interaction with the mitochondrial voltage-dependent anion channel and protection against apoptotic cell death |
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