Short communicationOxidative damage to synovial fluid from the inflamed rheumatoid joint detected by 1H NMR spectroscopy
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A systematic review of the small molecule studies of osteoarthritis using nuclear magnetic resonance and mass spectroscopy
2019, Osteoarthritis and CartilageCitation Excerpt :Hyaluronan cleavage in SF is observed by an increase in the terminal N-acetyl (N-Ac) group peak, verified by treating SF with hyaluronidase enzyme30. Concurrent formation of lactate, citrate and acetate, (known products of N-acetylglucosamine) is also reported31,32. Unfortunately, NMR cannot distinguish between the N-Ac liberation of hyaluronic acid and other proteoglycans, although both are present in joint destruction.
Metabolomics to identify biomarkers and as a predictive tool in inflammatory diseases
2015, Best Practice and Research: Clinical RheumatologyCitation Excerpt :Hyaluronic acid, as mentioned, is important for the functional integrity of the extracellular matrix of articular cartilage. In RA, ROS depolymerises synovial fluid hyaluronate [70]. Hyaluronidase activity is non-existent in both normal and inflamed synovial fluid.
Hyaluronic Acid: Its Function and Degradation in in vivo Systems
2008, Studies in Natural Products ChemistryIn vitro screening of the action of non-steroidal anti-inflammatory drugs on hypochlorous acid-induced hyaluronan degradation
2007, Polymer Degradation and StabilityCitation Excerpt :Oxygen derived free radicals produced by polymorphonuclear leukocytes (PMNLs) are involved in tissue damage associated with inflammatory joint diseases. Rheumatoid arthritis is accompanied by a decrease in viscosity of the synovial fluid due to the degradation of high-molecular weight hyaluronan (HA) [1–4]. HA is degraded by hydroxyl radicals produced as a result of the Fenton reaction [5–10].
A Survey of Metabonomics Approaches for Disease Characterisation
2007, The Handbook of Metabonomics and MetabolomicsInvolvement of a ferroprotein sensor in hypoxia-mediated inhibition of neutrophil apoptosis
2002, BloodCitation Excerpt :Persistent accumulation of primed and activated neutrophils is a cardinal feature of a number of lung diseases, including acute lung injury, bronchiectasis, and chronic obstructive airways disease, and it is associated with disease progression and destruction of lung tissue.2 Similarly, in myocardial infarction, neutrophils have been implicated in extending the area of primary myocardial injury by releasing protease-rich granule contents into adjacent viable tissue,3 and, in rheumatoid arthritis, neutrophil-derived reactive-oxygen species and granule enzymes have been demonstrated in synovial fluid and again implicated in disease pathogenesis.4, 5 Understanding the mechanisms that modulate neutrophil influx, activation, and longevity is therefore of major pathophysiologic importance to a number of organ systems.