大鼠骨骼肌线粒体代谢的实验性诱导缺陷。线粒体解偶联剂2,4-二硝基苯酚的生物学效应。
Experimentally induced defects of mitochondrial metabolism in rat skeletal muscle. Biological effects of the mitochondrial uncoupling agent 2,4-dinitrophenol.
作者信息
Byrne E, Hayes D J, Shoubridge E A, Morgan-Hughes J A, Clark J B
出版信息
Biochem J. 1985 Jul 1;229(1):101-8. doi: 10.1042/bj2290101.
Abstract
Infusion of dinitrophenol intra-arterially into rat hind limb caused an irreversible failure of isometric twitch tension and the induction of a severe progressive contracture. Metabolite analysis of muscle in which the twitch response had grossly fatigued revealed low levels of ATP and phosphocreatine together with lactate accumulation. Studies using 31P-n.m.r. confirmed the decrease in ATP and creatine phosphate concentrations and indicated a fall in intracellular pH. It is concluded that dinitrophenol-induced myopathy does not represent a good model for the human mitochondrial myopathic condition as has been previously suggested.
摘要
将二硝基苯酚动脉内注入大鼠后肢，会导致等长收缩张力不可逆丧失，并引发严重的进行性挛缩。对抽搐反应严重疲劳的肌肉进行代谢物分析发现，三磷酸腺苷（ATP）和磷酸肌酸水平较低，同时伴有乳酸积累。使用磷-31核磁共振（31P-n.m.r.）的研究证实了ATP和磷酸肌酸浓度的降低，并表明细胞内pH值下降。得出的结论是，二硝基苯酚诱导的肌病并不像之前所认为的那样，是人类线粒体肌病状况的良好模型。
相似文献
1
Experimentally induced defects of mitochondrial metabolism in rat skeletal muscle. Biological effects of the mitochondrial uncoupling agent 2,4-dinitrophenol.大鼠骨骼肌线粒体代谢的实验性诱导缺陷。线粒体解偶联剂2,4-二硝基苯酚的生物学效应。
Biochem J. 1985 Jul 1;229(1):101-8. doi: 10.1042/bj2290101.
2
Relationship of oxypurine release to contractile failure in dinitrophenol-treated rat skeletal muscle.二硝基苯酚处理的大鼠骨骼肌中氧嘌呤释放与收缩功能衰竭的关系。
Acta Physiol Scand. 1993 Nov;149(3):249-55. doi: 10.1111/j.1748-1716.1993.tb09620.x.
3
Experimentally induced defects of mitochondrial metabolism in rat skeletal muscle. Biological effects of the NADH: coenzyme Q reductase inhibitor diphenyleneiodonium.大鼠骨骼肌中线粒体代谢的实验性诱导缺陷。NADH：辅酶Q还原酶抑制剂二苯碘鎓的生物学效应。
Biochem J. 1985 Jul 1;229(1):109-17. doi: 10.1042/bj2290109.
4
Energy dependence of cytosolic enzyme efflux from rat skeletal muscle.大鼠骨骼肌胞质酶流出的能量依赖性
Clin Chim Acta. 1990 Aug 15;189(2):163-72. doi: 10.1016/0009-8981(90)90088-a.
5
Downregulation of uncoupling protein-3 in vivo is linked to changes in muscle mitochondrial energy metabolism as a result of capsiate administration.体内解偶联蛋白-3的下调与辣椒素给药后肌肉线粒体能量代谢的变化有关。
Am J Physiol Endocrinol Metab. 2007 May;292(5):E1474-82. doi: 10.1152/ajpendo.00292.2006. Epub 2007 Jan 30.
6
Metformin increases mitochondrial energy formation in L6 muscle cell cultures.二甲双胍可增加 L6 肌细胞培养物中线粒体的能量生成。
J Biol Chem. 2013 Jul 12;288(28):20369-77. doi: 10.1074/jbc.M113.482646. Epub 2013 May 29.
7
Morphogenesis of the mitochondrial alterations in muscle diseases.肌肉疾病中线粒体改变的形态发生。
J Neurol Sci. 1982 Jul;55(1):25-37. doi: 10.1016/0022-510x(82)90167-8.
8
Glutathione depletion during experimental damage to rat skeletal muscle and its relevance to Duchenne muscular dystrophy.实验性大鼠骨骼肌损伤过程中的谷胱甘肽耗竭及其与杜兴氏肌营养不良症的相关性。
Clin Sci (Lond). 1991 Jun;80(6):559-64. doi: 10.1042/cs0800559.
9
10
Force, relaxation and energy metabolism of rat soleus muscle during anaerobic contraction.大鼠比目鱼肌无氧收缩过程中的力量、松弛和能量代谢
Acta Physiol Scand. 1987 Jan;129(1):1-7. doi: 10.1111/j.1748-1716.1987.tb08033.x.
引用本文的文献
1
Direct real-time quantification of mitochondrial oxidative phosphorylation efficiency in permeabilized skeletal muscle myofibers.通透化骨骼肌肌纤维中线粒体氧化磷酸化效率的直接实时定量分析。
Am J Physiol Cell Physiol. 2016 Aug 1;311(2):C239-45. doi: 10.1152/ajpcell.00124.2016. Epub 2016 Jun 22.
2
Mitochondrial disease: a historical, biochemical, and London perspective.线粒体疾病：历史、生物化学及伦敦视角
Neurochem Res. 2004 Mar;29(3):483-91. doi: 10.1023/b:nere.0000014819.53972.b0.
3
Experimentally induced defects of mitochondrial metabolism in rat skeletal muscle. Biological effects of the NADH: coenzyme Q reductase inhibitor diphenyleneiodonium.大鼠骨骼肌中线粒体代谢的实验性诱导缺陷。NADH：辅酶Q还原酶抑制剂二苯碘鎓的生物学效应。
Biochem J. 1985 Jul 1;229(1):109-17. doi: 10.1042/bj2290109.
4
An investigation of arterial insufficiency in rat hindlimb. A combined 31P-n.m.r. and bloodflow study.大鼠后肢动脉供血不足的研究。31P核磁共振与血流联合研究。
Biochem J. 1986 Jun 1;236(2):461-7. doi: 10.1042/bj2360461.
5
Secondary mitochondrial pathology.
J Inherit Metab Dis. 1987;10 Suppl 1:98-104. doi: 10.1007/BF01812850.
本文引用的文献
1
2
A case of severe hypermetabolism of nonthyroid origin with a defect in the maintenance of mitochondrial respiratory control: a correlated clinical, biochemical, and morphological study.一例非甲状腺源性严重高代谢伴线粒体呼吸控制维持缺陷：一项临床、生化及形态学相关性研究。
J Clin Invest. 1962 Sep;41(9):1776-804. doi: 10.1172/JCI104637.
3
4
Effect of dinitrophenol on phosphorylation and bioelectric phenomena of excitable tissues.二硝基苯酚对可兴奋组织磷酸化及生物电现象的影响。
Am J Physiol. 1961 Mar;200:431-6. doi: 10.1152/ajplegacy.1961.200.3.431.
5
The behaviour of mammalian striated muscle in the presence of 2:4-dinitrophenol.哺乳动物横纹肌在2,4-二硝基苯酚存在下的行为。
J Physiol. 1955 Dec 29;130(3):585-600. doi: 10.1113/jphysiol.1955.sp005429.
6
Mapping of metabolites in whole animals by 31P NMR using surface coils.使用表面线圈通过31P核磁共振对全动物体内代谢物进行图谱分析。
Nature. 1980 Jan 10;283(5743):167-70. doi: 10.1038/283167a0.
7
Application of 31P-NMR spectroscopy to the study of striated muscle metabolism.31P-核磁共振波谱在横纹肌代谢研究中的应用。
Am J Physiol. 1982 Jan;242(1):C1-11. doi: 10.1152/ajpcell.1982.242.1.C1.
8
Mechanical relaxation rate and metabolism studied in fatiguing muscle by phosphorus nuclear magnetic resonance.通过磷核磁共振研究疲劳肌肉中的机械松弛率和代谢。
J Physiol. 1980 Feb;299:465-84. doi: 10.1113/jphysiol.1980.sp013137.
9
Fatigue in human metabolic myopathy.人类代谢性肌病中的疲劳
Ciba Found Symp. 1981;82:264-82. doi: 10.1002/9780470715420.ch16.
10
Shortage of chemical fuel as a cause of fatigue: studies by nuclear magnetic resonance and bicycle ergometry.化学燃料短缺作为疲劳原因的研究：通过核磁共振和自行车测力计进行的研究
Ciba Found Symp. 1981;82:102-19. doi: 10.1002/9780470715420.ch7.
Zotero 插件