MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle-aged men

Purpose Excess production of reactive oxygen species (ROS) from the mitochondria can promote mitochondrial dysfunction and has been implicated in the development of a range of chronic diseases. As such there is interest in whether mitochondrial-targeted antioxidant supplementation can attenuate mito...

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Veröffentlicht in:European journal of applied physiology 2020-07, Vol.120 (7), p.1657-1669
Hauptverfasser: Pham, Toan, MacRae, Caitlin L., Broome, Sophie C., D’souza, Randall F., Narang, Ravi, Wang, Hsiang W., Mori, Trevor A., Hickey, Anthony J. R., Mitchell, Cameron J., Merry, Troy L.
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container_end_page 1669
container_issue 7
container_start_page 1657
container_title European journal of applied physiology
container_volume 120
creator Pham, Toan
MacRae, Caitlin L.
Broome, Sophie C.
D’souza, Randall F.
Narang, Ravi
Wang, Hsiang W.
Mori, Trevor A.
Hickey, Anthony J. R.
Mitchell, Cameron J.
Merry, Troy L.
description Purpose Excess production of reactive oxygen species (ROS) from the mitochondria can promote mitochondrial dysfunction and has been implicated in the development of a range of chronic diseases. As such there is interest in whether mitochondrial-targeted antioxidant supplementation can attenuate mitochondrial-associated oxidative stress. We investigated the effect of MitoQ and CoQ10 supplementation on oxidative stress and skeletal muscle mitochondrial ROS levels and function in healthy middle-aged men. Methods Skeletal muscle and blood samples were collected from twenty men (50 ± 1 y) before and following six weeks of daily supplementation with MitoQ (20 mg) or CoQ10 (200 mg). High-resolution respirometry was used to determine mitochondrial respiration and H 2 O 2 levels, markers of mitochondrial mass and antioxidant defences were measured in muscle samples and oxidative stress markers in urine and blood samples. Results Both MitoQ and CoQ10 supplementation suppressed mitochondrial net H 2 O 2 levels during leak respiration, while MitoQ also elevated muscle catalase expression. However, neither supplement altered urine F 2 -isoprostanes nor plasma TBARS levels. Neither MitoQ nor CoQ10 supplementation had a significant impact on mitochondrial respiration or mitochondrial density markers (citrate synthase, mtDNA/nDNA, PPARGC1A , OXPHOS expression). Conclusion Our results suggest that neither MitoQ and CoQ10 supplements impact mitochondrial function, but both can mildly suppress mitochondrial ROS levels in healthy middle-aged men, with some indication that MitoQ may be more effective than CoQ10.
doi_str_mv 10.1007/s00421-020-04396-4
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High-resolution respirometry was used to determine mitochondrial respiration and H 2 O 2 levels, markers of mitochondrial mass and antioxidant defences were measured in muscle samples and oxidative stress markers in urine and blood samples. Results Both MitoQ and CoQ10 supplementation suppressed mitochondrial net H 2 O 2 levels during leak respiration, while MitoQ also elevated muscle catalase expression. However, neither supplement altered urine F 2 -isoprostanes nor plasma TBARS levels. Neither MitoQ nor CoQ10 supplementation had a significant impact on mitochondrial respiration or mitochondrial density markers (citrate synthase, mtDNA/nDNA, PPARGC1A , OXPHOS expression). Conclusion Our results suggest that neither MitoQ and CoQ10 supplements impact mitochondrial function, but both can mildly suppress mitochondrial ROS levels in healthy middle-aged men, with some indication that MitoQ may be more effective than CoQ10.</description><identifier>ISSN: 1439-6319</identifier><identifier>EISSN: 1439-6327</identifier><identifier>DOI: 10.1007/s00421-020-04396-4</identifier><identifier>PMID: 32458156</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adult ; Antioxidants ; Antioxidants - pharmacology ; Biomedical and Life Sciences ; Biomedicine ; Catalase ; Chronic illnesses ; Citrate synthase ; Dietary Supplements ; Human Physiology ; Humans ; Hydrogen peroxide ; Hydrogen Peroxide - metabolism ; Isoprostanes ; Male ; Middle age ; Middle Aged ; Mitochondria ; Mitochondria - metabolism ; Mitochondrial DNA ; Muscle, Skeletal - metabolism ; Musculoskeletal system ; Occupational Medicine/Industrial Medicine ; Original Article ; Oxidative stress ; Oxidative Stress - drug effects ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Respiration ; Skeletal muscle ; Sports Medicine ; Supplements ; Ubiquinone - analogs &amp; derivatives ; Ubiquinone - metabolism</subject><ispartof>European journal of applied physiology, 2020-07, Vol.120 (7), p.1657-1669</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020</rights><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-ae7e1654ba0154266cdcd5dace1b7be72574c5a137e70ea8ba5c28ddf42d578b3</citedby><cites>FETCH-LOGICAL-c428t-ae7e1654ba0154266cdcd5dace1b7be72574c5a137e70ea8ba5c28ddf42d578b3</cites><orcidid>0000-0001-8699-500X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00421-020-04396-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00421-020-04396-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32458156$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pham, Toan</creatorcontrib><creatorcontrib>MacRae, Caitlin L.</creatorcontrib><creatorcontrib>Broome, Sophie C.</creatorcontrib><creatorcontrib>D’souza, Randall F.</creatorcontrib><creatorcontrib>Narang, Ravi</creatorcontrib><creatorcontrib>Wang, Hsiang W.</creatorcontrib><creatorcontrib>Mori, Trevor A.</creatorcontrib><creatorcontrib>Hickey, Anthony J. R.</creatorcontrib><creatorcontrib>Mitchell, Cameron J.</creatorcontrib><creatorcontrib>Merry, Troy L.</creatorcontrib><title>MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle-aged men</title><title>European journal of applied physiology</title><addtitle>Eur J Appl Physiol</addtitle><addtitle>Eur J Appl Physiol</addtitle><description>Purpose Excess production of reactive oxygen species (ROS) from the mitochondria can promote mitochondrial dysfunction and has been implicated in the development of a range of chronic diseases. As such there is interest in whether mitochondrial-targeted antioxidant supplementation can attenuate mitochondrial-associated oxidative stress. We investigated the effect of MitoQ and CoQ10 supplementation on oxidative stress and skeletal muscle mitochondrial ROS levels and function in healthy middle-aged men. Methods Skeletal muscle and blood samples were collected from twenty men (50 ± 1 y) before and following six weeks of daily supplementation with MitoQ (20 mg) or CoQ10 (200 mg). High-resolution respirometry was used to determine mitochondrial respiration and H 2 O 2 levels, markers of mitochondrial mass and antioxidant defences were measured in muscle samples and oxidative stress markers in urine and blood samples. Results Both MitoQ and CoQ10 supplementation suppressed mitochondrial net H 2 O 2 levels during leak respiration, while MitoQ also elevated muscle catalase expression. However, neither supplement altered urine F 2 -isoprostanes nor plasma TBARS levels. Neither MitoQ nor CoQ10 supplementation had a significant impact on mitochondrial respiration or mitochondrial density markers (citrate synthase, mtDNA/nDNA, PPARGC1A , OXPHOS expression). 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R.</au><au>Mitchell, Cameron J.</au><au>Merry, Troy L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle-aged men</atitle><jtitle>European journal of applied physiology</jtitle><stitle>Eur J Appl Physiol</stitle><addtitle>Eur J Appl Physiol</addtitle><date>2020-07-01</date><risdate>2020</risdate><volume>120</volume><issue>7</issue><spage>1657</spage><epage>1669</epage><pages>1657-1669</pages><issn>1439-6319</issn><eissn>1439-6327</eissn><abstract>Purpose Excess production of reactive oxygen species (ROS) from the mitochondria can promote mitochondrial dysfunction and has been implicated in the development of a range of chronic diseases. As such there is interest in whether mitochondrial-targeted antioxidant supplementation can attenuate mitochondrial-associated oxidative stress. We investigated the effect of MitoQ and CoQ10 supplementation on oxidative stress and skeletal muscle mitochondrial ROS levels and function in healthy middle-aged men. Methods Skeletal muscle and blood samples were collected from twenty men (50 ± 1 y) before and following six weeks of daily supplementation with MitoQ (20 mg) or CoQ10 (200 mg). High-resolution respirometry was used to determine mitochondrial respiration and H 2 O 2 levels, markers of mitochondrial mass and antioxidant defences were measured in muscle samples and oxidative stress markers in urine and blood samples. Results Both MitoQ and CoQ10 supplementation suppressed mitochondrial net H 2 O 2 levels during leak respiration, while MitoQ also elevated muscle catalase expression. However, neither supplement altered urine F 2 -isoprostanes nor plasma TBARS levels. Neither MitoQ nor CoQ10 supplementation had a significant impact on mitochondrial respiration or mitochondrial density markers (citrate synthase, mtDNA/nDNA, PPARGC1A , OXPHOS expression). Conclusion Our results suggest that neither MitoQ and CoQ10 supplements impact mitochondrial function, but both can mildly suppress mitochondrial ROS levels in healthy middle-aged men, with some indication that MitoQ may be more effective than CoQ10.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>32458156</pmid><doi>10.1007/s00421-020-04396-4</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-8699-500X</orcidid></addata></record>
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subjects Adult
Antioxidants
Antioxidants - pharmacology
Biomedical and Life Sciences
Biomedicine
Catalase
Chronic illnesses
Citrate synthase
Dietary Supplements
Human Physiology
Humans
Hydrogen peroxide
Hydrogen Peroxide - metabolism
Isoprostanes
Male
Middle age
Middle Aged
Mitochondria
Mitochondria - metabolism
Mitochondrial DNA
Muscle, Skeletal - metabolism
Musculoskeletal system
Occupational Medicine/Industrial Medicine
Original Article
Oxidative stress
Oxidative Stress - drug effects
Reactive oxygen species
Reactive Oxygen Species - metabolism
Respiration
Skeletal muscle
Sports Medicine
Supplements
Ubiquinone - analogs & derivatives
Ubiquinone - metabolism
title MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle-aged men
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