Respiratory System
David Sturgeon in Introduction to Anatomy and Physiology for Healthcare Students, 2018
Everybody knows that breathing is an essential requirement for good health and that failure to do so will, in a relatively short period of time, lead to asphyxia and death. However, it is important to recognise that there are three types of respiration occurring simultaneously at different locations within the human body: external, internal and cellular respiration. External respiration describes the process of gaseous exchange that takes place in the lungs. That is to say: oxygen (O2) from the atmosphere is exchanged for carbon dioxide (CO2) from the pulmonary blood supply (capillaries). Internal respiration refers to the process by which oxygen in the blood is made available to the cells and exchanged for carbon dioxide across the plasma membrane. Lastly, cellular respiration refers to the production of energy (ATP) within the cells (by oxidative metabolism) described in Chapter 2 (glucose + O2→ ATP + CO2+ H2O). All three processes are absolutely essential for health and take place at the same time. In general terms, external and internal respiration ensure that the blood is provided with a constant supply of oxygen for cellular metabolism and provide a means for the excretion of carbon dioxide. However, before we look at how the respiratory tract facilitates this process, it is necessary to first consider the air that we breathe.
Experimental studies with antioxidants
Ronald R. Watson in NUTRIENTS and FOODS in AIDS, 2017
These are phenolic fat-soluble antioxidants of which the protype member is Coenzyme Q10 (CoQ10). The latter is an important component of the electron transport chain within the mitochondria involved in cellular respiration and ATP generation. Its reduced form (ubiquinol 10) is a powerful membrane antioxidant that can scavenge peroxyl radicals after lipid peroxidation has been initiated. In the inner mitochondrial membrane, Coenzyme Q10 and vitamin E function in a complementary fashion to reduce free radical production.78 Coenzyme Q10 has been extensively studied in patients with heart disease and shown to have benefits in improving cardiac function and survival.79,80 It has been reported by Folkers and colleagues that patients with HIV infection, ARC, and AIDS have decreased levels of CoQ10 in blood compared to healthy subjects.81 The same research group published findings from a small study in healthy volunteers showing improvement in T4/T8 ratios following supplementation with 100 mg/d of CoQ10 over a 2-month period.78 Based on these observations it has been postulated that CoQ10 may have value in ARC or AIDS patients with low T4/T8 ratios. This proposal needs to be put to experimental test.
Liver, GI and Metabolism
Sarah Armstrong, Barry Clifton, Lionel Davis in Primary FRCA in a Box, 2019
Final metabolic pathway of cellular respiration that occurs on inner mitochondrial membraneTendency for electrons to be transferred from activated carriers (e.g. NADH – ‘loaded’ during CAC) to cascade of lower potential carriers (electron transfer chain)Process involves many enzymes, including those of cytochrome oxidase systemProton pumps in inner mitochondrial membrane are activated by flow of electrons through them pumping H+ ions out and creating gradient that generates ATP (via ATP synthase) by driving H+ ions back across inner membraneRequires oxygen and results in liberation of 30 ATP molecules per molecule of glucose
Manganese dioxide nanosheets induce mitochondrial toxicity in fish gill epithelial cells
Published in Nanotoxicology, 2021
Cynthia L. Browning, Allen Green, Evan P. Gray, Robert Hurt, Agnes B. Kane
One major consequence of impaired mitochondrial respiration is inhibition of ATP production. Mitochondrial respiration is a major source of ATP production and contributes most of the cell’s energy (Attene-Ramos et al. 2015; Bonora et al. 2012). The Seahorse Mito Stress assay was utilized to calculate mitochondrial ATP production after exposure to MnO2 nanosheets, MnO2 microparticles or soluble MnCl2 (Figure 8). Mitochondrial ATP production was significantly inhibited after 48 h exposure to MnO2 nanosheets (Figure 8(B)). This inhibition of ATP production occurred in a concentration dependent manner. No effect on ATP production was observed following exposure to MnO2 microparticles or soluble MnCl2. Broader impacts of these functional changes are discussed next.
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).
Pathological mechanisms of abnormal iron metabolism and mitochondrial dysfunction in systemic lupus erythematosus
Published in Expert Review of Clinical Immunology, 2021
Chris Wincup, Natalie Sawford, Anisur Rahman
Aside from its role in hemopoiesis, iron has an essential role in mitochondrial function [32]. Mitochondria are specialized organelles that conduct a wide array of vital cellular process, most notably known for their key role in energy metabolism via the production of adenosine triphosphate [ATP]. The generation of ATP is dependent upon oxidative phosphorylation [OXPHOS] that results from a series of metabolic processes that are broadly referred to as mitochondrial respiration. The primary site of this reaction is across the electron transport chain [ETC] on the inner mitochondrial membrane [as summarized in Figure 1]. The ETC is comprised of five individual complexes [I–V], which drive protons across the membrane in order to generate an electrochemical gradient that is required for the conversion of adenosine diphosphate [ADP] to ATP via the fifth complex [also known as ATP synthase]. Iron plays an important role in complexes I, II, and II, where it is contained within iron-sulfur [IS] clusters in the ferrous [Fe2+] state. Clinically, abnormalities relating to IS clusters have been shown to play a pathogenic role in both Parkinson’s disease [33,34] and Friedreich ataxia [35]. However, before considering the role of abnormal iron metabolism in SLE, it is important to understand the way in which iron homeostasis is maintained in health.
Related Knowledge Centers
- Combustion
- Oxygen
- Metabolism
- Catabolism
- Oxidation State
- Adenosine Triphosphate
- Cell
- Nutrient
- Redox
- Sugar