Reductive stress impairs myoblasts mitochondrial function and triggers mitochondrial hormesis

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 (mit...

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Vydáno v:	Biochimica et biophysica acta Ročník 1853; číslo 7; s. 1574 - 1585
Hlavní autoři:	Singh, François, Charles, Anne-Laure, Schlagowski, Anna-Isabel, Bouitbir, Jamal, Bonifacio, Annalisa, Piquard, François, Krähenbühl, Stephan, Geny, Bernard, Zoll, Joffrey
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Netherlands Elsevier B.V 01.07.2015
Témata:	Acetylcysteine - pharmacology Animals Apoptosis Cell Respiration - drug effects Cell Survival - drug effects Cytoprotection - drug effects Hormesis - drug effects Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Mitochondria - drug effects Mitochondria - metabolism Mitochondrial Turnover - drug effects Mitohormesis Myoblast Myoblasts - drug effects Myoblasts - metabolism N-acetylcysteine Oxidation-Reduction - drug effects Protective Agents - pharmacology Rats Reactive Oxygen Species - metabolism Reductive stress Statin Stress, Physiological - drug effects Time Factors Myoblast Reductive stress Statin Mitohormesis N-acetylcysteine Apoptosis
ISSN:	0167-4889, 0006-3002, 1879-2596
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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 H2O2 production. 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 failed to protect cells from the deleterious effects of statins. On the other hand, NAC pretreatment during one week triggered mitochondrial hormesis and reduced the deleterious effect of statins. These results contribute to a better understanding of the redox-dependant pathways linked to mitochondria, showing that reductive stress could trigger mitochondrial hormesis phenomenon. •NAC reductive stress impairs myoblasts mitochondrial respiratory chain function.•Mitochondrial malfunction leads to mitochondrial ROS production.•Mitochondrial oxidation triggers the mitochondrial hormesis phenomenon.•Mitochondrial hormesis protects myoblasts from the toxic effects of statins.
AbstractList	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 failed to protect cells from the deleterious effects of statins. On the other hand, NAC pretreatment during one week triggered mitochondrial hormesis and reduced the deleterious effect of statins. These results contribute to a better understanding of the redox-dependant pathways linked to mitochondria, showing that reductive stress could trigger mitochondrial hormesis phenomenon.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 failed to protect cells from the deleterious effects of statins. On the other hand, NAC pretreatment during one week triggered mitochondrial hormesis and reduced the deleterious effect of statins. These results contribute to a better understanding of the redox-dependant pathways linked to mitochondria, showing that reductive stress could trigger mitochondrial hormesis phenomenon. 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 H2O2 production. 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 failed to protect cells from the deleterious effects of statins. On the other hand, NAC pretreatment during one week triggered mitochondrial hormesis and reduced the deleterious effect of statins. These results contribute to a better understanding of the redox-dependant pathways linked to mitochondria, showing that reductive stress could trigger mitochondrial hormesis phenomenon. •NAC reductive stress impairs myoblasts mitochondrial respiratory chain function.•Mitochondrial malfunction leads to mitochondrial ROS production.•Mitochondrial oxidation triggers the mitochondrial hormesis phenomenon.•Mitochondrial hormesis protects myoblasts from the toxic effects of statins. 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 failed to protect cells from the deleterious effects of statins. On the other hand, NAC pretreatment during one week triggered mitochondrial hormesis and reduced the deleterious effect of statins. These results contribute to a better understanding of the redox-dependant pathways linked to mitochondria, showing that reductive stress could trigger mitochondrial hormesis phenomenon.
Author	Zoll, Joffrey Singh, François Charles, Anne-Laure Bonifacio, Annalisa Geny, Bernard Schlagowski, Anna-Isabel Piquard, François Krähenbühl, Stephan Bouitbir, Jamal
Author_xml	– sequence: 1 givenname: François surname: Singh fullname: Singh, François organization: University of Strasbourg, Faculty of Medicine, Fédération de Médecine Translationelle, EA 3072, 11 rue Humann, Strasbourg, France – sequence: 2 givenname: Anne-Laure surname: Charles fullname: Charles, Anne-Laure organization: University of Strasbourg, Faculty of Medicine, Fédération de Médecine Translationelle, EA 3072, 11 rue Humann, Strasbourg, France – sequence: 3 givenname: Anna-Isabel surname: Schlagowski fullname: Schlagowski, Anna-Isabel organization: University of Strasbourg, Faculty of Medicine, Fédération de Médecine Translationelle, EA 3072, 11 rue Humann, Strasbourg, France – sequence: 4 givenname: Jamal surname: Bouitbir fullname: Bouitbir, Jamal organization: Department of Clinical Pharmacology & Toxicology, Department of Biomedicine, University Hospital, Hebelstrasse 20, 4031 Basel, Switzerland – sequence: 5 givenname: Annalisa surname: Bonifacio fullname: Bonifacio, Annalisa organization: Department of Clinical Pharmacology & Toxicology, Department of Biomedicine, University Hospital, Hebelstrasse 20, 4031 Basel, Switzerland – sequence: 6 givenname: François surname: Piquard fullname: Piquard, François organization: University of Strasbourg, Faculty of Medicine, Fédération de Médecine Translationelle, EA 3072, 11 rue Humann, Strasbourg, France – sequence: 7 givenname: Stephan surname: Krähenbühl fullname: Krähenbühl, Stephan organization: Department of Clinical Pharmacology & Toxicology, Department of Biomedicine, University Hospital, Hebelstrasse 20, 4031 Basel, Switzerland – sequence: 8 givenname: Bernard surname: Geny fullname: Geny, Bernard organization: University of Strasbourg, Faculty of Medicine, Fédération de Médecine Translationelle, EA 3072, 11 rue Humann, Strasbourg, France – sequence: 9 givenname: Joffrey surname: Zoll fullname: Zoll, Joffrey email: zolljoffrey@yahoo.com organization: University of Strasbourg, Faculty of Medicine, Fédération de Médecine Translationelle, EA 3072, 11 rue Humann, Strasbourg, France
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Keywords	Myoblast Reductive stress Statin Mitohormesis N-acetylcysteine Apoptosis
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Snippet	Even though oxidative stress damage from excessive production of ROS is a well known phenomenon, the impact of reductive stress remains poorly understood. This...
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SubjectTerms	Acetylcysteine - pharmacology Animals Apoptosis Cell Respiration - drug effects Cell Survival - drug effects Cytoprotection - drug effects Hormesis - drug effects Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Mitochondria - drug effects Mitochondria - metabolism Mitochondrial Turnover - drug effects Mitohormesis Myoblast Myoblasts - drug effects Myoblasts - metabolism N-acetylcysteine Oxidation-Reduction - drug effects Protective Agents - pharmacology Rats Reactive Oxygen Species - metabolism Reductive stress Statin Stress, Physiological - drug effects Time Factors
Title	Reductive stress impairs myoblasts mitochondrial function and triggers mitochondrial hormesis
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