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Metabolic Syndrome
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Metabolic syndrome is a risk factor for cardiac events even with other risk factors such as dyslipidemia, coagulopathy, and hypertension. This may be due to the link with endothelial dysfunction. Nitric oxide production is sufficient when the endothelium is healthy. It allows the arteries to vasodilate, provides surfaces that are not sticky so that clots do not attach, and suppresses atheromas from forming due to stopping leukocytes from breaching the endothelium. With metabolic syndrome’s inflammation, excessive superoxide is produced, leading to increased atheroma formation, thrombosis, and vasoconstriction.
Immunologic Mechanisms in Renal Disease
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Brian D. Schreiber, Gerald C. Groggel
A free radical may be defined as an atom or molecule that contains an unpaired electron in its outer orbit. If one electron is added to the oxygen molecule, superoxide is formed. Superoxide itself is an OFR. The subsequent products formed by chemical modification of superoxide are even more reactive. Superoxide is spontaneously converted to hydrogen peroxide, but this reaction is accelerated greatly by superoxide dismutase (SOD), an enzyme widely distributed in nature. Though in certain systems hydrogen peroxide itself can cause cellular damage, that damage is likely due to the hydroxyl radical it forms by the so-called Haber-Weiss reaction in which hydrogen peroxide is catalyzed to form hydroxyl radicals by iron salts. Other highly reactive products of hydrogen peroxide are the hypohalous acids, whose formation is catalyzed by myeloperoxidase, another widely distributed enzyme.
Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The degranulation is associated with a strong respiratory process which generates highly reactive agents. The respiratory burst increases oxygen uptake, hydrogen peroxide (H2O2) and superoxide (O2–) production, and hexose monophosphate shunt.17,19 NADPH represents the electron donor, and the enzyme responsible for these catalytic activities is localized on the plasma membrane. The enhanced respiration produces many oxidizing agents which are used by phagocytes for the destruction of microorganisms. Part of the microbial killing system is oxygen-dependent and functions with H2O2 and myeloperoxidase, superoxide, hydroxyl radicals, and singlet oxygen.17 The antimicrobial potency of H2O2 is increased by myeloperoxidase. Superoxide is produced during phagocytosis. Singlet oxygen (IO2) is also formed during the enhanced respiration as an end-product of the myeloperoxidase reaction. The latter is different from the atmospheric oxygen in electron distribution around the two oxygen nuclei.
Screening the immunotoxicity of different food preservative agents on the model organism Galleria mellonella L. (Lepidoptera: Pyralidae) larvae
Published in Drug and Chemical Toxicology, 2023
Emine Duman Erbaş, Rehemah Gwokyalya, Hülya Altuntaş, Bilal Kutrup
Additionally, the reduced number of granulocytes after force-feeding with SB, SNi, and SNa could also be related to increased toxicity of the food additives, which induce granulocyte-targeted apoptosis. Moreover, the possibility that granulocytes in circulation reduced due to food preservative-induced respiratory burst cannot be ruled out. Previous research has shown that the respiratory burst pathway involving NADPH oxidase activity is activated during phagocytosis of foreign agents by hemocytes. Superoxide production has also been shown to be critical for effective microbial killing by both neutrophils and hemocytes (Reeves et al.2002, Bergin et al.2005). Yet, treating G. mellonella larvae with potassium nitrate, which is a food preservative, increased SOD enzyme activity in the larval hemolymph (Maguire et al.2017). Accordingly, we argue that food preservatives may have induced a respiratory burst in the G. mellonella larval granulocytes due to increased concentration of superoxide anions leading to low granulocyte counts.
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).
3,4-Dihydroxybenzaldehyde attenuates pentachlorophenol-induced cytotoxicity, DNA damage and collapse of mitochondrial membrane potential in isolated human blood cells
Published in Drug and Chemical Toxicology, 2022
Nikhil Maheshwari, Riaz Mahmood
PCP-induced oxidative modification of proteins, lipids and GSH suggests increased production of ROS and RNS. ROS include oxygen free radicals like hydroxyl radical (OH•), superoxide radical (O2•−) and the non-radical H2O2. Fluorescent probes DCFH-DA and DHE were used to measure general ROS and superoxide radical formation, respectively. A twofold enhancement in fluorescence intensity of DCF and DHE was observed in PCP-treated cells (Figure 5). This elevated level of ROS and superoxide will damage the affected cells and impair both enzymatic and non-enzymatic AO defense systems. However, prior treatment with DHB decreased the DCF and DHE fluorescence intensity in a DHB concentration-dependent manner and at 2.0 mM DHB it was only 1.2- and 1.1-fold of the control values. Superoxide radicals are anionic form of O2 and are capable of inactivating metabolic pathways. They also liberate free iron in cells that can undergo Fenton-reaction to generate the extremely reactive and damaging hydroxyl radicals (Di Meo et al.2016).