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Bioenergetics
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Regulation of the Krebs cycle is partially controlled by the need for energy (ATP) and therefore by reactions producing NADH2+ or FADH2+ and the ratio of oxidized to reduced coenzymes (O:Rc). The O:Rc is controlled by ADP and Pi availability for oxidative phosphorylation in the ETS. The rate at which the Krebs cycle proceeds becomes limited if the coenzymes FAD+ and NAD+ are not available to accept electrons (along with H+ in biological systems). Additionally, accumulation of guanine triphosphate (GTP) can result in an increase in succinyl-CoA which inhibits the initial Krebs cycle reaction: oxaloacetate + acetyl-CoA → citrate + CoA. Isocitrate → α-ketoglutarate is the rate-limiting step for the Krebs cycle, which is catalyzed by isocitrate dehydrogenase. Isocitrate dehydrogenase is generally inhibited by ATP and strongly allosterically stimulated by the accumulation of ADP. Secondarily, the Krebs cycle is controlled by α-ketoglutarate dehydrogenase which catalyzes the conversion of α-ketoglutarate to succinyl-CoA and produces NADH, thus, providing electrons for the ETS. α-ketoglutarate dehydrogenase is inhibited by increased concentrations of succinyl-CoA and NADH, which are produced by the reaction that it catalyzes. α-ketoglutarate dehydrogenase and the Krebs cycle rate are inhibited by a high energy charge (high concentration of ATP). General control of the ETS is relatively simple: stimulated by ADP and inhibited by ATP (35, 171, 283).
Cellular and Immunobiology
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Masood Moghul, Sarah McClelland, Prabhakar Rajan
TCA (Krebs) cycle takes place within the mitochondria.As acetyl CoA is oxidised, it de-oxidises (reduces) electron carriers NAD and FAD → NADH, FADH2.NAD and FAD pass their electrons into the electron transport chain—oxidative phosphorylation.As electrons pass along the chain, they lose energy, which is used to pump hydrogen ions into inter-membrane space of mitochondria, causing an electrochemical gradient.Hydrogen flows back down the electrochemical current and through membrane enzyme ATP synthase, producing ATP.This process is called chemiosmosis and yields the most ATP from glucose.
The cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
In the presence of oxygen, the pyruvic acid moves into the mitochondria and is converted into acetyl coenzyme A (acetyl CoA) and enters the Krebs or citric acid cycle. This part of the process produces the hydrogen ions that will combine with oxygen in the next phase. It is the Krebs cycle that produces the carbon dioxide that we exhale. During the cycle, the coenzyme A is released and the pick-up molecule, oxaloacetic acid, is regenerated, ready for the next cycle. During the cycle, molecules that are the building blocks for non-essential amino acids and fatty acids are produced. It can therefore be seen that this is a very efficient energy production system.
Harel Yoon syndrome: a novel mutation in ATAD3A gene and expansion of the clinical spectrum
Published in Ophthalmic Genetics, 2023
Caroline Atef Tawfik, Raghda Zaitoun, Aliaa Ahmed Farag
Harel-Yoon syndrome (HAYOS: OMIM# 617183) is a rare, recently described neurodevelopmental disorder characterized by psychomotor delay, truncal hypotonia, spasticity, and peripheral neuropathy. There are other more variable features described in association with HAYOS including optic atrophy and hypertrophic cardiomyopathy. It can be inherited either in autosomal dominant or autosomal recessive manner (1). Laboratory evidence of mitochondrial dysfunction is usually detected in the form of lactic acidosis and/or excessive urinary excretion of metabolites from Krebs cycle. A classic and severe presentation is characterized by cerebellar and brainstem atrophy, hypotonia, encephalopathy, and death in the first days or weeks of life. This form is usually the result of bi-allelic deletions in the ATPase Family AAA Domain Containing 3A (ATAD3) gene cluster (containing ATAD3A, ATAD3B, and ATAD3C) (2). A less severe presentation has been reported in those with biallelic missense variants. This attenuated and later-onset form of HAYOS presents with developmental delay, cataracts, seizures, and optic and cerebellar atrophy with individuals living into adulthood (1–3)
Hyperglycaemia and the risk of post-surgical adhesion
Published in Archives of Physiology and Biochemistry, 2022
Gordon A. Ferns, Seyed Mahdi Hassanian, Mohammad-Hassan Arjmand
Hyperglycaemia increases superoxide production (Nishikawa et al.2000). Under hyperglycaemic conditions, there is increased glucose entering the glycolytic pathway (important biochemical pathway in the cells for glucose metabolism) that produced two molecules of pyruvate. In aerobic conditions, pyruvates are converted to acetyl-CoA by pyruvate dehydrogenase. Acetyl-CoA produced by pyruvate entered to the Krebs cycle in mitochondria. Three molecules of NADH are produced by each Krebs cycle (Sabri 1984). NADH is an electron carrier to transport electron in complex 1 of the electron transport chain in mitochondria for ATP synthesis. An excessive amount of NADH causes reductive stress by intracellular production of superoxide O2– (Liu et al.2002) (Figure 3). Superoxide is one of the most important ROS factors and can damage biomolecules and increase of inflammation (McCord 1980). Increase of ROS such as superoxide causes excessive production of proinflammatory cytokines and growth factors by immune cells which are associated with adhesion formation post-surgical (Fortin et al.2015).
Prevalence of succinate dehydrogenase deficiency in paragangliomas and phaeochromocytomas at a tertiary hospital in Cape Town: a retrospective review
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2021
Cassandra Bruce-Brand, Abraham C van Wyk
The SDH enzyme complex (mitochondrial complex II) catalyses the conversion of succinate to fumarate in the Krebs cycle.16 Loss of heterozygosity with inactivating germline mutations results in destabilisation of the SDH protein complex and abolishes its enzymatic activity leading to an accumulation of succinate.16,18–20 This results in reactive oxygen species causing free radical damage and activation of a pseudohypoxia pathway by increasing hypoxia-inducible factors.16,18–21 A third mechanism that has been proposed to explain how Krebs cycle dysfunction can lead to neoplasia is through a decrease in apoptosis.21 The SDH complex consists of four subunits, SDHA, SDHB, SDHC and SDHD. Hereditary PC/PGL syndrome can be caused by germline mutations in any of the SDH subunits as well as in SDHAF2, a mitochondrial protein that flavinates SDHA and promotes maturation of SDHB.16,21–24