کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738571 | 1046716 | 2011 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Increased mitochondrial matrix-directed superoxide production by fatty acid hydroperoxides in skeletal muscle mitochondria
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کلمات کلیدی
DIPPMPORCRFETROS - ROSHydrogen peroxide - آب اکسیژنهreverse electron transfer - انتقال الکترون معکوس استElectron paramagnetic resonance - تشدید پارامغناطیس الکترونEPR - تشدید پارامغناطیس الکترونOxidative stress - تنش اکسیداتیوRET - حقFree radicals - رادیکال آزادelectron transport chain - زنجیره انتقال الکترونSuperoxide - سوپر اکسیدMitochondria - میتوکندریاrespiratory control ratio - نسبت کنترل تنفسیFatty acid hydroperoxides - هیدروپراکسید اسید چربFatty acid hydroperoxide - هیدروپراکسید اسید چربETc - و غیرهReactive 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: Increased mitochondrial matrix-directed superoxide production by fatty acid hydroperoxides in skeletal muscle mitochondria Increased mitochondrial matrix-directed superoxide production by fatty acid hydroperoxides in skeletal muscle mitochondria](/preview/png/10738571.png)
چکیده انگلیسی
Previous studies have shown that muscle atrophy is associated with mitochondrial dysfunction and an increased rate of mitochondrial reactive oxygen species production. We recently demonstrated that fatty acid hydroperoxides (FA-OOHs) are significantly elevated in mitochondria isolated from atrophied muscles. The purpose of this study was to determine whether FA-OOHs can alter skeletal muscle mitochondrial function. We found that FA-OOHs (at low-micromolar concentrations) induce mitochondrial dysfunction assessed by a decrease in the rate of ATP production, oxygen consumption, and activity of respiratory chain complexes I and III. Using methods to distinguish superoxide release toward the matrix and toward the intermembrane space, we demonstrate that FA-OOHs significantly elevate oxidative stress in the mitochondrial matrix (and not the intermembrane space), with complex I as the major site of superoxide production (most probably from a site upstream of the ubiquinone binding site but downstream from the flavin binding site-the iron sulfur clusters). Our results are the first to indicate that FA-OOHs are important modulators of mitochondrial function and oxidative stress in skeletal muscle mitochondria and may play an important role in muscle atrophies that are associated with increased generation of FA-OOHs, e.g., denervation-induced muscle atrophy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 50, Issue 5, 1 March 2011, Pages 592-601
Journal: Free Radical Biology and Medicine - Volume 50, Issue 5, 1 March 2011, Pages 592-601
نویسندگان
Arunabh Bhattacharya, Michael Lustgarten, Yun Shi, Yuhong Liu, Youngmok C. Jang, Daniel Pulliam, Amanda L. Jernigan, Holly Van Remmen,