scholarly journals On the Mechanism of Respiratory Control

1965 ◽  
Vol 49 (1) ◽  
pp. 149-162 ◽  
Author(s):  
Ronald A. Butow ◽  
Efraim Racker
Keyword(s):  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Electron Flow ◽  
Respiratory Control ◽  
Model System ◽  
Physiological Significance ◽  
Tight Coupling ◽  
Submitochondrial Particles ◽  
Loosely Coupled ◽  
The Subject

Control of oxidation is the key mechanism in the regulation of energy metabolism. In glycolysis the oxidation of glyceraldehyde-3-phosphate is controlled by DPNH, which inhibits glyceraldehyde-3-phosphate dehydrogenase. In oxidative phosphorylation the inhibition of electron flow from DPNH to oxygen, called "respiratory control," is the subject of this paper. After a discussion of the physiological significance of the "tight coupling" between phosphorylation and oxidation, studies on "loosely coupled" submitochondrial particles are reported. These particles are capable of oxidative phosphorylation in the presence of a suitable phosphate acceptor system, but in contrast to controlled, intact mitochondria they oxidize DPNH in the absence of phosphate and ADP. The addition of o-phenanthroline to submitochondrial particles gives rise to an inhibition of respiration, which is partly reversed by phosphate and ADP or by dinitrophenol. The properties of this model system of respiratory control will be described.

Sulphide oxidation and oxidative phosphorylation in the mitochondria of the lugworm

1997 ◽  
Vol 200 (1) ◽  
pp. 83-92 ◽  
Author(s):  
S Vökel ◽  
M K Grieshaber
Keyword(s):  
Oxygen Consumption ◽  
Cytochrome C ◽  
Oxidative Phosphorylation ◽  
Cytochrome C Oxidase ◽  
Electron Flow ◽  
Respiratory Control ◽  
Sulphide Oxidation ◽  
Atp Production ◽  
Sulphide Concentration ◽  
Flow Through

Oxygen consumption, ATP production and cytochrome c oxidase activity of isolated mitochondria from body-wall tissue of Arenicola marina were measured as a function of sulphide concentration, and the effect of inhibitors of the respiratory complexes on these processes was determined. Concentrations of sulphide between 6 and 9 µmol l-1 induced oxygen consumption with a respiratory control ratio of 1.7. Production of ATP was stimulated by the addition of sulphide, reaching a maximal value of 67 nmol min-1 mg-1 protein at a sulphide concentration of 8 µmol l-1. Under these conditions, 1 mole of ATP was formed per mole of sulphide consumed. Higher concentrations of sulphide led to a decrease in ATP production until complete inhibition occurred at approximately 50 µmol l-1. The production of ATP with malate and succinate was stimulated by approximately 15 % in the presence of 4 µmol l-1 sulphide, but decreased at sulphide concentrations higher than 15­20 µmol l-1. Cytochrome c oxidase was also inhibited by sulphide, showing half-maximal inhibition at 1.5 µmol l-1 sulphide. Sulphide-induced ATP production was inhibited by antimycin, cyanide and oligomycin but not by rotenone or salicylhydroxamic acid. The present data indicate that sulphide oxidation is coupled to oxidative phosphorylation solely by electron flow through cytochrome c oxidase, whereas the alternative oxidase does not serve as a coupling site. At sulphide concentrations higher than 20 µmol l-1, oxidation of sulphide serves mainly as a detoxification process rather than as a source of energy.

scholarly journals Studies on the Energy Metabolism of Human Leukocytes

Blood ◽  
1967 ◽  
Vol 30 (2) ◽  
pp. 168-175 ◽  
Author(s):  
JOHN M. FOSTER ◽  
MARY L. TERRY ◽  
Harriet Gunther
Keyword(s):  
Energy Metabolism ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Respiratory Control ◽  
Endogenous Respiration ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Human Leukocytes ◽  
Endogenous Activity ◽  
Stimulation Of

Abstract 1. Oxidative phosphorylation has been studied in mitochondrial preparations from human leukocytes, using recently developed methods for homogenization, measuring respiration, and assaying for ATP. 2. Appreciable stimulation of both respiration and phosphorylation was limited to 3 substrates: succinate, malate, and α-glycerophosphate. The effects of other substrates were minimal. 3. The stimulating effects of these 3 substrates responded to inhibitors in a manner typical of mitochondrial oxidative phosphorylation. There was also considerable endogenous activity which, however, was insensitive to inhibitors. It is concluded the endogenous respiration and phosphorylation are not associated with electron transport. Subtracting their values from the data, P/O ratios consistent with good phosphorylation with the 3 substrates are obtained. 4. Studies with oligomycin and dinitrophenol suggest the presence of respiratory control. This indicates the mitochondria are intact. It is concluded that in the intact leukocyte the mitochondria are a major source of ATP.

scholarly journals Remodeling Pathway Control of Oxidative Phosphorylation by Temperature in the Heart

2017 ◽  
Author(s):  
Hélène Lemieux ◽  
Pierre U. Blier ◽  
Erich Gnaiger
Keyword(s):  
Oxidative Phosphorylation ◽  
Electron Flow ◽  
Respiratory Control ◽  
Muscle Performance ◽  
Mouse Heart ◽  
Strong Temperature Dependence ◽  
Excess Capacity ◽  
Respiratory Capacity ◽  
Disease Evolution ◽  
Mitochondrial Respiratory

AbstractThe capacity of mitochondrial oxidative phosphorylation (OXPHOS) and fuel substrate supply are key determinants of cardiac muscle performance. Although temperature exerts a strong effect on energy metabolism, until recently numerous respiratory studies of mammalian mitochondria have been carried out below physiological temperature, with substrates supporting submaximal respiratory capacity. We measured mitochondrial respiration as a function of temperature in permeabilized fibers from the left ventricle of the mouse heart. At 37 °C, OXPHOS capacity with electron entry through either Complex I or Complex II into the Q-junction was about half of respiratory capacity with the corresponding physiological substrate combination reconstituting tricarboxylic acid cycle function with convergent electron flow through the NADH&succinate (NS) pathway. When separating the component core mitochondrial pathways, the relative contribution of the NADH pathway increased with a decrease of temperature from 37 to 25 ºC. The additive effect of convergent electron flow has profound consequences for optimization of mitochondrial respiratory control. The apparent excess capacity of cytochrome c oxidase (CIV) was 0.7 above convergent NS-pathway capacity, but would be overestimated nearly 2-fold with respect to respiration restricted by provision of NADH-linked substrates only. The apparent excess capacity of CIV increased sharply at 4 °C, caused by a strong temperature dependence of and OXPHOS limitation by NADH-linked dehydrogenases. This mechanism of mitochondrial respiratory control in the hypothermic mammalian heart is comparable to the pattern in ectotherm species, pointing towards NADH-linked mt-matrix dehydrogenases and the phosphorylation system rather than electron transfer complexes as the primary drivers of thermal sensitivity at low temperature and likely modulators of temperature adaptation and acclimatization. Delineating the link between stress and remodeling of OXPHOS is critically important for improving our understanding of metabolic perturbations in disease evolution and cardiac protection. Temperature is not a trivial experimental parameter to consider when addressing these questions.

scholarly journals Senescence-associated changes in respiration and oxidative phosphorylation in primary human fibroblasts

2004 ◽  
Vol 380 (3) ◽  
pp. 919-928 ◽  
Author(s):  
Eveline HUTTER ◽  
Kathrin RENNER ◽  
Gerald PFISTER ◽  
Petra STÖCKL ◽  
Pidder JANSEN-DÜRR ◽  
...  
Keyword(s):  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Replicative Senescence ◽  
Citrate Synthase ◽  
Human Fibroblasts ◽  
Respiratory Control ◽  
Compensatory Mechanisms ◽  
Intact Cells ◽  
Atp Production ◽  
Human Diploid Fibroblasts

Limitation of lifespan in replicative senescence is related to oxidative stress, which is probably both the cause and consequence of impaired mitochondrial respiratory function. The respiration of senescent human diploid fibroblasts was analysed by highresolution respirometry. To rule out cell-cycle effects, proliferating and growth-arrested young fibroblasts were used as controls. Uncoupled respiration, as normalized to citrate synthase activity, remained unchanged, reflecting a constant capacity of the respiratory chain. Oligomycin-inhibited respiration, however, was significantly increased in mitochondria of senescent cells, indicating a lower coupling of electron transport with phosphorylation. In contrast, growth-arrested young fibroblasts exhibited a higher coupling state compared with proliferating controls. In intact cells, partial uncoupling may lead to either decreased oxidative ATP production or a compensatory increase in routine respiration. To distinguish between these alternatives, we subtracted oligomycin-inhibited respiration from routine respiration, which allowed us to determine the part of respiratory activity coupled with ATP production. Despite substantial differences in the respiratory control ratio, ranging from 4 to 11 in the different experimental groups, a fixed proportion of respiratory capacity was maintained for coupled oxidative phosphorylation in all the experimental groups. This finding indicates that the senescent cells fully compensate for increased proton leakage by enhanced electron-transport activity in the routine state. These results provide a new insight into age-associated defects in mitochondrial function and compensatory mechanisms in intact cells.

Internet of Things Service Provisioning Platform for Cross-Application Cooperation

2016 ◽  
Vol 13 (1) ◽  
pp. 1-22 ◽  
Author(s):  
Shuai Zhao ◽  
Bo Cheng ◽  
Le Yu ◽  
Shou-lu Hou ◽  
Yang Zhang ◽  
...  
Keyword(s):  
Internet Of Things ◽  
Large Scale ◽  
Physical Space ◽  
Service Provisioning ◽  
Problem Domain ◽  
Tight Coupling ◽  
User Requirement ◽  
Loosely Coupled ◽  
Heterogeneous Devices ◽  
On Demand

With the development of Internet of Things (IoT), large-scale of resources and applications atop them emerge. However, most of existing efforts are “silo” solutions, there is a tight-coupling between the device and the application. The paradigm for IoT and its corresponding infrastructure are required to move away from isolated solutions towards cooperative models. Recent works have focused on applying Service Oriented Architecture (SOA) to IoT service provisioning. Other than the traditional services of cyberspace which are oriented to a two-tuple problem domain, IoT services are faced with a three-tuple problem domain of user requirement, cyberspace and physical space. One challenge of existing works is lacking of efficient mechanism to on-demand provisioning the sensing information in a loosely-coupled, decentralized way and then dynamically coordinate the relevant services to rapidly respond to changes in the physical world. Another challenge is how to systematically and effectively access (plug) the heterogeneous devices without intrusive changing. This paper proposes a service provisioning platform which enables to access heterogeneous devices and expose device capabilities as light-weighted service, and presents an event-based message interaction mode to facilitate the asynchronous, on-demand sharing of sensing information in distributed, loosely-coupled IoT environment. It provides the basic infrastructure for IoT application pattern: inner-domain high-degree autonomy and inter-domain dynamic coordination. The practicability of platform is validated by experimental evaluations and a District Heating Control and Information System (DHCIS).

scholarly journals Increased Oxidative Phosphorylation Is Required for Stemness Maintenance in Liver Cancer Stem Cells from Hepatocellular Carcinoma Cell Line HCCLM3 Cells

2020 ◽  
Vol 21 (15) ◽  
pp. 5276 ◽  
Author(s):  
Ge Liu ◽  
Qing Luo ◽  
Hong Li ◽  
Qiuping Liu ◽  
Yang Ju ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Energy Metabolism ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Oxidative Phosphorylation ◽  
Carcinoma Cell ◽  
Hepatocellular Carcinoma Cell Line ◽  
Hepatocellular Carcinoma Cell ◽  
The Relationship

Cancer stem cells (CSCs) are considered to be the main cause of tumor recurrence, metastasis, and an unfavorable prognosis. Energy metabolism is closely associated with cell stemness. However, how the stemness of liver cancer stem cells (LCSCs) is regulated by metabolic/oxidative stress remains poorly understood. In this study, we compare the metabolic differences between LCSCs and the hepatocellular carcinoma cell line HCCLM3, and explore the relationship between metabolism and LCSC stemness. We found that LCSCs from the hepatocellular carcinoma cell HCCLM3 exhibited more robust glucose metabolism than HCCLM3, including glycolysis, oxidative phosphorylation (OXPHOS), and pyruvate produced by glycolysis entering mitochondria for OXPHOS. Moreover, 2-deoxy-D-glucose (2-DG) enhanced the LCSC stemness by upregulating OXPHOS. In contrast, Mdivi-1 reduced the levels of OXPHOS and weakened the stemness by inhibiting mitochondrial fission. Together, our findings clarify the relationship between energy metabolism and LCSC stemness and may provide theoretical guidance and potential therapeutic approaches for liver cancer.

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