Chapter Paper 1 Answers
James Day, Amy Thomson, Tamsin McAllister, Nawal Bahal in Get Through, 2014
Oxidative phosphorylation takes place inside mitochondria: Electrons from the electron carriers NADH and FADH2 are passed to a chain of electron carriers within the inner mitochondrial membrane.These electron carriers are a series of proton pumps, activated by the flow of electrons through them.They pump H+ out of the inner mitochondrial membrane.H+ moves back in along its concentration gradient through channels of ATP synthase, which catalyzes the generation of ATP.
Cell structure, function and adaptation
C. Simon Herrington in Muir's Textbook of Pathology, 2020
In the cytoplasm, a variety of organelles are responsible for the remainder of the cellular function. In some cases, these are permanent features, e.g. mitochondria (Figure 2.2). In other cases, a macromolecular complex may be assembled only when needed, for example the proteasome which is involved in protein degradation, or the ‘apoptosome’ that catalyses cell death by apoptosis (see Chapter 3). Ribosomes translate messenger ribonucleic acid (mRNA) into peptide sequences (proteins) and further processing, including splicing, glycosylation, and possible packaging for secretion, occurs in the endoplasmic reticulum. The mitochondria are the primary site of oxidative phosphorylation. As part of this function, they generate free radicals that damage membranes, enzymes, and DNA, but are also part of the redox signalling system that indirectly regulates the expression of several genes involved in protection. The mitochondria are also key players in executing apoptosis in some situations.
Burkholderia
Dongyou Liu in Handbook of Foodborne Diseases, 2018
Toxoflavin is toxic because it acts as an electron carrier, resulting in the production of hydrogen peroxide. Under normal conditions, NADH and FADH2 produced during glycolysis and the citric acid cycle (in the cytosol and mitochondrial matrix, respectively) transfer their electrons to a series of carriers in the inner mitochondrial membrane, including cytochromes, which are organized into Complex I–IV.94 The electrons are shuttled down this chain based on redox potential, and the energy released is used to pump protons into the intermembrane space of the mitochondria. This transport creates a proton gradient that powers the ATP synthase, which produces the majority of ATP used by the cell in a process called oxidative phosphorylation.94 It was discovered by Latuasan and Berends95 that toxoflavin interferes with this process. When antimycin A, which blocks Complex III of the electron transport chain, is added to yeast, respiration is inhibited.94,95 However, when antimycin A and toxoflavin are added together, no inhibitory effects are observed. Similarly, the addition of potassium cyanide blocks Complex IV and inhibits respiration, but not in the presence of toxoflavin.94,95 These results suggest that toxoflavin facilitates cytochrome-independent electron transfer.95
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.
Pearson syndrome
Published in Expert Review of Hematology, 2018
Piero Farruggia, Floriana Di Marco, Carlo Dufour
Epidemiological studies indicate the prevalence of mitochondrial diseases to be 1/4300 newborns [7,8] and 11.5/100,000 in the general population [9]. In Italy, the likely incidence of PS is approximately 1 in 1,000,000 newborns, with no sex predilection [6]. Mitochondria are subcellular organelles normally inherited exclusively from the mother, with sperm-derived mitochondria being disposed of inside the fertilized egg [10]. They are involved in many important cellular processes, such as the regulation of intracellular calcium concentrations, iron–sulfur cluster biogenesis, and apoptosis. However, mitochondria mainly function as the primary energy-generating system in most eukaryotic cells. Through the electron transport chain in the inner mitochondrial membrane, these organelles act as the site of oxidative phosphorylation (OXPHOS) to generate adenosine triphosphate (ATP) from energy-rich molecules. Approximately 90% of oxygen in the cell is consumed by mitochondria with some of it being converted to reactive oxygen species (ROS). The presence of mitochondrial DNA (mtDNA) close to ROS producing OXPHOS may explain the observed higher mutation rate of the mtDNA compared to nuclear DNA (nDNA) [11–14]. Interestingly, the vast majority of proteins necessary for mitochondrial function are encoded by nDNA, with approximately 13 proteins being encoded by mtDNA [15]. Nevertheless, mitochondria maintain a genome that is essential for mitochondrial function, with each mitochondrion containing 2–10 copies of mtDNA [15].
Related Knowledge Centers
- Enzyme
- Eukaryote
- Fermentation
- Metabolic Pathway
- Cell
- Redox
- Nutrient
- Adenosine Triphosphate
- Mitochondrion
- Aerobic Organism