Investigation of oxidative phosphorylation in continuous cultures. A non-equilibrium thermodynamic approach to energy transduction for Escherichia coli in aerobic condition

2015 ◽  
Vol 40 (1) ◽  
Author(s):  
Mohazabeh Ghafuri ◽  
Mohsen Nosrati ◽  
Saman Hosseinkhani

AbstractAdenosine triphosphate (ATP) production in living cells is very important. Different researches have shown that in terms of mathematical modeling, the domain of these investigations is essentially restricted. Recently the thermodynamic models have been suggested for calculation of the efficiency of oxidative phosphorylation process and rate of energy loss in animal cells using chemiosmotic theory and non-equilibrium thermodynamics equations. In our previous work, we developed a mathematical model for mitochondria of animal cells. In this research, according to similarities between oxidative phosphorylation process in microorganisms and animal cells, Golfar's model was developed to predict the non-equilibrium thermodynamic behavior of the oxidative phosphorylation process for bacteria in aerobic condition. With this model the rate of energy loss,

Author(s):  
Mohazabeh Ghafuri ◽  
Bahareh Golfar ◽  
Mohsen Nosrati ◽  
Saman Hoseinkhani

AbstractThe process of ATP production is one of the most vital processes in living cells which happens with a high efficiency. Thermodynamic evaluation of this process and the factors involved in oxidative phosphorylation can provide a valuable guide for increasing the energy production efficiency in research and industry. Although energy transduction has been studied qualitatively in several researches, there are only few brief reviews based on mathematical models on this subject. In our previous work, we suggested a mathematical model for ATP production based on non-equilibrium thermodynamic principles. In the present study, based on the new discoveries on the respiratory chain of animal mitochondria, Golfar's model has been used to generate improved results for the efficiency of oxidative phosphorylation and the rate of energy loss. The results calculated from the modified coefficients for the proton pumps of the respiratory chain enzymes are closer to the experimental results and validate the model.


2019 ◽  
Vol 3 (5) ◽  
pp. 573-578 ◽  
Author(s):  
Kwanwoo Shin

Living cells naturally maintain a variety of metabolic reactions via energy conversion mechanisms that are coupled to proton transfer across cell membranes, thereby producing energy-rich compounds. Until now, researchers have been unable to maintain continuous biochemical reactions in artificially engineered cells, mainly due to the lack of mechanisms that generate energy-rich resources, such as adenosine triphosphate (ATP) and reduced nicotinamide adenine dinucleotide (NADH). If these metabolic activities in artificial cells are to be sustained, reliable energy transduction strategies must be realized. In this perspective, this article discusses the development of an artificially engineered cell containing a sustainable energy conversion process.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Weiwei Zou ◽  
Qixin Chen ◽  
Jesse Slone ◽  
Li Yang ◽  
Xiaoting Lou ◽  
...  

AbstractSLC25A46 mutations have been found to lead to mitochondrial hyper-fusion and reduced mitochondrial respiratory function, which results in optic atrophy, cerebellar atrophy, and other clinical symptoms of mitochondrial disease. However, it is generally believed that mitochondrial fusion is attributable to increased mitochondrial oxidative phosphorylation (OXPHOS), which is inconsistent with the decreased OXPHOS of highly-fused mitochondria observed in previous studies. In this paper, we have used the live-cell nanoscope to observe and quantify the structure of mitochondrial cristae, and the behavior of mitochondria and lysosomes in patient-derived SLC25A46 mutant fibroblasts. The results show that the cristae have been markedly damaged in the mutant fibroblasts, but there is no corresponding increase in mitophagy. This study suggests that severely damaged mitochondrial cristae might be the predominant cause of reduced OXPHOS in SLC25A46 mutant fibroblasts. This study demonstrates the utility of nanoscope-based imaging for realizing the sub-mitochondrial morphology, mitophagy and mitochondrial dynamics in living cells, which may be particularly valuable for the quick evaluation of pathogenesis of mitochondrial morphological abnormalities.


Children ◽  
2021 ◽  
Vol 8 (7) ◽  
pp. 532
Author(s):  
Dorota Wesół-Kucharska ◽  
Dariusz Rokicki ◽  
Aleksandra Jezela-Stanek

Mitochondrial diseases are a heterogeneous group of diseases resulting from energy deficit and reduced adenosine triphosphate (ATP) production due to impaired oxidative phosphorylation. The manifestation of mitochondrial disease is usually multi-organ. Epilepsy is one of the most common manifestations of diseases resulting from mitochondrial dysfunction, especially in children. The onset of epilepsy is associated with poor prognosis, while its treatment is very challenging, which further adversely affects the course of these disorders. Fortunately, our knowledge of mitochondrial diseases is still growing, which gives hope for patients to improve their condition in the future. The paper presents the pathophysiology, clinical picture and treatment options for epilepsy in patients with mitochondrial disease.


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