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The Metabolic Cart
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
But I would like to propose an even more fundamental reason for using the metabolic cart. It has to do with oxygen dynamics. Our pulmonary colleagues are thinking about oxygen in terms of lung function. Our cardiology colleagues are thinking about the pump’s role in oxygen delivery. The surgeons, about tissue perfusion. As Metabolists, we place our attention and consideration at the cellular level. We are looking at oxygen in terms of the production of energy derived from nutrients. We are looking at oxygen’s essential function: cellular respiration.
Asphyxia
Published in Kevin L. Erskine, Erica J. Armstrong, Water-Related Death Investigation, 2021
Cyanide acts as an asphyxiant at the cellular level by blocking the enzyme cytochrome oxidase present in all cells except mature red and white blood cells. This enzyme is partly necessary for cellular respiration and the production of a form of energy called adenosine triphosphate (ATP). The whole process of cellular respiration also requires oxygen, and thus its utilization by the cells is also impaired.
Biochemical and Metabolic Limitations to Athletic Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Ultimately, oxygen bioavailability is crucial at a biochemical level, as oxygen is the final electron acceptor in the process of cellular respiration. This allows oxidative phosphorylation and generation of adenosine triphosphate (ATP) (biochemical energy), whereas a deficient matching of oxygen delivery to the working mitochondria results in reliance on anaerobic respiration. Both aerobic and anaerobic respiration result in the build-up of biochemical intermediates, which limit performance. The biochemical and metabolic limits of athletic endurance and performance can be essentially boiled down to three abilities:The ability to match oxygen requirement to mitochondrial respiration in a temporally and spatially specific mannerThe ability to prevent accumulation of by-products of anaerobic and aerobic respiration, which are detrimental to performanceThe ability to efficiently metabolize readily available fuel or metabolites
Assessment of single-nucleotide variant discovery protocols in RNA-seq data from human cells exposed to mycotoxins
Published in Toxicology Mechanisms and Methods, 2023
M. Alonso-Garrido, M. Lozano, A. L. Riffo-Campos, G. Font, P. Vila-Donat, L. Manyes
In order to study BEA and ENB toxicological mechanisms, transcriptomics RNA-seq technique was previously applied using Jurkat cells. Those results showed how BEA and ENB individual exposures in vitro were responsible of mitochondrial damage and confirmed Tonshin et al. (2010) previous results (Escrivá et al 2018; Alonso-Garrido et al. 2018). When exposing cells to BEA, results showed 43 differentially expressed genes (DEGs) overlapped in the three studied concentrations. Several biological processes related to electron transport chain, oxidative phosphorylation, and cellular respiration were significantly altered (Escrivá et al. 2018). In the three ENB concentrations studied, same than for BEA, 245 differentially expressed genes were found overlapped and the biological processes related to nucleoside monophosphate metabolic process, respiratory chain complex, electron transport chain, oxidative phosphorylation and cellular respiration were the most perturbed (Alonso-Garrido et al. 2018). Moreover, after BEA and ENB mixture exposure at low levels, transcriptional changes in the respiratory chain were revealed too by qPCR. The expression profile found was slightly upregulated, the opposite effect than after individual and higher concentration exposures (Escrivá et al. 2018).
Effect of mycobacterial proteins that target mitochondria on the alveolar macrophages activation during Mycobacterium tuberculosis infection
Published in Experimental Lung Research, 2022
Iris Selene Paredes-González, Omar Emiliano Aparicio-Trejo, Octavio Ramos-Espinosa, Manuel Othoniel López-Torres, Milena Maya-Hoyos, Monserrat Mendoza-Trujillo, Alejandra Barrera-Rosales, Dulce Mata-Espinosa, Juan Carlos León-Contreras, José Pedraza-Chaverri, Clara Espitia, Rogelio Hernández-Pando
Mitochondria are involved in catabolic and anabolic reactions and are critical for respiratory ATP production. Interestingly, the organelle’s morphology is directly related to their function. The fusion and fission processes constantly modify the mitochondrial network. Fission exscinds a mitochondrial tubule into two, while fusion connects two tubules to form a longer one.15,16 Cycles of mitochondrial fusion and fission are essential for maintaining mitochondrial activity, influenced by metabolic and cellular signals, depending on the cell type and organism.17,18 Interconnected (fused) mitochondria are frequently present in cells with active mitochondrial respiration, while metabolically quiescent cells are characterized by presenting small fragmented (fission) mitochondria.19,20 Thus, part of the mitochondrial morphology can be represented by changes in cellular respiration.21
Detrimental effects of fructose on mitochondria in mouse motor neurons and on C. elegans healthspan
Published in Nutritional Neuroscience, 2022
Divya Lodha, Sudarshana Rajasekaran, Tamilselvan Jayavelu, Jamuna R. Subramaniam
Neurodegeneration is a major concern in the world today because of the increase in prevalence of the neurodegenerative diseases – Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and Amyotrophic Lateral Sclerosis (ALS). None of the neurons, including hippocampal neurons and motor neurons, and non –neuronal cells, astrocytes10 and other glial cells11, can escape the fate of degeneration. Mitochondrial impairment in ALS is well documented12. Mitochondria, responsible for nutrient metabolism and energy (ATP) production, are the hub of cellular respiration. Previous studies have shown that excessive amounts of fructose when metabolized, generate Reactive Oxygen Species (ROS) in the mitochondria of skeletal muscles, resulting in cell death13,14. This ROS generation and accumulation causes oxidative stress in the mitochondria of neurons15 and leads to neurodegeneration. But the direct effect of fructose on the mitochondrial function in neurons has not been studied in detail.