The discovery of oxidative phosphorylation: a conceptual off-shoot from the study of glycolysis

Qc, John Prebble

doi:10.1016/j.shpsc.2010.07.014

Cited by 14 publications

(16 citation statements)

References 66 publications

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“…The derivation of oxidative metabolism research from studies of lactate/glycolysis are clearly discernible from Meyerhof's studies in the 1920s. This is evidenced by his proposition that respiratory oxidation in some unknown process provided the energy for glycogen resynthesis from lactate in isolated muscles following contractions (Meyerhof, 1927; Prebble, 2010). This of course followed from the classic paper of Fletcher and Hopkins in 1907 (Fletcher & Hopkins, 1907) which reported the disappearance of lactate in the presence of O 2 in previously stimulated muscles.…”

Section: Brief History Of Glycolytic and Oxidative Metabolismmentioning

confidence: 99%

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Mitochondrial lactate metabolism: history and implications for exercise and disease

Glancy

Kane

Kavazis

et al. 2020

The Journal of Physiology

127

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Mitochondrial structures were probably observed microscopically in the 1840s, but the idea of oxidative phosphorylation (OXPHOS) within mitochondria did not appear until the 1930s. The foundation for research into energetics arose from Meyerhof's experiments on oxidation of lactate in isolated muscles recovering from electrical contractions in an O2 atmosphere. Today, we know that mitochondria are actually reticula and that the energy released from electron pairs being passed along the electron transport chain from NADH to O2 generates a membrane potential and pH gradient of protons that can enter the molecular machine of ATP synthase to resynthesize ATP. Lactate stands at the crossroads of glycolytic and oxidative energy metabolism. Based on reported research and our own modelling in silico, we contend that lactate is not directly oxidized in the mitochondrial matrix. Instead, the interim glycolytic products (pyruvate and NADH) are held in cytosolic equilibrium with the products of the lactate dehydrogenase (LDH) reaction and the intermediates of the malate‐aspartate and glycerol 3‐phosphate shuttles. This equilibrium supplies the glycolytic products to the mitochondrial matrix for OXPHOS. LDH in the mitochondrial matrix is not compatible with the cytoplasmic/matrix redox gradient; its presence would drain matrix reducing power and substantially dissipate the proton motive force. OXPHOS requires O2 as the final electron acceptor, but O2 supply is sufficient in most situations, including exercise and often acute illness. Recent studies suggest that atmospheric normoxia may constitute a cellular hyperoxia in mitochondrial disease. As research proceeds appropriate oxygenation levels should be carefully considered.

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Section: Brief History Of Glycolytic and Oxidative Metabolismmentioning

confidence: 99%

“…2018). Prebble (2010) offers insights and interpretations into these discoveries and Needham (1971) provides details of the studies that revealed the entirety of these pathways. A succinct overview of these advances follows.…”

Section: Brief History Of Glycolytic and Oxidative Metabolismmentioning

confidence: 99%

Mitochondrial lactate metabolism: history and implications for exercise and disease

Glancy

Kane

Kavazis

et al. 2020

The Journal of Physiology

127

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“…Although the process of oxygen utilization through mitochondrial oxidative phosphorylation was discovered over a century ago (31), aspects governing its control are still being elucidated. To this end, recent studies demonstrate that signal transducer and activator of transcription 3 (STAT3), which has historically been considered for its cytokine-induced nuclear transcriptional activity (21), can localize to the mitochondria in a number of tissues and cells, including heart, liver, brain, kidney (42,45), Pro-B cells (45), astrocytes (34), and Rastransformed mouse embryonic fibroblasts (MEFS) (12).…”

Section: Introductionmentioning

confidence: 99%

Skeletal muscle mitochondrial function and exercise capacity are not impaired in mice with knockout of STAT3

Dent

Hetrick

Tahvilian

et al. 2019

Journal of Applied Physiology

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Signal transducer and activator of transcription 3 (STAT3) was recently found to be localized to mitochondria in a number of tissues and cell types, where it modulates oxidative phosphorylation via interactions with the electron transport proteins, complex I and complex II. Skeletal muscle is densely populated with mitochondria although whether STAT3 contributes to skeletal muscle oxidative capacity is unknown. In the present study, we sought to elucidate the contribution of STAT3 to mitochondrial and skeletal muscle function by studying mice with muscle-specific knockout of STAT3 (mKO). First, we developed a novel flow cytometry-based approach to confirm that STAT3 is present in skeletal muscle mitochondria. However, contrary to findings in other tissue types, complex I and complex II activity and maximal mitochondrial respiratory capacity in skeletal muscle were comparable between mKO mice and floxed/wild-type littermates. Moreover, there were no genotype differences in endurance exercise performance, skeletal muscle force-generating capacity, or the adaptive response of skeletal muscle to voluntary wheel running. Collectively, although we confirm the presence of STAT3 in skeletal muscle mitochondria, our data establish that STAT3 is dispensable for mitochondrial and physiological function in skeletal muscle. NEW & NOTEWORTHY Whether signal transducer and activator of transcription 3 (STAT3) can regulate the activity of complex I and II of the electron transport chain and mitochondrial oxidative capacity in skeletal muscle, as it can in other tissues, is unknown. By using a mouse model lacking STAT3 in muscle, we demonstrate that skeletal muscle mitochondrial and physiological function, both in vivo and ex vivo, is not impacted by the loss of STAT3.

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“…The reconversion of photosynthetically-derived ATP back to ADP provides the rubisco enzymes in plants with chemical energy to link carbon dioxide with water to form glucose and to release oxygen [7]. The linking of carbon dioxide to water is reversible using a different set of enzymes in an oxygen requiring process called oxidative phosphorylation [8]. The oxidation of glucose in plants, as well as animals, occurs in the cells' mitochondria [9] and yields ATP from ADP for numerous cellular activities [10].…”

Section: Introductionmentioning

confidence: 99%

Hyper-Excitability Followed by Functional Quiescence in Neuronal Cells Caused by Insufficient Cellular Energy (ICE): Treatable by Enhancing the Alternative Cellular Energy (ACE) Pathway

Martin¹

2017

WJNS

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Living organisms derive energy for cellular activities through three primary mechanisms. The first is photosynthesis, which is restricted to plants and certain bacteria. It uses energy in sunlight to combine carbon dioxide with water to form carbohydrates plus oxygen. The second is chemical energy, which is obtainable by all organisms from the cellular metabolism of carbohydrates and other organic molecules. The third mechanism of obtaining cellular energy is the alternative cellular energy (ACE) pathway. The ACE pathway is expressed as an added dynamic (kinetic) quality of the body's fluids. It results from the absorption of an environmental force termed KELEA (kinetic energy limiting electrostatic attraction). The fundamental role of KELEA is presumably to prevent the fusion and annihilation of electrostatically attracted opposing electrical charges. KELEA can loosen the hydrogen bonding between fluid molecules. KELEA benefits living organisms in part by enabling more efficient biochemical reactions. Cells require a minimal amount of energy to remain viable. Additional energy is required to undertake specialized cellular functions. Illnesses result if cells have insufficient cellular energy (ICE) for their specialized functions. Since KELEA is attracted to separated electrical charges, it is presumably attracted to the electrical charges comprising the membrane potential of cells. It is proposed that the depolarization of neuronal cells leads to the partial release of KELEA for use by the depolarized cell and as a contribution to the overall activation of the body's fluids. Many brain illnesses currently attributed to cellular neurodegeneration are explainable as neuronal cells' adaptations to ICE. The adaptations likely comprise initial hyper-excitability to obtain additional KELEA, followed by functional quiescence prior How to cite this paper: Martinto actual neuronal cell death. Clinical recovery during both the hyper-excitable and hypoactive phases is potentially achievable by enhancing the ACE pathway. Furthermore, among the restored specialized functions of quiescent neuronal cells may be the capacity to again attract KELEA, leading to sustainable recovery. The opportunity exists for extended clinical trials involving the ACE pathway in neurological and psychiatric illnesses.

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The discovery of oxidative phosphorylation: a conceptual off-shoot from the study of glycolysis

Cited by 14 publications

References 66 publications

Mitochondrial lactate metabolism: history and implications for exercise and disease

Mitochondrial lactate metabolism: history and implications for exercise and disease

Skeletal muscle mitochondrial function and exercise capacity are not impaired in mice with knockout of STAT3

Hyper-Excitability Followed by Functional Quiescence in Neuronal Cells Caused by Insufficient Cellular Energy (ICE): Treatable by Enhancing the Alternative Cellular Energy (ACE) Pathway

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