The antioxidant Trolox restores mitochondrial membrane potential and Ca2+-stimulated ATP production in human complex I deficiency
Malfunction of mitochondrial complex I caused by nuclear gene mutations causes early-onset neurodegenerative diseases. Previous work using cultured fibroblasts of complex-I-deficient patients revealed elevated levels of reactive oxygen species (ROS) and reductions in both total Ca 2+ content of the...
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| Veröffentlicht in: | Journal of molecular medicine (Berlin, Germany) Germany), 2009-05, Vol.87 (5), p.515-522 |
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| creator | Distelmaier, Felix Visch, Henk-Jan Smeitink, Jan A. M. Mayatepek, Ertan Koopman, Werner J. H. Willems, Peter H. G. M. |
| description | Malfunction of mitochondrial complex I caused by nuclear gene mutations causes early-onset neurodegenerative diseases. Previous work using cultured fibroblasts of complex-I-deficient patients revealed elevated levels of reactive oxygen species (ROS) and reductions in both total Ca
2+
content of the endoplasmic reticulum (ER
Ca
) and bradykinin(Bk)-induced increases in cytosolic and mitochondrial free Ca
2+
([Ca
2+
]
C
; [Ca
2+
]
M
) and ATP ([ATP]
C
; [ATP]
M
) concentration. Here, we determined the mitochondrial membrane potential (Δ
ψ
) in patient skin fibroblasts and show significant correlations with cellular ROS levels and ER
Ca
, i.e., the less negative Δ
ψ
, the higher these levels and the lower ER
Ca
. Treatment with 6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox) normalized Δ
ψ
and Bk-induced increases in [Ca
2+
]
M
and [ATP]
M
. These effects were accompanied by an increase in ER
Ca
and Bk-induced increase in [Ca
2+
]
C
. Together, these results provide evidence for an integral role of increased ROS levels in complex I deficiency and point to the potential therapeutic value of antioxidant treatment. |
| doi_str_mv | 10.1007/s00109-009-0452-5 |
| format | Article |
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2+
content of the endoplasmic reticulum (ER
Ca
) and bradykinin(Bk)-induced increases in cytosolic and mitochondrial free Ca
2+
([Ca
2+
]
C
; [Ca
2+
]
M
) and ATP ([ATP]
C
; [ATP]
M
) concentration. Here, we determined the mitochondrial membrane potential (Δ
ψ
) in patient skin fibroblasts and show significant correlations with cellular ROS levels and ER
Ca
, i.e., the less negative Δ
ψ
, the higher these levels and the lower ER
Ca
. Treatment with 6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox) normalized Δ
ψ
and Bk-induced increases in [Ca
2+
]
M
and [ATP]
M
. These effects were accompanied by an increase in ER
Ca
and Bk-induced increase in [Ca
2+
]
C
. Together, these results provide evidence for an integral role of increased ROS levels in complex I deficiency and point to the potential therapeutic value of antioxidant treatment.</description><identifier>ISSN: 0946-2716</identifier><identifier>EISSN: 1432-1440</identifier><identifier>DOI: 10.1007/s00109-009-0452-5</identifier><identifier>PMID: 19255735</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Adenosine Triphosphate - metabolism ; Age ; Antioxidants ; Antioxidants - pharmacology ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Bradykinin ; Bradykinin - pharmacology ; Calcium (mitochondrial) ; Calcium (reticular) ; Calcium - metabolism ; Carboxylic acids ; Cell Line ; Chromans - pharmacology ; Dose-Response Relationship, Drug ; Electron transport chain ; Electron Transport Complex I - deficiency ; Endoplasmic reticulum ; Endoplasmic Reticulum - drug effects ; Endoplasmic Reticulum - metabolism ; Errors of metabolism ; Fibroblasts ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; General aspects ; Human Genetics ; Humans ; Internal Medicine ; Medical sciences ; Membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Metabolic diseases ; Miscellaneous hereditary metabolic disorders ; Mitochondria ; Mitochondrial Diseases - metabolism ; Mitochondrial Diseases - pathology ; Mitochondrial Diseases - physiopathology ; Molecular Medicine ; NADH-ubiquinone oxidoreductase ; Neurodegenerative diseases ; Nitric oxide ; Original Aricle ; Oxidative stress ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Vitamin E</subject><ispartof>Journal of molecular medicine (Berlin, Germany), 2009-05, Vol.87 (5), p.515-522</ispartof><rights>The Author(s) 2009</rights><rights>2009 INIST-CNRS</rights><rights>Springer-Verlag 2009</rights><rights>The Author(s) 2009. This work is published under https://creativecommons.org/licenses/by-nc/2.0 (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-eda536c64112662d5be7592b4e61e9bc9c4aa23e2a2a060b9a12e788eb06c9513</citedby><cites>FETCH-LOGICAL-c486t-eda536c64112662d5be7592b4e61e9bc9c4aa23e2a2a060b9a12e788eb06c9513</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00109-009-0452-5$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00109-009-0452-5$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,315,782,786,887,27933,27934,41497,42566,51328</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21398507$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19255735$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Distelmaier, Felix</creatorcontrib><creatorcontrib>Visch, Henk-Jan</creatorcontrib><creatorcontrib>Smeitink, Jan A. M.</creatorcontrib><creatorcontrib>Mayatepek, Ertan</creatorcontrib><creatorcontrib>Koopman, Werner J. H.</creatorcontrib><creatorcontrib>Willems, Peter H. G. M.</creatorcontrib><title>The antioxidant Trolox restores mitochondrial membrane potential and Ca2+-stimulated ATP production in human complex I deficiency</title><title>Journal of molecular medicine (Berlin, Germany)</title><addtitle>J Mol Med</addtitle><addtitle>J Mol Med (Berl)</addtitle><description>Malfunction of mitochondrial complex I caused by nuclear gene mutations causes early-onset neurodegenerative diseases. Previous work using cultured fibroblasts of complex-I-deficient patients revealed elevated levels of reactive oxygen species (ROS) and reductions in both total Ca
2+
content of the endoplasmic reticulum (ER
Ca
) and bradykinin(Bk)-induced increases in cytosolic and mitochondrial free Ca
2+
([Ca
2+
]
C
; [Ca
2+
]
M
) and ATP ([ATP]
C
; [ATP]
M
) concentration. Here, we determined the mitochondrial membrane potential (Δ
ψ
) in patient skin fibroblasts and show significant correlations with cellular ROS levels and ER
Ca
, i.e., the less negative Δ
ψ
, the higher these levels and the lower ER
Ca
. Treatment with 6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox) normalized Δ
ψ
and Bk-induced increases in [Ca
2+
]
M
and [ATP]
M
. These effects were accompanied by an increase in ER
Ca
and Bk-induced increase in [Ca
2+
]
C
. Together, these results provide evidence for an integral role of increased ROS levels in complex I deficiency and point to the potential therapeutic value of antioxidant treatment.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Age</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bradykinin</subject><subject>Bradykinin - pharmacology</subject><subject>Calcium (mitochondrial)</subject><subject>Calcium (reticular)</subject><subject>Calcium - metabolism</subject><subject>Carboxylic acids</subject><subject>Cell Line</subject><subject>Chromans - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Electron transport chain</subject><subject>Electron Transport Complex I - deficiency</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum - drug effects</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Errors of metabolism</subject><subject>Fibroblasts</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>General aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medical sciences</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Metabolic diseases</subject><subject>Miscellaneous hereditary metabolic disorders</subject><subject>Mitochondria</subject><subject>Mitochondrial Diseases - metabolism</subject><subject>Mitochondrial Diseases - pathology</subject><subject>Mitochondrial Diseases - physiopathology</subject><subject>Molecular Medicine</subject><subject>NADH-ubiquinone oxidoreductase</subject><subject>Neurodegenerative diseases</subject><subject>Nitric oxide</subject><subject>Original Aricle</subject><subject>Oxidative stress</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Vitamin E</subject><issn>0946-2716</issn><issn>1432-1440</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kk2LFDEQhoMo7jj6A7xIUPQirUk6SXcuwjL4sbCgh_Ec0umanSzdyZh0L7NH_7k1zLCrwh4qgdRTb-qLkJecfeCMNR8LY5yZih1MKlGpR2TBZS0qLiV7TBbMSF2Jhusz8qyUa6QbZeRTcsaNUKqp1YL8Xm-BujiFtA893nSd05D2NEOZEh50DFPy2xT7HNxARxi77CLQXZoAo_DJxZ6unHhflSmM8-Am6On5-gfd5dTPHoUjDZFu59FF6tO4G2BPL2gPm-ADRH_7nDzZuKHAi9O9JD-_fF6vvlWX379erM4vKy9bPVXQO1VrryXnQmvRqw6wGNFJ0BxM542XzokahBOOadYZxwU0bQsd094oXi_Jp6Pubu5G6D2mn91gdzmMLt_a5IL91xPD1l6lGyvaWgtZo8C7k0BOv2bsjx1D8TAM2I80Fys411pxg-Cb_8DrNOeIxVmhatNIY1BzSV4_SPFGt1JLgRA_Qj6nUjJs7vLlzB52wB53wLKD4Q5YhTGv_i70PuI0dATengBXvBs2OFAfyh0neG1axRrkxJEr6IpXkO8zfPj3P4KIywQ</recordid><startdate>20090501</startdate><enddate>20090501</enddate><creator>Distelmaier, Felix</creator><creator>Visch, Henk-Jan</creator><creator>Smeitink, Jan A. M.</creator><creator>Mayatepek, Ertan</creator><creator>Koopman, Werner J. H.</creator><creator>Willems, Peter H. G. 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M. ; Mayatepek, Ertan ; Koopman, Werner J. H. ; Willems, Peter H. G. M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-eda536c64112662d5be7592b4e61e9bc9c4aa23e2a2a060b9a12e788eb06c9513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Age</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bradykinin</topic><topic>Bradykinin - pharmacology</topic><topic>Calcium (mitochondrial)</topic><topic>Calcium (reticular)</topic><topic>Calcium - metabolism</topic><topic>Carboxylic acids</topic><topic>Cell Line</topic><topic>Chromans - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Electron transport chain</topic><topic>Electron Transport Complex I - deficiency</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum - drug effects</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Errors of metabolism</topic><topic>Fibroblasts</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>General aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medical sciences</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Metabolic diseases</topic><topic>Miscellaneous hereditary metabolic disorders</topic><topic>Mitochondria</topic><topic>Mitochondrial Diseases - metabolism</topic><topic>Mitochondrial Diseases - pathology</topic><topic>Mitochondrial Diseases - physiopathology</topic><topic>Molecular Medicine</topic><topic>NADH-ubiquinone oxidoreductase</topic><topic>Neurodegenerative diseases</topic><topic>Nitric oxide</topic><topic>Original Aricle</topic><topic>Oxidative stress</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Vitamin E</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Distelmaier, Felix</creatorcontrib><creatorcontrib>Visch, Henk-Jan</creatorcontrib><creatorcontrib>Smeitink, Jan A. 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M.</au><au>Mayatepek, Ertan</au><au>Koopman, Werner J. H.</au><au>Willems, Peter H. G. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The antioxidant Trolox restores mitochondrial membrane potential and Ca2+-stimulated ATP production in human complex I deficiency</atitle><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle><stitle>J Mol Med</stitle><addtitle>J Mol Med (Berl)</addtitle><date>2009-05-01</date><risdate>2009</risdate><volume>87</volume><issue>5</issue><spage>515</spage><epage>522</epage><pages>515-522</pages><issn>0946-2716</issn><eissn>1432-1440</eissn><abstract>Malfunction of mitochondrial complex I caused by nuclear gene mutations causes early-onset neurodegenerative diseases. Previous work using cultured fibroblasts of complex-I-deficient patients revealed elevated levels of reactive oxygen species (ROS) and reductions in both total Ca
2+
content of the endoplasmic reticulum (ER
Ca
) and bradykinin(Bk)-induced increases in cytosolic and mitochondrial free Ca
2+
([Ca
2+
]
C
; [Ca
2+
]
M
) and ATP ([ATP]
C
; [ATP]
M
) concentration. Here, we determined the mitochondrial membrane potential (Δ
ψ
) in patient skin fibroblasts and show significant correlations with cellular ROS levels and ER
Ca
, i.e., the less negative Δ
ψ
, the higher these levels and the lower ER
Ca
. Treatment with 6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox) normalized Δ
ψ
and Bk-induced increases in [Ca
2+
]
M
and [ATP]
M
. These effects were accompanied by an increase in ER
Ca
and Bk-induced increase in [Ca
2+
]
C
. Together, these results provide evidence for an integral role of increased ROS levels in complex I deficiency and point to the potential therapeutic value of antioxidant treatment.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>19255735</pmid><doi>10.1007/s00109-009-0452-5</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0946-2716 |
| ispartof | Journal of molecular medicine (Berlin, Germany), 2009-05, Vol.87 (5), p.515-522 |
| issn | 0946-2716 1432-1440 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2836243 |
| source | MEDLINE; SpringerNature Journals |
| subjects | Adenosine Triphosphate - metabolism Age Antioxidants Antioxidants - pharmacology Biological and medical sciences Biomedical and Life Sciences Biomedicine Bradykinin Bradykinin - pharmacology Calcium (mitochondrial) Calcium (reticular) Calcium - metabolism Carboxylic acids Cell Line Chromans - pharmacology Dose-Response Relationship, Drug Electron transport chain Electron Transport Complex I - deficiency Endoplasmic reticulum Endoplasmic Reticulum - drug effects Endoplasmic Reticulum - metabolism Errors of metabolism Fibroblasts Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism General aspects Human Genetics Humans Internal Medicine Medical sciences Membrane potential Membrane Potential, Mitochondrial - drug effects Metabolic diseases Miscellaneous hereditary metabolic disorders Mitochondria Mitochondrial Diseases - metabolism Mitochondrial Diseases - pathology Mitochondrial Diseases - physiopathology Molecular Medicine NADH-ubiquinone oxidoreductase Neurodegenerative diseases Nitric oxide Original Aricle Oxidative stress Reactive oxygen species Reactive Oxygen Species - metabolism Vitamin E |
| title | The antioxidant Trolox restores mitochondrial membrane potential and Ca2+-stimulated ATP production in human complex I deficiency |
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