کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8271243 | 1534977 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The effects of acetaldehyde and acrolein on muscle catabolism in C2 myotubes
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کلمات کلیدی
GAPDHMyHCMuRF1RNSAtrogin-1NACGSHMAPK - MAPKN-acetylcysteine - N-استیل سیستئینp38 MAPK - P38 MAPKROS - ROSAcrolein - آکرولئین، آکرولینacetaldehyde - استالدهید Oxidative stress - تنش اکسیداتیوCigarette smoke - دود سیگارFree radicals - رادیکال آزادMyosin heavy chain - زنجیره سنگین میوزینE3 ubiquitin ligases - لیگاز ubiquitin E3mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenMuscle catabolism - کاتابولیسم عضلانیreduced glutathione - کاهش گلوتاتیونglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژنازreactive nitrogen species - گونه های واکنش پذیر نیتروژنReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: The effects of acetaldehyde and acrolein on muscle catabolism in C2 myotubes The effects of acetaldehyde and acrolein on muscle catabolism in C2 myotubes](/preview/png/8271243.png)
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 65, December 2013, Pages 190-200
Journal: Free Radical Biology and Medicine - Volume 65, December 2013, Pages 190-200
نویسندگان
Oren Rom, Sharon Kaisari, Dror Aizenbud, Abraham Z. Reznick,