The effects of acetaldehyde and acrolein on muscle catabolism in C2 myotubes
Autor: | Dror Aizenbud, Abraham Z. Reznick, Sharon Kaisari, Oren Rom |
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Rok vydání: | 2013 |
Předmět: |
medicine.medical_specialty
Cell Survival Blotting Western Muscle Fibers Skeletal Acetaldehyde Real-Time Polymerase Chain Reaction medicine.disease_cause Biochemistry Cell Line Mice chemistry.chemical_compound Physiology (medical) Internal medicine Myosin medicine Animals Myocyte Acrolein Myogenesis Catabolism Skeletal muscle Endocrinology medicine.anatomical_structure chemistry Oxidative stress Signal Transduction |
Zdroj: | Free Radical Biology and Medicine. 65:190-200 |
ISSN: | 0891-5849 |
DOI: | 10.1016/j.freeradbiomed.2013.06.024 |
Popis: | The toxic aldehydes acetaldehyde and acrolein were previously suggested to damage skeletal muscle. Several conditions in which exposure to acetaldehyde and acrolein is increased were associated with muscle wasting and dysfunction. These include alcoholic myopathy, renal failure, oxidative stress, and inflammation. A main exogenous source of both acetaldehyde and acrolein is cigarette smoking, which was previously associated with increased muscle catabolism. Recently, we have shown that exposure of skeletal myotubes to cigarette smoke stimulated muscle catabolism via increased oxidative stress, activation of p38 MAPK, and upregulation of muscle-specific E3 ubiquitin ligases. In this study, we aimed to investigate the effects of acetaldehyde and acrolein on catabolism of skeletal muscle. Skeletal myotubes differentiated from the C2 myoblast cell line were exposed to acetaldehyde or acrolein and their effects on signaling pathways related to muscle catabolism were studied. Exposure of myotubes to acetaldehyde did not promote muscle catabolism. However, exposure to acrolein caused increased generation of free radicals, activation of p38 MAPK, upregulation of the muscle-specific E3 ligases atrogin-1 and MuRF1, degradation of myosin heavy chain, and atrophy of myotubes. Inhibition of p38 MAPK by SB203580 abolished acrolein-induced muscle catabolism. Our findings demonstrate that acrolein but not acetaldehyde activates a signaling cascade resulting in muscle catabolism in skeletal myotubes. Although within the limitations of an in vitro study, these findings indicate that acrolein may promote muscle wasting in conditions of increased exposure to this aldehyde. |
Databáze: | OpenAIRE |
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