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Muscle and Nerve Histology
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
Within the matrix space, the enzymes facilitate the process of glycolysis to produce pyruvate and acetyl-CoA and help in the subsequent oxidation of these intermediates in the Krebs cycle. Called oxidative phosphorylation, this process is responsible for ATP production.
Fuel Metabolism in the Fetus
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
As a general rule, except in Brown Adipose Tissue, coupling between substrate oxidation and ADP phosphorylation in the mitochondria is due to an electrochemical gradient of protons, on either side of the mitochondrial membrane. During the transfer of electrons to oxygen, protons are extruded from the mitochondrial matrix. These protons cannot be readily reintroduced into the matrix, except in the part of the membrane where ATP-synthase is located. This results in ATP production (Figure 3a left side). Thus electron transfer from substrates to oxygen leads to stochiometric amounts of ATP (coupled oxidative phosphorylation). By contrast, in brown adipocyte mitochondria, the permeability of the inner membrane to protons is abnormally high and protons can readily cross the mitochondrial membrane. The free energy of substrates will therefore be released without ATP synthesis (uncoupled oxidative phosphorylation) and this will result in heat production22 (Figure 3a right side). The high permeability of the inner membrane to protons is related to a specific protein called the uncoupling protein or thermogenin. Interestingly, recent data indicate that thermogenin is present in late gestation in brown adipose tissue of fetuses from many species.25,26
Metabolism
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Oxidative phosphorylation is the primary mechanism by which ATP is produced in the body. Electrons are donated to the electron transport chain by the carriers NADH + H+ and FADH2 and are passed along a series of cytochromes until, at the end of the chain, they are accepted by oxygen to form water. The final cytochrome, which handles oxygen, is cytochrome a3 – the site of action of the poison cyanide. As they pass down the transport chain, the electrons release energy, which is used to form ATP – the process of oxidative phosphorylation. Mitochondria are therefore the primary site of cellular ATP production, carbon dioxide release and oxygen consumption.
Passive heat stress induces mitochondrial adaptations in skeletal muscle
Published in International Journal of Hyperthermia, 2023
Erik D. Marchant, W. Bradley Nelson, Robert D. Hyldahl, Jayson R. Gifford, Chad R. Hancock
Oxidative phosphorylation is the process by which the majority of ATP is produced in muscle cells. This process involves a series of redox reactions which result in electrons being transferred through protein complexes (referred to as complexes I-IV), ultimately reacting with molecular oxygen. These redox reactions are coupled with the transfer of protons (H+ ions) out of the matrix, resulting in an increase in membrane potential. Protons then flow down a gradient and drive the production of ATP, catalyzed by ATP synthase. In response to changes in energy demand, like muscle disuse or endurance exercise training, skeletal muscle is able to increase or decrease its capacity to perform oxidative phosphorylation via changes in the density of mitochondrial enzymes in existing mitochondria and/or alteration of mitochondrial volume [3,7].
Targeting ATP Synthase by Bedaquiline as a Therapeutic Strategy to Sensitize Ovarian Cancer to Cisplatin
Published in Nutrition and Cancer, 2023
Hongyan Zhu, Qitian Chen, Lingling Zhao, Pengchao Hu
Oxidative phosphorylation is a process that generate ATP through mitochondrial respiratory complexes I, II, III, IV and together with the F1F0 ATP synthase (complex V). Substantial evidence shows that oxidative phosphorylation is the main form of energy metabolism in some cancers, such as leukemia, ovarian cancer and renal cell carcinoma, and critically contributes to tumor progression and resistance (7–10). Specific agents targeting oxidative phosphorylation have been tested in pre-clinical and clinical settings to attenuate tumor progression, enhance chemosensitization and eradicate cancer stem cells in many cancers (5, 11). Bedaquiline is a FDA-approved antibiotic for treating pulmonary multidrug-resistant tuberculosis with the mechanism of action targeting ATP synthase and inducing energy crisis (12–14). Recent studies have revealed that bedaquiline decreased level of ATP synthase subunit, ATP5F1C in cancer cells, leading to mitochondrial respiration inhibition and ATP reduction, and subsequent growth arrest and inhibition of metastasis (15–17). Given the ability in inhibiting oxidative phosphorylation, we speculated that bedaquiline might be active against ovarian cancer. We thus systematically assessed the efficacy of bedaquiline using cell culturing and xenograft mouse models, and investigated the underlying mechanisms of bedaquiline focusing on oxidative phosphorylation.
A review of surgical management of progressive myogenic ptosis
Published in Orbit, 2023
Royce B. Park, Sruti S. Akella, Vinay K. Aakalu
Chronic progressive external ophthalmoplegia (CPEO) represents a group of neuromyopathic disorders with features of progressive bilateral ptosis and symmetric deficits in ocular motility.34 CPEO can occur in isolation (Isolated CPEO) or as part of a systemic disease entity with more widespread manifestations (CPEO plus).35 The disease is thought to be the result of genetic mutations associated with mitochondrial dysfunction and defective oxidative phosphorylation.36 Symptoms can present at any age,37 but typically begin by the third decade of life.9 The orbicularis oculi, levator palpebrae superioris, and extraocular muscles are preferentially affected, leading to ophthalmic findings of progressively worsening bilateral ptosis and symmetric ophthalmoparesis.34 This worsening ptosis will often force patients to compensate by adopting a chin-up head position (“backward head tilt”),7 and is usually the symptom that brings patients to seek care.34 By contrast, frontalis muscle function remains relatively preserved, and deep forehead furrows may be visible due to constant contraction to raise the lids.6