Differential cellular regulation of the mitochondrial permeability transition in an in vitro model of 1,3-dinitrobenzene-induced encephalopathy
Exposure to 1,3-dinitrobenzene (DNB) is associated with neuropathologic changes in specific brainstem nuclei, mediated by oxidative stress and mitochondrial dysfunction. The expression of Bcl-2-family proteins as a function of sensitivity to 1,3-dinitrobenzene (DNB)-induced mitochondrial permeabilit...
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| Veröffentlicht in: | Brain research 2000-08, Vol.874 (2), p.165-177 |
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| description | Exposure to 1,3-dinitrobenzene (DNB) is associated with neuropathologic changes in specific brainstem nuclei, mediated by oxidative stress and mitochondrial dysfunction. The expression of Bcl-2-family proteins as a function of sensitivity to 1,3-dinitrobenzene (DNB)-induced mitochondrial permeability transition (MPT) was examined in C6 glioma and SY5Y neuroblastoma cells. Neuroblastoma cells were 10-fold more sensitive than glioma cells to DNB-induced decreases in mitochondrial reducing potential, measured by reduction of the tetrazolium compound, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). The IC
50 values for DNB-related inhibition of MTT reduction were 107±25 μM in SY5Y cells and 1047±101 μM in C6 cells. Levels of reactive oxygen species (ROS) were increased in both SY5Y and C6 cells following DNB exposure by 4.6- and 6.0-fold above control, respectively. DNB caused abrupt depolarization of mitochondria in both neuroblastoma and glioma cells that was inhibited by trifluoperazine. The first order rate constants for mitochondrial depolarization were: C6,
k=0.31±0.02 min
−1; SY5Y,
k=0.14±0.01 min
−1. Onset of MPT occurred at 10-fold lower concentration of DNB in SY5Y cells than in C6 cells. The antioxidants, deferoxamine and α-tocopherol, effectively prevented DNB-induced MPT in C6 and SY5Y cells, suggesting involvement of ROS in the initiation of MPT. Exposure to DNB resulted in decreased cellular ATP content in SY5Y cells and efflux of mitochondrial calcium in both SY5Y and C6 cells, concurrent with onset of MPT. The expression of Bcl-2, Bcl-X
L, and Bax was evaluated in both cell types by Western blot analysis. C6 glioma cells strongly expressed Bcl-X
L and only weakly expressed Bcl-2 and Bax, whereas SY5Y neuroblastoma cells expressed lower levels of Bcl-X
L and higher levels of both Bcl-2 and Bax. Collectively, these results suggest that higher constitutive expression of Bcl-X
L, rather than Bcl-2, correlates with resistance to DNB-induced MPT in SY5Y and C6 cells and that differential regulation of the permeability transition pore may underlie the cell-specific neurotoxicity of DNB. |
| doi_str_mv | 10.1016/S0006-8993(00)02546-4 |
| format | Article |
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50 values for DNB-related inhibition of MTT reduction were 107±25 μM in SY5Y cells and 1047±101 μM in C6 cells. Levels of reactive oxygen species (ROS) were increased in both SY5Y and C6 cells following DNB exposure by 4.6- and 6.0-fold above control, respectively. DNB caused abrupt depolarization of mitochondria in both neuroblastoma and glioma cells that was inhibited by trifluoperazine. The first order rate constants for mitochondrial depolarization were: C6,
k=0.31±0.02 min
−1; SY5Y,
k=0.14±0.01 min
−1. Onset of MPT occurred at 10-fold lower concentration of DNB in SY5Y cells than in C6 cells. The antioxidants, deferoxamine and α-tocopherol, effectively prevented DNB-induced MPT in C6 and SY5Y cells, suggesting involvement of ROS in the initiation of MPT. Exposure to DNB resulted in decreased cellular ATP content in SY5Y cells and efflux of mitochondrial calcium in both SY5Y and C6 cells, concurrent with onset of MPT. The expression of Bcl-2, Bcl-X
L, and Bax was evaluated in both cell types by Western blot analysis. C6 glioma cells strongly expressed Bcl-X
L and only weakly expressed Bcl-2 and Bax, whereas SY5Y neuroblastoma cells expressed lower levels of Bcl-X
L and higher levels of both Bcl-2 and Bax. Collectively, these results suggest that higher constitutive expression of Bcl-X
L, rather than Bcl-2, correlates with resistance to DNB-induced MPT in SY5Y and C6 cells and that differential regulation of the permeability transition pore may underlie the cell-specific neurotoxicity of DNB.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(00)02546-4</identifier><identifier>PMID: 10960601</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>1,3-Dinitrobenzene ; Adenosine Triphosphate - metabolism ; Antioxidants - pharmacology ; Bcl-2 proteins ; bcl-2-Associated X Protein ; bcl-X Protein ; Biological and medical sciences ; Brain Diseases - chemically induced ; Brain Diseases - pathology ; Brain Diseases - physiopathology ; C6 glioma ; Calcium - metabolism ; Deferoxamine - pharmacology ; Dinitrobenzene ; Dinitrobenzenes - pharmacology ; Electrophysiology ; Glioma - metabolism ; Glioma - pathology ; Glioma - physiopathology ; Humans ; Medical sciences ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondria - physiology ; Mitochondrial permeability transition ; Nervous system involvement in other diseases. Miscellaneous ; Neuroblastoma - metabolism ; Neuroblastoma - pathology ; Neuroblastoma - physiopathology ; Neurology ; Oxidation-Reduction - drug effects ; Oxidative stress ; Permeability ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Reactive Oxygen Species - metabolism ; SYSY neuroblastoma ; Tetrazolium Salts - metabolism ; Thiazoles - metabolism ; Trifluoperazine - pharmacology ; Tumor Cells, Cultured ; Vitamin E - pharmacology</subject><ispartof>Brain research, 2000-08, Vol.874 (2), p.165-177</ispartof><rights>2000 Elsevier Science B.V.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-976aaacd10293a0d12ed2c20031083260c04e327e9f5d724c8b753233f6257743</citedby><cites>FETCH-LOGICAL-c487t-976aaacd10293a0d12ed2c20031083260c04e327e9f5d724c8b753233f6257743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-8993(00)02546-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1486643$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10960601$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tjalkens, Ronald B</creatorcontrib><creatorcontrib>Ewing, Megan M</creatorcontrib><creatorcontrib>Philbert, Martin A</creatorcontrib><title>Differential cellular regulation of the mitochondrial permeability transition in an in vitro model of 1,3-dinitrobenzene-induced encephalopathy</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Exposure to 1,3-dinitrobenzene (DNB) is associated with neuropathologic changes in specific brainstem nuclei, mediated by oxidative stress and mitochondrial dysfunction. The expression of Bcl-2-family proteins as a function of sensitivity to 1,3-dinitrobenzene (DNB)-induced mitochondrial permeability transition (MPT) was examined in C6 glioma and SY5Y neuroblastoma cells. Neuroblastoma cells were 10-fold more sensitive than glioma cells to DNB-induced decreases in mitochondrial reducing potential, measured by reduction of the tetrazolium compound, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). The IC
50 values for DNB-related inhibition of MTT reduction were 107±25 μM in SY5Y cells and 1047±101 μM in C6 cells. Levels of reactive oxygen species (ROS) were increased in both SY5Y and C6 cells following DNB exposure by 4.6- and 6.0-fold above control, respectively. DNB caused abrupt depolarization of mitochondria in both neuroblastoma and glioma cells that was inhibited by trifluoperazine. The first order rate constants for mitochondrial depolarization were: C6,
k=0.31±0.02 min
−1; SY5Y,
k=0.14±0.01 min
−1. Onset of MPT occurred at 10-fold lower concentration of DNB in SY5Y cells than in C6 cells. The antioxidants, deferoxamine and α-tocopherol, effectively prevented DNB-induced MPT in C6 and SY5Y cells, suggesting involvement of ROS in the initiation of MPT. Exposure to DNB resulted in decreased cellular ATP content in SY5Y cells and efflux of mitochondrial calcium in both SY5Y and C6 cells, concurrent with onset of MPT. The expression of Bcl-2, Bcl-X
L, and Bax was evaluated in both cell types by Western blot analysis. C6 glioma cells strongly expressed Bcl-X
L and only weakly expressed Bcl-2 and Bax, whereas SY5Y neuroblastoma cells expressed lower levels of Bcl-X
L and higher levels of both Bcl-2 and Bax. Collectively, these results suggest that higher constitutive expression of Bcl-X
L, rather than Bcl-2, correlates with resistance to DNB-induced MPT in SY5Y and C6 cells and that differential regulation of the permeability transition pore may underlie the cell-specific neurotoxicity of DNB.</description><subject>1,3-Dinitrobenzene</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Antioxidants - pharmacology</subject><subject>Bcl-2 proteins</subject><subject>bcl-2-Associated X Protein</subject><subject>bcl-X Protein</subject><subject>Biological and medical sciences</subject><subject>Brain Diseases - chemically induced</subject><subject>Brain Diseases - pathology</subject><subject>Brain Diseases - physiopathology</subject><subject>C6 glioma</subject><subject>Calcium - metabolism</subject><subject>Deferoxamine - pharmacology</subject><subject>Dinitrobenzene</subject><subject>Dinitrobenzenes - pharmacology</subject><subject>Electrophysiology</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>Glioma - physiopathology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - physiology</subject><subject>Mitochondrial permeability transition</subject><subject>Nervous system involvement in other diseases. Miscellaneous</subject><subject>Neuroblastoma - metabolism</subject><subject>Neuroblastoma - pathology</subject><subject>Neuroblastoma - physiopathology</subject><subject>Neurology</subject><subject>Oxidation-Reduction - drug effects</subject><subject>Oxidative stress</subject><subject>Permeability</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>SYSY neuroblastoma</subject><subject>Tetrazolium Salts - metabolism</subject><subject>Thiazoles - metabolism</subject><subject>Trifluoperazine - pharmacology</subject><subject>Tumor Cells, Cultured</subject><subject>Vitamin E - pharmacology</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctu1DAUhi1ERYfCI4C8QAikBo4vcZIVQuVSpEosgLXlsU8Yo8QOtlNp-hK8MsnMCNix8ZGPvnP7f0KeMHjFgKnXXwBAVW3XiRcAL4HXUlXyHtmwtuGV4hLuk80f5Jw8zPnH8hWigwfknEGnQAHbkF_vfN9jwlC8GajFYZgHk2jC70ssPgYae1p2SEdfot3F4NIKTphGNFs_-LKnJZmQ_QH2gZrDe-tLinSMDoe1A7sUlfNhTW4x3GHAygc3W3QUg8VpZ4Y4mbLbPyJnvRkyPj7FC_Ltw_uvV9fVzeePn67e3lRWtk2pukYZY6xjwDthwDGOjlu-HMigFVyBBYmCN9j1tWu4tO22qQUXole8bhopLsjzY98pxZ8z5qJHn9fzTcA4Z80axUQn2wWsj6BNMeeEvZ6SH03aawZ6dUIfnNCrzBpAH5zQ64CnpwHzdkT3T9VR-gV4dgJMtmboFxGtz3852SolxYK9OWK4qHHrMels_aqZ8wlt0S76_2zyG-2Ipv4</recordid><startdate>20000825</startdate><enddate>20000825</enddate><creator>Tjalkens, Ronald B</creator><creator>Ewing, Megan M</creator><creator>Philbert, Martin A</creator><general>Elsevier B.V</general><general>Elsevier</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>7TK</scope></search><sort><creationdate>20000825</creationdate><title>Differential cellular regulation of the mitochondrial permeability transition in an in vitro model of 1,3-dinitrobenzene-induced encephalopathy</title><author>Tjalkens, Ronald B ; Ewing, Megan M ; Philbert, Martin A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-976aaacd10293a0d12ed2c20031083260c04e327e9f5d724c8b753233f6257743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>1,3-Dinitrobenzene</topic><topic>Adenosine Triphosphate - metabolism</topic><topic>Antioxidants - pharmacology</topic><topic>Bcl-2 proteins</topic><topic>bcl-2-Associated X Protein</topic><topic>bcl-X Protein</topic><topic>Biological and medical sciences</topic><topic>Brain Diseases - chemically induced</topic><topic>Brain Diseases - pathology</topic><topic>Brain Diseases - physiopathology</topic><topic>C6 glioma</topic><topic>Calcium - metabolism</topic><topic>Deferoxamine - pharmacology</topic><topic>Dinitrobenzene</topic><topic>Dinitrobenzenes - pharmacology</topic><topic>Electrophysiology</topic><topic>Glioma - metabolism</topic><topic>Glioma - pathology</topic><topic>Glioma - physiopathology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - physiology</topic><topic>Mitochondrial permeability transition</topic><topic>Nervous system involvement in other diseases. Miscellaneous</topic><topic>Neuroblastoma - metabolism</topic><topic>Neuroblastoma - pathology</topic><topic>Neuroblastoma - physiopathology</topic><topic>Neurology</topic><topic>Oxidation-Reduction - drug effects</topic><topic>Oxidative stress</topic><topic>Permeability</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>SYSY neuroblastoma</topic><topic>Tetrazolium Salts - metabolism</topic><topic>Thiazoles - metabolism</topic><topic>Trifluoperazine - pharmacology</topic><topic>Tumor Cells, Cultured</topic><topic>Vitamin E - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tjalkens, Ronald B</creatorcontrib><creatorcontrib>Ewing, Megan M</creatorcontrib><creatorcontrib>Philbert, Martin A</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>Neurosciences Abstracts</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tjalkens, Ronald B</au><au>Ewing, Megan M</au><au>Philbert, Martin A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential cellular regulation of the mitochondrial permeability transition in an in vitro model of 1,3-dinitrobenzene-induced encephalopathy</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2000-08-25</date><risdate>2000</risdate><volume>874</volume><issue>2</issue><spage>165</spage><epage>177</epage><pages>165-177</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Exposure to 1,3-dinitrobenzene (DNB) is associated with neuropathologic changes in specific brainstem nuclei, mediated by oxidative stress and mitochondrial dysfunction. The expression of Bcl-2-family proteins as a function of sensitivity to 1,3-dinitrobenzene (DNB)-induced mitochondrial permeability transition (MPT) was examined in C6 glioma and SY5Y neuroblastoma cells. Neuroblastoma cells were 10-fold more sensitive than glioma cells to DNB-induced decreases in mitochondrial reducing potential, measured by reduction of the tetrazolium compound, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). The IC
50 values for DNB-related inhibition of MTT reduction were 107±25 μM in SY5Y cells and 1047±101 μM in C6 cells. Levels of reactive oxygen species (ROS) were increased in both SY5Y and C6 cells following DNB exposure by 4.6- and 6.0-fold above control, respectively. DNB caused abrupt depolarization of mitochondria in both neuroblastoma and glioma cells that was inhibited by trifluoperazine. The first order rate constants for mitochondrial depolarization were: C6,
k=0.31±0.02 min
−1; SY5Y,
k=0.14±0.01 min
−1. Onset of MPT occurred at 10-fold lower concentration of DNB in SY5Y cells than in C6 cells. The antioxidants, deferoxamine and α-tocopherol, effectively prevented DNB-induced MPT in C6 and SY5Y cells, suggesting involvement of ROS in the initiation of MPT. Exposure to DNB resulted in decreased cellular ATP content in SY5Y cells and efflux of mitochondrial calcium in both SY5Y and C6 cells, concurrent with onset of MPT. The expression of Bcl-2, Bcl-X
L, and Bax was evaluated in both cell types by Western blot analysis. C6 glioma cells strongly expressed Bcl-X
L and only weakly expressed Bcl-2 and Bax, whereas SY5Y neuroblastoma cells expressed lower levels of Bcl-X
L and higher levels of both Bcl-2 and Bax. Collectively, these results suggest that higher constitutive expression of Bcl-X
L, rather than Bcl-2, correlates with resistance to DNB-induced MPT in SY5Y and C6 cells and that differential regulation of the permeability transition pore may underlie the cell-specific neurotoxicity of DNB.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>10960601</pmid><doi>10.1016/S0006-8993(00)02546-4</doi><tpages>13</tpages></addata></record> |
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| ispartof | Brain research, 2000-08, Vol.874 (2), p.165-177 |
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| subjects | 1,3-Dinitrobenzene Adenosine Triphosphate - metabolism Antioxidants - pharmacology Bcl-2 proteins bcl-2-Associated X Protein bcl-X Protein Biological and medical sciences Brain Diseases - chemically induced Brain Diseases - pathology Brain Diseases - physiopathology C6 glioma Calcium - metabolism Deferoxamine - pharmacology Dinitrobenzene Dinitrobenzenes - pharmacology Electrophysiology Glioma - metabolism Glioma - pathology Glioma - physiopathology Humans Medical sciences Mitochondria - drug effects Mitochondria - metabolism Mitochondria - physiology Mitochondrial permeability transition Nervous system involvement in other diseases. Miscellaneous Neuroblastoma - metabolism Neuroblastoma - pathology Neuroblastoma - physiopathology Neurology Oxidation-Reduction - drug effects Oxidative stress Permeability Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Reactive Oxygen Species - metabolism SYSY neuroblastoma Tetrazolium Salts - metabolism Thiazoles - metabolism Trifluoperazine - pharmacology Tumor Cells, Cultured Vitamin E - pharmacology |
| title | Differential cellular regulation of the mitochondrial permeability transition in an in vitro model of 1,3-dinitrobenzene-induced encephalopathy |
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