Abstract

Uric acid, the final product of purine metabolism, is one of the most recognized biological markers, a catalyzed reaction by xantina oxidoreductasa (XOR). This bifunctional enzyme in its dehydrogenated shape (XDH), produces AU, and nicotidamide adenine dinucleotide and in oxidase (XO), AU and Superoxide (O2•-). Hyperuricemia (HAU) is an indicator of over-regulation of XO activity, a powerful system producer of species of reactive oxygen (ROS), in human physiology. Accumulation of these radicals contribute to endothelial malfunction, metabolic and functional deterioration, inflammatory activation and other events. HAU is currently considered one of the characteristic alterations of metabolic syndrome (MS). HAU presence in the MS may be explained through its connection to hypertension, hypertriglyceridemia or obesity, as well as with renal vascular injury. The purpose of this article is to show importance of AU in diagnostic of MS, its structural and functional characteristics and implications on physiopathology of metabolic alteration. Information was search in Spanish language and English language, using as key words: Uric acid, xanthine, oxidase, hyperuricemia, metabolic syndrome. Motors or data bases used to collect information were: Science Direct, Scopus, Pubmed and Scielo. Information was selected with a search temporal window of 30 years (1985 – 2015). Many researches show a strong association between plasmatic concentrations of AU and MS and/or their components. Transversal studies performed in various ethnic groups have shown that MS prevalence increases through increase of AU serum concentrations.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call