Molybdenum cofactor deficiency.
Houston, United States. In Mol Genet Metab, Jan 2016
MoCD results in deficiency of the molybdenum cofactor dependent enzymes sulfite oxidase, xanthine dehydrogenase, aldehyde oxidase and mitochondrial amidoxime reducing component.
Serum uric acid and the risk of cardiovascular and renal disease.
Milano, Italy. In J Hypertens, Sep 2015
Another important question is whether lowering serum uric acid can improve cardiovascular and renal outcomes, and what therapeutic mechanism of action could provide more clinical benefits to patients; the available literature shows a trend toward improvement associated with administration of urate-lowering drugs, in particular for the xanthine oxidase inhibitors.
A new paradigm for XOR-catalyzed reactive species generation in the endothelium.
Pittsburgh, United States. In Pharmacol Rep, Aug 2015
To establish the micro-environmental conditions requisite for in vivo XOR-catalyzed oxidant and NO production, this review assesses the impact of pH, O2 tension, enzyme-endothelial interactions, substrate concentrations and catalytic differences between xanthine oxidase (XO) and xanthine dehydrogenase (XDH).
Gout therapeutics: new drugs for an old disease.
United States. In Lancet, 2011
The approval of febuxostat, a non-purine-analogue inhibitor of xanthine oxidase, by the European Medicines Agency and the US Food and Drug Administration heralds a new era in the treatment of gout.
Antioxidants in Sport Nutrition: All the Same Effectiveness?
Boca Raton, United States. In Unknown Journal, 0001
Depending on the type of exercise, a number of potential mechanisms for the generation of ROS within the muscle have been proposed, such as (a) increased formation of in the mitochondrial respiratory chain, (b) xanthine oxidase (XO) catalysed degradation of AMP (adenosine monophosphate) during ischaemic muscular work leading to increased production of , (c) increased ROS formation in the oxidative-burst reaction due to activation of polymorphoneutrophils (PMNs) after exercise-induced muscle damage, (d) loss of calcium homeostasis in stressed muscles, (e) enhanced cytokine production and activation of nuclear factor kappa B (NF-κB), catecholamine autooxidation and many more (König et al. 2007; Niess et al. 1999; Vina et al. 2000).