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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
Energy is generated from metabolic fuels (carbohydrates, fats and proteins) and from reduced molecules, which are oxidized to release energy. Oxidation involves removing electrons at high potential from the fuel molecules and transferring them to a lower potential, thus releasing energy. The removed electrons must be transferred to a suitable electron acceptor, which has to be transportable, soluble in water and generally available. In cells, oxygen is the electron acceptor used. Unfortunately, oxygen is too reactive to be the immediate oxidizing agent and, so, intermediates, nicotinamide adenine dinucleotide (NAD+) and flavin adenine dinucleotide (FAD), are employed as carriers of electrons between the metabolic pathways and the site of oxygen consumption in mitochondria. NAD+ and FAD are reduced by the major metabolic pathways (e.g. glycolysis and citric acid (Krebs) cycle) to NADH + H+ and FADH2 and carry electrons to the electron transport chain. In the electron transport chain, the electrons are transferred through a series of carriers of lower potential until they finally combine with oxygen to form water. In this process, energy is released, and ATP is formed from adenosine diphosphate (ADP) by the process of oxidative phosphorylation (Figure 65.1).
Emerging Potential of In Vitro Diagnostic Devices: Applications and Current Status
Published in Debarshi Kar Mahapatra, Sanjay Kumar Bharti, Medicinal Chemistry with Pharmaceutical Product Development, 2019
Swarnali Das Paul, Gunjan Jeswani
Major achievement of IVD’s has been gained by the invention of glucose monitoring devices. Glucose monitoring devices can be categorized into four types according to their principle of working. First generation devices were based on the amperometric detection of hydrogen peroxide which was expensive due to platinum electrode. The improvements were achieved with redox mediators, which are non-physiological electron acceptors. The electrons are carried to the working electrode from the enzymes easily by these mediators. Further specificity was attained by preparing reagent less biosensors based on direct transfer between the enzyme and the electrode without mediators. These are third generation glucose biosensors and preclude the disadvantage of toxic mediators.
Metabolism, nutrition, exercise and temperature regulation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2015
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Energy is generated from metabolic fuels (carbohydrates, fats and proteins) and from reduced molecules, which are oxidized to release energy. Oxidation involves removing electrons at high potential from the fuel molecules and transferring them to a lower potential, thus releasing energy. The removed electrons must be transferred to a suitable electron acceptor, which has to be transportable, soluble in water and generally available. In cells, oxygen is the electron acceptor used. Unfortunately, oxygen is too reactive to be the immediate oxidizing agent and so intermediates, nicotinamide adenine dinucleotide (NAD+) and flavin adenine dinucleotide (FAD), are employed as carriers of electrons between the metabolic pathways and the site of oxygen consumption in mitochondria. NAD+ and FAD are reduced by the major metabolic pathways (e.g. glycolysis and citric acid [Krebs] cycle) to NADH + H+ and FADH2 and carry electrons to the electron transport chain. In the electron transport chain, the electrons are transferred through a series of carriers of lower potential until they finally combine with oxygen to form water. In this process energy is released, and ATP is formed from adenosine diphosphate (ADP) by the process of oxidative phosphorylation (Figure 12.1).
Morin and isoquercitrin protect against ischemic neuronal injury by modulating signaling pathways and stimulating mitochondrial biogenesis
Published in Nutritional Neuroscience, 2023
Vanesa Carmona Mata, Joshua Goldberg
Based on our results, it is clear that flavonols can reverse the viability loss caused by IAA, but not those due to most OXPHOS inhibitors. Furthermore, the presence of inhibitors of complexes I (rotenone and DPI), III (antimycin A) or ATP synthase (oligomycin A) simultaneously with IAA makes the protective effect of flavonoids disappear, so we could suggest that both morin and isoquercitrin’s protective mechanism involves oxidative phosphorylation. Previous studies indicate that some flavonoids and other molecules structurally related to them interact with complex I and even modify its activity [13] although they do not influence directly the activity of complexes II and III [14]. According to the most recent reports, flavonoids could favor the mitochondrial electron flow through complex I by copying the action of coenzyme Q in its role as an electron acceptor, and then transfer the electrons to complex III. The electron acceptor role proposed could be explained by the presence of a carbonyl group at the C4 position of its pyrone ring, which resembles the reducible carbonyl present at the C4 position of the benzoquinone ring [13, 15]. This hypothesis would also explain why complex II inhibition did not interfere with the protective mechanism of the flavonoids. Furthermore, the ATP measurements demonstrated that flavonol increases ATP levels when glycolysis is inhibited, and mitochondrial inhibitors (but TTFA) abolish this effect, confirming that the beneficial effects of flavonols during chemical ischemia include favoring the generation of ATP through the mitochondrial oxidative phosphorylation pathway.
Pharmacology of apocynin: a natural acetophenone
Published in Drug Metabolism Reviews, 2021
Shreya R. Savla, Ankit P. Laddha, Yogesh A. Kulkarni
NADPH oxidase(s) (NOX) are multi-subunit enzymes whose primary function is to generate reactive oxygen species (ROS) (Laddha and Kulkarni 2020). They play a role in electron transport, utilizing a reduced NADPH as the electron donor and oxygen in its molecular state (O2) as the electron acceptor. This redox reaction results in the generation of superoxide (O2−) and hydrogen peroxide (H2O2) (Buvelot et al. 2019). In diseased conditions, the phagocytic leukocyte NOX generates ROS as a response to varying stimuli. Different organs of the human body show presence of different isoforms of NOX, which are NOX 1–5, DUOX 1 and 2 (Brown and Griendling 2009; Konior et al. 2014). NOX 1 expression has been mainly reported in the smooth muscles, endothelium, plasma membrane, and fibroblasts. However other tissues of NOX 1 expression include the placenta, uterus, and prostate (Buvelot et al. 2019). Owing to the predominance of its expression in macrophages and neutrophils, NOX 2 is also known as the ‘phagocyte NOX.’ However, the presence of NOX 2 has also been reported in other cell types such as skeletal muscle cells, endothelial cells, stem cells, microglia, hepatocytes, and cardiomyocytes (Buvelot et al. 2019). NOX 3 is predominantly expressed in the inner ear, including the vestibular and cochlear sensory epithelium. The wide expression of NOX 4 was found in the endoplasmic reticulum and perinuclear space of endothelial cells (Bánfi et al. 2004).
Lactoferrin for Mental Health: Neuro-Redox Regulation and Neuroprotective Effects across the Blood-Brain Barrier with Special Reference to Neuro-COVID-19
Published in Journal of Dietary Supplements, 2021
Sreus A. G. Naidu, Taylor C. Wallace, Kelvin J. A. Davies, A. Satyanarayan Naidu
SARS-CoV-2 binding to ACE2 receptors on brain capillary endothelia may disrupt the BBB and facilitate viral entry into the CNS. SARS-CoV-2 infection of brainstem neurons may disrupt cardio-respiratory regulation and cause severe pneumonia, and hypoxia-mediated brain damage (Steardo et al. 2020). Secondary mechanisms involve hypoxia (due to respiratory failure); as well as, various forms of encephalopathy, white matter damage, and abnormal blood clotting that may result in stroke. Cerebral microhemorrhage due to hypoxia has been recognized as a severe complication in Neuro-COVID-19, which triggers neuronal swelling, brain edema and damage to the CNS (Jaunmuktane et al. 2020). Oxygen levels play an essential role in cellular metabolism and O2 fluctuations are known to regulate the expression of several proteins, including hypoxia-inducible factor (HIF), the redox-sensitive transcription factor (Wang et al. 1995). Hypoxia lowers the terminal electron acceptor (O2) and increases the oxidative stress within a cell due to insufficient terminal electron acceptors, a prerequisite for oxidative phosphorylation. Stabilization of HIF is critical for survival of neurons during hypoxia. Accordingly, the stabilized HIF upregulates aerobic glycolysis to generate ATP to meet the metabolic energy demand (Semenza 2000).