Methylenedioxymethamphetamine inhibits mitochondrial complex I activity in mice: a possible mechanism underlying neurotoxicity
Background and purpose: 3,4‐methylenedioxymethamphetamine (MDMA) causes a persistent loss of dopaminergic cell bodies in the substantia nigra of mice. Current evidence indicates that such neurotoxicity is due to oxidative stress but the source of free radicals remains unknown. Inhibition of mitocho...
Gespeichert in:
| Veröffentlicht in: | British journal of pharmacology 2010-05, Vol.160 (2), p.233-245 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 245 |
|---|---|
| container_issue | 2 |
| container_start_page | 233 |
| container_title | British journal of pharmacology |
| container_volume | 160 |
| creator | Puerta, Elena Hervias, Isabel Goñi‐Allo, Beatriz Zhang, Steven F Jordán, Joaquín Starkov, Anatoly A Aguirre, Norberto |
| description | Background and purpose: 3,4‐methylenedioxymethamphetamine (MDMA) causes a persistent loss of dopaminergic cell bodies in the substantia nigra of mice. Current evidence indicates that such neurotoxicity is due to oxidative stress but the source of free radicals remains unknown. Inhibition of mitochondrial electron transport chain complexes by MDMA was assessed as a possible source.
Experimental approach: Activities of mitochondrial complexes after MDMA were evaluated spectrophotometrically. In situ visualization of superoxide production in the striatum was assessed by ethidium fluorescence and striatal dopamine levels were determined by HPLC as an index of dopaminergic toxicity.
Key results: 3,4‐methylenedioxymethamphetamine decreased mitochondrial complex I activity in the striatum of mice, an effect accompanied by an increased production of superoxide radicals and the inhibition of endogenous aconitase. α‐Lipoic acid prevented superoxide generation and long‐term toxicity independent of any effect on complex I inhibition. These effects of α‐lipoic acid were also associated with a significant increase of striatal glutathione levels. The relevance of glutathione was supported by reducing striatal glutathione content with L‐buthionine‐(S,R)‐sulfoximine, which exacerbated MDMA‐induced dopamine deficits, effects suppressed by α‐lipoic acid. The nitric oxide synthase inhibitor, NG‐nitro‐L‐arginine, partially prevented MDMA‐induced dopamine depletions, an effect reversed by L‐arginine but not D‐arginine. Finally, a direct relationship between mitochondrial complex I inhibition and long‐term dopamine depletions was found in animals treated with MDMA in combination with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine.
Conclusions and implications: Inhibition of mitochondrial complex I following MDMA could be the source of free radicals responsible for oxidative stress and the consequent neurotoxicity of this drug in mice.
This article is commented on by Moncada, pp. 217–219 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00706.x and to view related papers in this issue by Pravdic et al. and Kurz et al. visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00698.x and http://dx.doi.org/10.1111/j.1476‐5381.2010.00656.x |
| doi_str_mv | 10.1111/j.1476-5381.2010.00663.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2874846</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3376142391</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5963-2d549fb92e3fe329b0adad7222b3df298dbcf82a016d24ecf36d042eeb45a3f93</originalsourceid><addsrcrecordid>eNqNkUtv1DAUhS1ERaeFv4AsIZYZHDsPByEkqAqtVAQLWFuOfdN4lNjBTkqy4bfjMNOh7OqNH_c718c-COGUbNM43uy2aVYWSc54uqUknhJSFGw7P0GbY-Ep2hBCyiRNOT9FZyHsCInFMn-GTinJKGOMb9DvLzC2SwcWtHHz0sed7IcWRtkbC9jY1tRmDLg3o1Ots9ob2WHl-qGDGV9jqUZzZ8YlkpFR8BZLPLgQTN0B7kG10prQ48lq8N1i7C22MHk3utmoKHuOThrZBXhxmM_Rj0-X3y-ukpuvn68vPtwkKq8KllCdZ1VTVxRYA4xWNZFa6pJSWjPd0IrrWjWcSpIWmmagGlbo-ESAOsslayp2jt7v-w5T3YNWYEcvOzF400u_CCeN-L9iTStu3Z2gvMx4VsQGrw4NvPs5QRjFzk3eRs8izbO8pJxzEim-p5SPf-ChOd6QErEmJ3ZiDUisAYk1OfE3OTFH6cuHDo_C-6gi8PoAyKBk13hplQn_OFqUeU5Wp-_23C_TwfJoA-Ljt6u4YH8A14y5ig</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1545728880</pqid></control><display><type>article</type><title>Methylenedioxymethamphetamine inhibits mitochondrial complex I activity in mice: a possible mechanism underlying neurotoxicity</title><source>Wiley Free Content</source><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Puerta, Elena ; Hervias, Isabel ; Goñi‐Allo, Beatriz ; Zhang, Steven F ; Jordán, Joaquín ; Starkov, Anatoly A ; Aguirre, Norberto</creator><creatorcontrib>Puerta, Elena ; Hervias, Isabel ; Goñi‐Allo, Beatriz ; Zhang, Steven F ; Jordán, Joaquín ; Starkov, Anatoly A ; Aguirre, Norberto</creatorcontrib><description>Background and purpose: 3,4‐methylenedioxymethamphetamine (MDMA) causes a persistent loss of dopaminergic cell bodies in the substantia nigra of mice. Current evidence indicates that such neurotoxicity is due to oxidative stress but the source of free radicals remains unknown. Inhibition of mitochondrial electron transport chain complexes by MDMA was assessed as a possible source.
Experimental approach: Activities of mitochondrial complexes after MDMA were evaluated spectrophotometrically. In situ visualization of superoxide production in the striatum was assessed by ethidium fluorescence and striatal dopamine levels were determined by HPLC as an index of dopaminergic toxicity.
Key results: 3,4‐methylenedioxymethamphetamine decreased mitochondrial complex I activity in the striatum of mice, an effect accompanied by an increased production of superoxide radicals and the inhibition of endogenous aconitase. α‐Lipoic acid prevented superoxide generation and long‐term toxicity independent of any effect on complex I inhibition. These effects of α‐lipoic acid were also associated with a significant increase of striatal glutathione levels. The relevance of glutathione was supported by reducing striatal glutathione content with L‐buthionine‐(S,R)‐sulfoximine, which exacerbated MDMA‐induced dopamine deficits, effects suppressed by α‐lipoic acid. The nitric oxide synthase inhibitor, NG‐nitro‐L‐arginine, partially prevented MDMA‐induced dopamine depletions, an effect reversed by L‐arginine but not D‐arginine. Finally, a direct relationship between mitochondrial complex I inhibition and long‐term dopamine depletions was found in animals treated with MDMA in combination with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine.
Conclusions and implications: Inhibition of mitochondrial complex I following MDMA could be the source of free radicals responsible for oxidative stress and the consequent neurotoxicity of this drug in mice.
This article is commented on by Moncada, pp. 217–219 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00706.x and to view related papers in this issue by Pravdic et al. and Kurz et al. visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00698.x and http://dx.doi.org/10.1111/j.1476‐5381.2010.00656.x</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/j.1476-5381.2010.00663.x</identifier><identifier>PMID: 20423338</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Antioxidants - pharmacology ; Biological and medical sciences ; complex I ; Corpus Striatum - drug effects ; Corpus Striatum - metabolism ; Dopamine ; Dopamine - metabolism ; Ecstasy ; Electron Transport Complex I - antagonists & inhibitors ; Free radicals ; Free Radicals - metabolism ; Hallucinogens - toxicity ; lipoic acid ; Male ; MDMA ; Medical sciences ; Mice ; mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; N-Methyl-3,4-methylenedioxyamphetamine - toxicity ; Neurotoxicity ; Neurotoxicity Syndromes - etiology ; Nitric oxide ; Oxidative stress ; Oxidative Stress - drug effects ; Pharmacology. Drug treatments ; Research Papers with Commentaries ; Rodents ; Thioctic Acid - pharmacology</subject><ispartof>British journal of pharmacology, 2010-05, Vol.160 (2), p.233-245</ispartof><rights>2010 The Authors. Journal compilation © 2010 The British Pharmacological Society</rights><rights>2015 INIST-CNRS</rights><rights>Journal compilation © 2010 The British Pharmacological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5963-2d549fb92e3fe329b0adad7222b3df298dbcf82a016d24ecf36d042eeb45a3f93</citedby><cites>FETCH-LOGICAL-c5963-2d549fb92e3fe329b0adad7222b3df298dbcf82a016d24ecf36d042eeb45a3f93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874846/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874846/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22675506$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20423338$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Puerta, Elena</creatorcontrib><creatorcontrib>Hervias, Isabel</creatorcontrib><creatorcontrib>Goñi‐Allo, Beatriz</creatorcontrib><creatorcontrib>Zhang, Steven F</creatorcontrib><creatorcontrib>Jordán, Joaquín</creatorcontrib><creatorcontrib>Starkov, Anatoly A</creatorcontrib><creatorcontrib>Aguirre, Norberto</creatorcontrib><title>Methylenedioxymethamphetamine inhibits mitochondrial complex I activity in mice: a possible mechanism underlying neurotoxicity</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and purpose: 3,4‐methylenedioxymethamphetamine (MDMA) causes a persistent loss of dopaminergic cell bodies in the substantia nigra of mice. Current evidence indicates that such neurotoxicity is due to oxidative stress but the source of free radicals remains unknown. Inhibition of mitochondrial electron transport chain complexes by MDMA was assessed as a possible source.
Experimental approach: Activities of mitochondrial complexes after MDMA were evaluated spectrophotometrically. In situ visualization of superoxide production in the striatum was assessed by ethidium fluorescence and striatal dopamine levels were determined by HPLC as an index of dopaminergic toxicity.
Key results: 3,4‐methylenedioxymethamphetamine decreased mitochondrial complex I activity in the striatum of mice, an effect accompanied by an increased production of superoxide radicals and the inhibition of endogenous aconitase. α‐Lipoic acid prevented superoxide generation and long‐term toxicity independent of any effect on complex I inhibition. These effects of α‐lipoic acid were also associated with a significant increase of striatal glutathione levels. The relevance of glutathione was supported by reducing striatal glutathione content with L‐buthionine‐(S,R)‐sulfoximine, which exacerbated MDMA‐induced dopamine deficits, effects suppressed by α‐lipoic acid. The nitric oxide synthase inhibitor, NG‐nitro‐L‐arginine, partially prevented MDMA‐induced dopamine depletions, an effect reversed by L‐arginine but not D‐arginine. Finally, a direct relationship between mitochondrial complex I inhibition and long‐term dopamine depletions was found in animals treated with MDMA in combination with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine.
Conclusions and implications: Inhibition of mitochondrial complex I following MDMA could be the source of free radicals responsible for oxidative stress and the consequent neurotoxicity of this drug in mice.
This article is commented on by Moncada, pp. 217–219 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00706.x and to view related papers in this issue by Pravdic et al. and Kurz et al. visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00698.x and http://dx.doi.org/10.1111/j.1476‐5381.2010.00656.x</description><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Biological and medical sciences</subject><subject>complex I</subject><subject>Corpus Striatum - drug effects</subject><subject>Corpus Striatum - metabolism</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Ecstasy</subject><subject>Electron Transport Complex I - antagonists & inhibitors</subject><subject>Free radicals</subject><subject>Free Radicals - metabolism</subject><subject>Hallucinogens - toxicity</subject><subject>lipoic acid</subject><subject>Male</subject><subject>MDMA</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>N-Methyl-3,4-methylenedioxyamphetamine - toxicity</subject><subject>Neurotoxicity</subject><subject>Neurotoxicity Syndromes - etiology</subject><subject>Nitric oxide</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pharmacology. Drug treatments</subject><subject>Research Papers with Commentaries</subject><subject>Rodents</subject><subject>Thioctic Acid - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUtv1DAUhS1ERaeFv4AsIZYZHDsPByEkqAqtVAQLWFuOfdN4lNjBTkqy4bfjMNOh7OqNH_c718c-COGUbNM43uy2aVYWSc54uqUknhJSFGw7P0GbY-Ep2hBCyiRNOT9FZyHsCInFMn-GTinJKGOMb9DvLzC2SwcWtHHz0sed7IcWRtkbC9jY1tRmDLg3o1Ots9ob2WHl-qGDGV9jqUZzZ8YlkpFR8BZLPLgQTN0B7kG10prQ48lq8N1i7C22MHk3utmoKHuOThrZBXhxmM_Rj0-X3y-ukpuvn68vPtwkKq8KllCdZ1VTVxRYA4xWNZFa6pJSWjPd0IrrWjWcSpIWmmagGlbo-ESAOsslayp2jt7v-w5T3YNWYEcvOzF400u_CCeN-L9iTStu3Z2gvMx4VsQGrw4NvPs5QRjFzk3eRs8izbO8pJxzEim-p5SPf-ChOd6QErEmJ3ZiDUisAYk1OfE3OTFH6cuHDo_C-6gi8PoAyKBk13hplQn_OFqUeU5Wp-_23C_TwfJoA-Ljt6u4YH8A14y5ig</recordid><startdate>201005</startdate><enddate>201005</enddate><creator>Puerta, Elena</creator><creator>Hervias, Isabel</creator><creator>Goñi‐Allo, Beatriz</creator><creator>Zhang, Steven F</creator><creator>Jordán, Joaquín</creator><creator>Starkov, Anatoly A</creator><creator>Aguirre, Norberto</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing Group</general><scope>IQODW</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>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>5PM</scope></search><sort><creationdate>201005</creationdate><title>Methylenedioxymethamphetamine inhibits mitochondrial complex I activity in mice: a possible mechanism underlying neurotoxicity</title><author>Puerta, Elena ; Hervias, Isabel ; Goñi‐Allo, Beatriz ; Zhang, Steven F ; Jordán, Joaquín ; Starkov, Anatoly A ; Aguirre, Norberto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5963-2d549fb92e3fe329b0adad7222b3df298dbcf82a016d24ecf36d042eeb45a3f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Biological and medical sciences</topic><topic>complex I</topic><topic>Corpus Striatum - drug effects</topic><topic>Corpus Striatum - metabolism</topic><topic>Dopamine</topic><topic>Dopamine - metabolism</topic><topic>Ecstasy</topic><topic>Electron Transport Complex I - antagonists & inhibitors</topic><topic>Free radicals</topic><topic>Free Radicals - metabolism</topic><topic>Hallucinogens - toxicity</topic><topic>lipoic acid</topic><topic>Male</topic><topic>MDMA</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>N-Methyl-3,4-methylenedioxyamphetamine - toxicity</topic><topic>Neurotoxicity</topic><topic>Neurotoxicity Syndromes - etiology</topic><topic>Nitric oxide</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pharmacology. Drug treatments</topic><topic>Research Papers with Commentaries</topic><topic>Rodents</topic><topic>Thioctic Acid - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Puerta, Elena</creatorcontrib><creatorcontrib>Hervias, Isabel</creatorcontrib><creatorcontrib>Goñi‐Allo, Beatriz</creatorcontrib><creatorcontrib>Zhang, Steven F</creatorcontrib><creatorcontrib>Jordán, Joaquín</creatorcontrib><creatorcontrib>Starkov, Anatoly A</creatorcontrib><creatorcontrib>Aguirre, Norberto</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Puerta, Elena</au><au>Hervias, Isabel</au><au>Goñi‐Allo, Beatriz</au><au>Zhang, Steven F</au><au>Jordán, Joaquín</au><au>Starkov, Anatoly A</au><au>Aguirre, Norberto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methylenedioxymethamphetamine inhibits mitochondrial complex I activity in mice: a possible mechanism underlying neurotoxicity</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2010-05</date><risdate>2010</risdate><volume>160</volume><issue>2</issue><spage>233</spage><epage>245</epage><pages>233-245</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Background and purpose: 3,4‐methylenedioxymethamphetamine (MDMA) causes a persistent loss of dopaminergic cell bodies in the substantia nigra of mice. Current evidence indicates that such neurotoxicity is due to oxidative stress but the source of free radicals remains unknown. Inhibition of mitochondrial electron transport chain complexes by MDMA was assessed as a possible source.
Experimental approach: Activities of mitochondrial complexes after MDMA were evaluated spectrophotometrically. In situ visualization of superoxide production in the striatum was assessed by ethidium fluorescence and striatal dopamine levels were determined by HPLC as an index of dopaminergic toxicity.
Key results: 3,4‐methylenedioxymethamphetamine decreased mitochondrial complex I activity in the striatum of mice, an effect accompanied by an increased production of superoxide radicals and the inhibition of endogenous aconitase. α‐Lipoic acid prevented superoxide generation and long‐term toxicity independent of any effect on complex I inhibition. These effects of α‐lipoic acid were also associated with a significant increase of striatal glutathione levels. The relevance of glutathione was supported by reducing striatal glutathione content with L‐buthionine‐(S,R)‐sulfoximine, which exacerbated MDMA‐induced dopamine deficits, effects suppressed by α‐lipoic acid. The nitric oxide synthase inhibitor, NG‐nitro‐L‐arginine, partially prevented MDMA‐induced dopamine depletions, an effect reversed by L‐arginine but not D‐arginine. Finally, a direct relationship between mitochondrial complex I inhibition and long‐term dopamine depletions was found in animals treated with MDMA in combination with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine.
Conclusions and implications: Inhibition of mitochondrial complex I following MDMA could be the source of free radicals responsible for oxidative stress and the consequent neurotoxicity of this drug in mice.
This article is commented on by Moncada, pp. 217–219 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00706.x and to view related papers in this issue by Pravdic et al. and Kurz et al. visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00698.x and http://dx.doi.org/10.1111/j.1476‐5381.2010.00656.x</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20423338</pmid><doi>10.1111/j.1476-5381.2010.00663.x</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0007-1188 |
| ispartof | British journal of pharmacology, 2010-05, Vol.160 (2), p.233-245 |
| issn | 0007-1188 1476-5381 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2874846 |
| source | Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Antioxidants - pharmacology Biological and medical sciences complex I Corpus Striatum - drug effects Corpus Striatum - metabolism Dopamine Dopamine - metabolism Ecstasy Electron Transport Complex I - antagonists & inhibitors Free radicals Free Radicals - metabolism Hallucinogens - toxicity lipoic acid Male MDMA Medical sciences Mice mitochondria Mitochondria - drug effects Mitochondria - metabolism N-Methyl-3,4-methylenedioxyamphetamine - toxicity Neurotoxicity Neurotoxicity Syndromes - etiology Nitric oxide Oxidative stress Oxidative Stress - drug effects Pharmacology. Drug treatments Research Papers with Commentaries Rodents Thioctic Acid - pharmacology |
| title | Methylenedioxymethamphetamine inhibits mitochondrial complex I activity in mice: a possible mechanism underlying neurotoxicity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T22%3A54%3A58IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Methylenedioxymethamphetamine%20inhibits%20mitochondrial%20complex%20I%20activity%20in%20mice:%20a%20possible%20mechanism%20underlying%20neurotoxicity&rft.jtitle=British%20journal%20of%20pharmacology&rft.au=Puerta,%20Elena&rft.date=2010-05&rft.volume=160&rft.issue=2&rft.spage=233&rft.epage=245&rft.pages=233-245&rft.issn=0007-1188&rft.eissn=1476-5381&rft.coden=BJPCBM&rft_id=info:doi/10.1111/j.1476-5381.2010.00663.x&rft_dat=%3Cproquest_pubme%3E3376142391%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1545728880&rft_id=info:pmid/20423338&rfr_iscdi=true |