脂溶耶氏菌呼吸小体和游离复合体I的动力学特性

IF 3.9 3区 生物学 Q2 CELL BIOLOGY
Giovanni García-Cruz, Mercedes Esparza-Perusquía, Alejandro Cruz-Cárdenas, Diana Cruz-Vilchis, Oscar Flores-Herrera
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引用次数: 0

摘要

线粒体是一种高度动态的细胞器,能够适应外部刺激和细胞的能量需求。线粒体是细胞ATP的主要来源,约占总量的90%,它促进呼吸复合物I、III2和IV结合成称为呼吸小体的超分子结构。这种超分子组织增强了线粒体内膜内的蛋白质密度,使能量产生均匀性。在这项研究中,我们研究了洋地黄苷溶解的呼吸小体和游离复合物I的亚基组成和动力学特征,以及它们在活性氧(ROS)产生中的作用。呼吸小体和游离复合体I的NADH:DBQ氧化还原酶活性相似。鱼藤酮、抗霉素A或氰化物抑制呼吸小体的呼吸作用,同时增加ROS的产生。测定呼吸小体活性的NADH氧化/氧还原比值为1.6±0.2。讨论了复合体之间的相互作用在呼吸小体功能中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Kinetic characterization of respirasomes and free complex I from Yarrowia lipolytica
The mitochondrion is a highly dynamic organelle capable of adapting to external stimuli and the energetic demands of the cell. As the primary source of cellular ATP, generating approximately 90 % of the total, mitochondrion facilitates the association of respiratory complexes I, III2, and IV into supramolecular structures called respirasomes. This supramolecular organization enhances protein density within the mitochondrial inner membrane, enabling homogenous energy production. In this study, we investigate the subunits composition and the kinetic characterization of digitonin-solubilized respirasomes and the free complex I from Yarrowia lipolytica as well as their role in reactive oxygen species (ROS) production. The NADH:DBQ oxido reductase activity of respirasome and free complex I was similar. Respiration by respirasome was inhibited with rotenone, antimycin A, or cyanide, simultaneously to an increase in the ROS production. A value of 1.6 ± 0.2 for the NADH oxidized/oxygen reduced ratio was determined for the respirasome activity. The role of interaction between complexes in the function of the respirasome is discussed.
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来源期刊
Mitochondrion
Mitochondrion 生物-细胞生物学
CiteScore
9.40
自引率
4.50%
发文量
86
审稿时长
13.6 weeks
期刊介绍: Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.
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