Reductive stress impairs myoblasts mitochondrial function and triggers mitochondrial hormesis

Biochimica Et Biophysica Acta
François SinghJoffrey Zoll

Abstract

Even though oxidative stress damage from excessive production of ROS is a well known phenomenon, the impact of reductive stress remains poorly understood. This study tested the hypothesis that cellular reductive stress could lead to mitochondrial malfunction, triggering a mitochondrial hormesis (mitohormesis) phenomenon able to protect mitochondria from the deleterious effects of statins. We performed several in vitro experiments on L6 myoblasts and studied the effects of N-acetylcysteine (NAC) at different exposure times. Direct NAC exposure (1mM) led to reductive stress, impairing mitochondrial function by decreasing maximal mitochondrial respiration and increasing H₂O₂production. After 24h of incubation, the reactive oxygen species (ROS) production was increased. The resulting mitochondrial oxidation activated mitochondrial biogenesis pathways at the mRNA level. After one week of exposure, mitochondria were well-adapted as shown by the decrease of cellular ROS, the increase of mitochondrial content, as well as of the antioxidant capacities. Atorvastatin (ATO) exposure (100μM) for 24h increased ROS levels, reduced the percentage of live cells, and increased the total percentage of apoptotic cells. NAC exposure during 3days fa...Continue Reading

References

Mar 1, 1985·Archives of Biochemistry and Biophysics·J F TurrensA L Lehninger
Jan 1, 1981·Current Topics in Cellular Regulation·A Meister
Mar 4, 2000·Free Radical Biology & Medicine·R G Allen, M Tresini
Mar 14, 2001·American Journal of Physiology. Cell Physiology·U J DumaswalaD W Jacobsen
Mar 6, 2003·Neuroscience Letters·Christian RamakersAntoon F M Moorman
Jul 4, 2003·The Journal of Biological Chemistry·Qun ChenEdward J Lesnefsky
Oct 1, 1964·Diseases of the Chest·I L BERNSTEIN, R W AUSDENMOORE
Oct 17, 2003·The Journal of Physiology·Julio F Turrens
May 18, 2004·The Journal of Clinical Investigation·Mitsuhiro WatanabeJohan Auwerx
Aug 2, 2005·Cell Metabolism·William G Kaelin
Oct 28, 2005·American Journal of Physiology. Cell Physiology·Ethan J Anderson, P Darrell Neufer
Dec 6, 2005·Journal of Cellular Biochemistry·Richard C Scarpulla
Oct 19, 2006·Cardiovascular Research·Renée Ventura-ClapierXavier Bigard
Dec 22, 2006·American Journal of Physiology. Cell Physiology·Leanne WilsonReza Halse
Dec 27, 2006·Free Radical Biology & Medicine·Navdeep S Chandel, G R Scott Budinger
Apr 17, 2007·Molecular Cell·Elizabeth A VealBrian A Morgan
Feb 5, 2008·Current Opinion in Pharmacology·Daniel R Schwartz, Michael N Sack
Mar 5, 2008·Cell Metabolism·David Gems, Linda Partridge
Apr 24, 2008·Cardiovascular Research·Renée Ventura-ClapierVladimir Veksler
Jun 24, 2008·The American Journal of Cardiology·Steven R Steinhubl
Nov 26, 2008·Circulation Research·Motoaki Sano, Keiichi Fukuda
Feb 23, 2010·Biochemical and Biophysical Research Communications·John M C Gutteridge, Barry Halliwell
Nov 19, 2010·Medicine and Science in Sports and Exercise·Natalie A StrobelGlenn D Wadley
Jul 1, 2011·Medicine and Science in Sports and Exercise·Frédéric N DaussinRuddy Richard
Oct 21, 2011·Antioxidants & Redox Signaling·David PimentelMarkus Michael Bachschmid
Dec 17, 2011·Journal of Signal Transduction·Elena Barbieri, Piero Sestili
Dec 29, 2011·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Huali ZhangIvor J Benjamin
Mar 1, 2012·Therapeutic Advances in Respiratory Disease·Anna M Sadowska
Jan 1, 2011·Polish Journal of Veterinary Sciences·I Otrocka-Domagała

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Citations

Sep 29, 2015·Antioxidants & Redox Signaling·Jamal BouitbirJoffrey Zoll
Sep 16, 2016·Cell Cycle·Marta Markiewicz-Potoczny, David Lydall
Jan 23, 2017·Free Radical Biology & Medicine·Motohiro NishidaTakaaki Akaike
Jun 27, 2017·Antioxidants & Redox Signaling·Wusheng XiaoJoseph Loscalzo
Oct 6, 2017·International Journal of Molecular Sciences·Israel Pérez-TorresMaría Esther Rubio-Ruiz
Dec 19, 2018·The Journal of Biological Chemistry·Eduard PerisIngrid Wernstedt Asterholm
Jun 21, 2019·Antioxidants & Redox Signaling·Wusheng Xiao, Joseph Loscalzo
Dec 10, 2019·FEMS Yeast Research·Ian W Dawes, Gabriel G Perrone
Dec 5, 2018·Archives of Toxicology·François SinghJamal Bouitbir
Jun 23, 2020·Oxidative Medicine and Cellular Longevity·Wei-Xing MaLiang-Jun Yan
Jul 16, 2020·Antioxidants·Maria Cristina Budani, Gian Mario Tiboni
Jun 16, 2017·Neural Regeneration Research·David Fisher, Shireen Mentor
May 23, 2015·American Journal of Physiology. Cell Physiology·Vladimir L KolossovH Rex Gaskins
Jan 8, 2021·Molecular Neurobiology·G MorrisB K Puri
May 21, 2017·Toxicology in Vitro : an International Journal Published in Association with BIBRA·David GrünigStephan Krähenbühl
Mar 21, 2021·Free Radical Biology & Medicine·Changhai TianIrving H Zucker
Jan 10, 2020·Biochimica Et Biophysica Acta. Molecular Cell Research·Natalia M GalignianaGraciela Piwien-Pilipuk
Apr 4, 2021·International Journal of Molecular Sciences·Alessandra FraternaleRita Crinelli
Jul 17, 2021·Nature Communications·Ivan GusarovEvgeny Nudler
Jul 27, 2021·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Fereshteh RadmaneshAli Shalizar-Jalali
May 13, 2019·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Chuanmei XieZhenyi Zhao

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