Reconstitution of the Respiratory Chain

King, Tsoo E.

doi:10.1002/9780470122730.ch3

Cited by 13 publications

(6 citation statements)

References 133 publications

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“…The enzymatic activities of OXPHOS CII and CS and their protein levels were assayed following previously described protocols ( Faloona and Srere, 1969 ; King, 1966 ; Tzagoloff et al, 1967 ). CIV activity and levels were determined using the Complex IV Human Specific Activity Microplate Assay Kit (Mitosciences, Abcam ® ) according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

OXPHOS xenobiotics alter adipogenic differentiation at concentrations found in human blood

Llobet

Toivonen

Montoya

et al. 2015

Disease Models &Amp; Mechanisms

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Adipogenesis is accompanied by differentiation of adipose tissue-derived stem cells to adipocytes. As part of this differentiation, biogenesis of the oxidative phosphorylation system occurs. Many chemical compounds used in medicine, agriculture or other human activities affect oxidative phosphorylation function. Therefore, these xenobiotics could alter adipogenesis. We have analyzed the effects on adipocyte differentiation of some xenobiotics that act on the oxidative phosphorylation system. The tested concentrations have been previously reported in human blood. Our results show that pharmaceutical drugs that decrease mitochondrial DNA replication, such as nucleoside reverse transcriptase inhibitors, or inhibitors of mitochondrial protein synthesis, such as ribosomal antibiotics, diminish adipocyte differentiation and leptin secretion. By contrast, the environmental chemical pollutant tributyltin chloride, which inhibits the ATP synthase of the oxidative phosphorylation system, can promote adipocyte differentiation and leptin secretion, leading to obesity and metabolic syndrome as postulated by the obesogen hypothesis.

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Section: Methodsmentioning

confidence: 99%

OXPHOS xenobiotics alter adipogenic differentiation at concentrations found in human blood

Llobet

Toivonen

Montoya

et al. 2015

Disease Models &Amp; Mechanisms

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“…Activity of complex I + III was determined as antimycin A-and rotenone-sensitive fraction of total NADH:cytochrome c oxidoreductase, modified according to the method by Hatefi [26]. Complex II and complex II + III were measured, as described by King [27]. Complex III was measured, as described by Krahenbuhl et al [28].…”

Section: Photospectrometric Measurements Of Enzyme Activities Of Oxphosmentioning

confidence: 99%

Mitochondrial OXPHOS Functions in R1H Rhabdomyosarcoma and Skeletal Muscles of the Rat

Kuhnt

Pelz

et al. 2007

Neurochem Res

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The aim of the study was to determinate mitochondrial oxidative phosphorylation (OXPHOS) functions in rat rhabdomyosarcoma R1H (R1H) and rat skeletal muscles. For that purpose skinned fiber technique and multiple substrate inhibitor titration were adapted to tumor samples. In our animal tumor model (R1H) functional abnormalities of OXPHOS were found compared to skeletal muscles. In R1H the state 3 respiration of pyruvate + malate was decreased: 0.56 +/- 0.28 nmol O(2)/mg/min versus 2.32 +/- 1.19 nmol O(2)/mg/min, P < 0.001, whereas the state 3 respiration of succinate + rotenone was increased: 36 +/- 14% versus 19 +/- 11%, P < 0.001. In R1H the rotenone-insensitive respiration reached higher levels than the antimycin A-insensitive respiration, whereas in normal muscles the converse was observed. Additionally, the obvious difference between the CAT- and the antimycin A-independent respiration indicates an increased part of leak respiration in R1H. By now, the high feasibility of these techniques is appreciated for the investigation of muscles and prospectively for tumors, too.

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“…Chemiosmotic hypothesis has long established that electron transport system (ETS) creates a proton gradient across the mitochondrion's inner membrane, which is used to drive ATP synthesis (1,2). Before this, most were convinced of the role of ETS in ATP synthesis with a provision that it is achieved based on a direct relationship through substrate-level phosphorylation (3)(4)(5). Reactive oxygen species (ROS) at complexes I and III are the by-products of ETS, which can contribute to mitochondrial damage when in excess, and are part of the signaling sequence leading to apoptosis (6).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial transplantation in cardiomyocytes: foundation, methods, and outcomes

Pour

Hosseinian

Kheradvar

2021

American Journal of Physiology-Cell Physiology

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Mitochondrial Transplantation is emerging as a novel cellular biotherapy to alleviate mitochondrial damage and dysfunction. Mitochondria play a crucial role in establishing cellular homeostasis and providing cell with the energy necessary to accomplish its function. Owing to its endosymbiotic origin, mitochondria share many features with their bacterial ancestors. Unlike the nuclear DNA, which is packaged into nucleosomes and protected from adverse environmental effects; mitochondrial DNA are more prone to harsh environmental effects, in particular that of the reactive oxygen species (ROS). Mitochondrial damage and dysfunction are implicated in many diseases ranging from metabolic diseases to cardiovascular and neurodegenerative diseases, among others. While it was once thought that transplantation of mitochondria would not be possible due to its semi-autonomous nature and reliance on the nucleus, recent advances have shown that it is possible to transplant viable functional intact mitochondria from autologous, allogenic, and xenogeneic sources into different cell types. Moreover, current research suggests that the transplantation could positively modulate bioenergetics and improve disease outcome. Mitochondrial transplantation techniques and consequences of transplantation in cardiomyocytes are the theme of this review. First, we outline the different mitochondrial isolation and transfer techniques. Second, we detail the consequences of mitochondrial transplantation in the cardiovascular system, more specifically in the context of cardiomyopathies and ischemia. Lastly, we elaborate our vision on how mitochondrial transplantation may mitigate other cardiac conditions secondary to mitochondrial damage and dysfunction, such as atherosclerosis and ST-elevated myocardial infarction.

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Reconstitution of the Respiratory Chain

Cited by 13 publications

References 133 publications

OXPHOS xenobiotics alter adipogenic differentiation at concentrations found in human blood

OXPHOS xenobiotics alter adipogenic differentiation at concentrations found in human blood

Mitochondrial OXPHOS Functions in R1H Rhabdomyosarcoma and Skeletal Muscles of the Rat

Mitochondrial transplantation in cardiomyocytes: foundation, methods, and outcomes

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