Conditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity

机译：有条件地敲除针对IIB型骨骼肌纤维的Mn-SOD会增加氧化应激足以改变有氧运动能力

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In vitro studies of isolated skeletal muscle have shown that oxidative stress is limiting with respect to contractile function. Mitochondria are a potential source of muscle function-limiting oxidants. To test the hypothesis that skeletal muscle-specific mitochondrial oxidative stress is sufficient to limit muscle function, we bred mice expressing Cre recombinase driven by the promoter for the inhibitory subunit of troponin (TnIFast-iCre) with mice containing a floxed Sod2 (Sod2^fl/fl) allele. Mn-SOD activity was reduced by 82% in glycolytic (mainly type II) muscle fiber homogenates from young TnIFastCreSod2^fl/fl mice. Furthermore, Mn-SOD content was reduced by 70% only in type IIB muscle fibers. Aconitase activity was decreased by 56%, which suggests an increase in mitochondrial matrix superoxide. Mitochondrial superoxide release was elevated more than twofold by mitochondria isolated from glycolytic skeletal muscle in TnIFastCreSod2^fl/fl mice. In contrast, the rate of mitochondrial H2O2 production was reduced by 33%, and only during respiration with complex II substrate. F2-isoprostanes were increased by 36% in tibialis anterior muscles isolated from TnIFastCreSod2^fl/fl mice. Elevated glycolytic muscle-specific mitochondrial oxidative stress and damage in TnIFastCreSod2^fl/fl mice were associated with a decreased ability of the extensor digitorum longus and gastrocnemius muscles to produce contractile force as a function of time, whereas force production by the soleus muscle was unaffected. TnIFastCreSod2^fl/fl mice ran 55% less distance on a treadmill than wild-type mice. Collectively, these data suggest that elevated mitochondrial oxidative stress and damage in glycolytic muscle fibers are sufficient to reduce contractile muscle function and aerobic exercise capacity.

机译：离体骨骼肌的体外研究表明，氧化应激在收缩功能方面受到限制。线粒体是限制肌肉功能的氧化剂的潜在来源。为了检验骨骼肌特异性线粒体氧化应激足以限制肌肉功能的假设，我们将含有肌钙蛋白抑制亚单位（TnIFast-iCre）启动子驱动的表达Cre重组酶的小鼠与含有Sod2（Sod2 ^{fl / fl ）等位基因。在来自年轻的TnIFastCreSod2 ^{fl / fl 小鼠的糖酵解（主要是II型）肌肉纤维匀浆中，Mn-SOD活性降低了82％。此外，仅IIB型肌肉纤维的Mn-SOD含量降低了70％。乌头酸酶活性降低了56％，这表明线粒体基质超氧化物的增加。 TnIFastCreSod2 ^{fl / fl 小鼠中从糖酵解骨骼肌分离的线粒体将线粒体超氧化物的释放提高了两倍以上。相比之下，线粒体H2O2的产生率降低了33％，并且仅在使用复杂II底物进行呼吸时才发生。从TnIFastCreSod2 ^{fl / fl 小鼠中分离出的胫骨前肌中F2-异前列腺素增加了36％。 TnIFastCreSod2 ^{fl / fl 小鼠中糖酵解性肌肉特异性线粒体氧化应激和损伤升高与指长伸肌和腓肠肌产生随时间变化的收缩力的能力降低，而产生力比目鱼肌不受影响。与野生型小鼠相比，TnIFastCreSod2 ^{fl / fl 小鼠在跑步机上的跑距要少55％。总的来说，这些数据表明线粒体氧化应激的升高和糖酵解性肌纤维的损伤足以降低收缩性肌肉功能和有氧运动能力。}}}}}}

著录项

期刊名称 American Journal of Physiology - Cell Physiology
作者
Michael S. Lustgarten; Youngmok C. Jang; Yuhong Liu; Florian L. Muller; Wenbo Qi; Mark Steinhelper; Susan V. Brooks; Lisa Larkin; Takahiko Shimizu; Takuji Shirasawa; Linda M. McManus; Arunabh Bhattacharya; Arlan Richardson; Holly Van Remmen;
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作者单位

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年(卷),期 -1(297),6
年度 -1
页码 C1520–C1532
总页数 8
原文格式 PDF
正文语种
中图分类细胞生物学;人体生理学;
关键词
muscle function contractile function oxidative damage free radical;

机译：肌肉功能;收缩功能;氧化损伤;自由基;

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机译：冷驯化增加线粒体氧化能力而不诱导金鱼白骨骼肌中的线粒体解偶联冷驯化增加线粒体氧化能力而不诱导金鱼白骨骼肌中的线粒体解偶联
2. Scientific Opinion on the substantiation of health claims related to whey protein and increase in satiety leading to a reduction in energy intake (ID 425), contribution to the maintenance or achievement of a normal body weight (ID 1683), growth or maintenance of muscle mass (ID 418, 419, 423, 426, 427, 429, 4307), increase in lean body mass during energy restriction and resistance training (ID 421), reduction of body fat mass during energy restriction and resistance training (ID 420, 421), increase in muscle strength (ID 422, 429), increase in endurance capacity during the subsequent exercise bout after strenuous exercise (ID 428), skeletal muscle tissue repair (ID 428) and faster recovery from muscle fatigue after exercise (ID 423, 428, 431), pursuant to Article 13(1) of Regulation (EC) No 1924/2006 [J] . EFSA Journal . 2010,第10期

机译：关于证实乳清蛋白和增加饱腹感的健康主张的科学见解，导致能量摄入减少（ID 425），对维持或达到正常体重的贡献（ID 1683），肌肉生长或维持（ID 418、419、423、426、427、429、4307），能量限制和抵抗训练中的瘦体重增加（ID 421），能量限制和抵抗训练期间的体脂肪减少（ID 420、421），增加肌肉力量（ID 422、429），在剧烈运动后进行的后续运动中增加耐力（ID 428），骨骼肌组织修复（ID 428）和运动后从肌肉疲劳中更快恢复（ID 423、428）（431），根据（EC）1924/2006号条例第13（1）条
3. Enzymatic alterations in single type IIB skeletal muscle fibers with inactivity and exercise in 12- and 30-month-old rats. [J] . Groskreutz JJ, Thompson LV Aging clinical and experimental research . 2002,第5期

机译：在12和30个月大的大鼠中，IIB型单一骨骼肌纤维的酶学改变与运动和运动无关。
4. FAST RUNNING INCREASES EXPRESSION OF MATRIX METALLOPROTEINASE-2 IN TYPE IIB MUSCLE FIBERS [C] . Eli Carmeli, Miri Moas, Shannon Lennonc, IASTED International Conference on Biomechanics . 2005

机译：快速运行增加了IIB型肌纤维类型的基质金属蛋白酶-2的表达
5. Influence of exercise training on oxidative capacity and ultrastructural damage in skeletal muscles of aged horses. [D] . Kim, Jeong-su. 2002

机译：运动训练对老年马骨骼肌氧化能力和超微结构损伤的影响。
6. MECHANISMS FOR EXERCISE TRAINING-INDUCED INCREASES IN SKELETAL MUSCLE BLOOD FLOW CAPACITY: DIFFERENCES WITH INTERVAL SPRINT TRAINING VERSUS AEROBIC ENDURANCE TRAINING [O] . M.H. LAUGHLIN, B. ROSEGUINI -1

机译：运动引起的骨骼肌血流量增加的机制：间歇性训练与有氧耐力训练的差异
7. Conditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity [O] . Lustgarten, Michael S., Jang, Youngmok C., Liu, Yuhong, 2009

机译：有条件地敲除针对IIB型骨骼肌纤维的Mn-SOD会增加氧化应激，足以改变有氧运动能力

Conditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity

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