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Nutritional Deficiencies
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Deepa Bhupali, Fernando D. Testai
Thiamine is a cofactor for: Transketolase: This enzyme links glycolysis to the hexose monophosphate shunt (Figure 17.1). The hexose monophosphate shunt is required for the synthesis of: Pentoses (such as ribose phosphate): necessary for the synthesis of nucleotides.Nicotinamide adenine dinucleotide phosphate (NADP): necessary for the synthesis of fatty acids, steroids, and antioxidants.Pyruvate dehydrogenase E1: Pyruvate dehydrogenase is a complex formed by three enzymes (E1, E2, and E3). This complex links the glycolytic pathway with the Krebs cycle. E1 requires thiamine pyrophosphate as a cofactor.Alpha-ketoglutarate dehydrogenase: This enzyme participates in the Krebs' cycle and is involved in the conversion of alpha-ketoglutarate to succinyl-CoA. The deficiencies of this enzyme and E1 lead to decreased adenosine triphosphate (ATP) production and cellular dysfunction.
Cellular Components of Blood
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
About 5% of glycolysis undergoes oxidation by the hexose monophospate (HMP) shunt in which glucose-6-phosphate is converted to 6-phosphogluconate and to ribulose-5-phosphate. NADPH is formed from NADP, and this is linked with glutathione that maintains sulphydryl (-SH) groups intact in the cell. Glutathione helps to maintain the integrity of the red cell membrane. Deficiency of NADPH leads to haemolysis because of the accumulation of hydrogen peroxide, which weakens the membrane. NADPH generated by the hexose monophosphate pathway is required by methaemoglobin reductase to reduce methaemoglobin to Hb. Some 1,3-DPG is converted to 2,3-DPG by the Rapoport–Luebering shunt.
Conclusion
Published in Jay A. Goldstein, Chronic Fatigue Syndromes, 2020
Malic acid has been advocated as a treatment for fibromyalgia. 67 Nitric oxide synthase has been identified as NADPH-diaphorase. Malic acid is involved in the function of an enzyme which converts NADP into NADPH, used as a substrate for NADPH-diaphorase, 68 and exogenous malic acid may work by enhancing nitric oxide synthase levels, even if sufficient LL-1 beta is not present.
Purification and characterisation of glutathione reductase from scorpionfish (scorpaena porcus) and investigation of heavy metal ions inhibition
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Glutathione reductase (EC 1.8.1.7; GR), a major enzyme in glutathione metabolism, is required for the maintenance of the reduced form of cellular glutathione, which is strongly nucleophilic for many reactive electrophiles10,11. The flavin enzyme GR acts as an antioxidant to protect cells from oxidative stress by reducing glutathione disulphide (GSSG) to its reduced form (GSH)12. It has an important role in the drug and detoxification mechanisms especially in the liver. This is due to the cytochrome P-450 system found in liver microsomes, which provides detoxifying events13. Maintaining the GSH/GSSG ratio in the cell environment is one of the most important known targets of the GR enzyme-catalysed reactions14. Glutathione reductase is involved in the reduction-oxidation of intracellular glutathione for GSSG, which is generated through the detoxification of hydroperoxides and reduction of some other chemicals catalysed by glutathione perdoxidase15. The NADP+ dependent malate dehydrogenase and pentose phosphate pathways provide the NADPH needed in this catalytic process16,17. NADPH, a key product of the pentose phosphate cycle, is employed extensively in reductive biosynthesis. Furthermore, it aids in the protection of the cell against oxidative damage9.
New insights into the metabolism of Th17 cells
Published in Immunological Medicine, 2023
Fatty acid oxidation is a mitochondrial aerobic process responsible for producing acetyl CoA from fatty acids. In contrast, fatty acid synthesis is the creation of fatty acids from acetyl CoA and Nicotinamide adenine dinucleotide phosphate (NADPH) [13]. Adenosine monophosphate-activated protein kinase (AMPK), a serine/threonine kinase, is a vital metabolic regulator that inhibits mTORC activity. AMPK-dependent phosphorylation of acetyl-CoA carboxylase 1 (ACC1) is the rate-limiting enzyme for fatty acid synthesis. ACC1 modulates the DNA binding of RORγt to target genes and enhances Th17 cell differentiation [79–81]. Cholesterol is synthesized from acetyl CoA by the hydroxymethylglutaryl-coenzyme A (HMG-CoA). Statin, an inhibitor of HMG-CoA reductase, reduces Th17 cell differentiation [82].
Prevalence of G6PD deficiency in Thai blood donors, the characteristics of G6PD deficient blood, and the efficacy of fluorescent spot test to screen for G6PD deficiency in a hospital blood bank setting
Published in Hematology, 2022
Phinyada Rojphoung, Thongbai Rungroung, Usanee Siriboonrit, Sasijit Vejbaesya, Parichart Permpikul, Janejira Kittivorapart
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked inherited disorder that is characterized by the insufficiency of an enzyme that is used in the pentose phosphate pathway to generate nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is a crucial oxidation reduction molecule that protects red blood cells (RBC) from reactive oxygen species (ROS). Patients with G6PD deficiency manifest varying degrees of acute hemolysis in response to oxidative stress precipitated by certain medications and foods. Transfusion of red cell products from G6PD enzyme deficient donors could cause a potentially unfavorable outcome, especially in newborns and those with hemoglobinopathies [1–3]. Current screening criteria of blood donors relative to red cell disorders in Thailand relies mostly on history taking and point-of-care hemoglobin (Hb) testing. The screening of G6PD deficiency is not performed in the donors at the moment. According to the World Health Organization (WHO) Blood Donor Selection guidelines, only donors with a previous history of hemolysis are to be permanently deferred [4]. However, countries with a high prevalence of G6PD deficiency should establish their own criteria for screening at-risk donors, and they should establish their own transfusion guidelines [5].