Abstract
With considering serum concentration of the uric acid in humans we are observing hyperuricemia and possible gout development. Many epidemiological studies have shown the relationship between the uric acid and different disorders such are obesity, metabolic syndrome, hypertension and coronary artery disease. Clinicians and investigators recognized serum uric acid concentration as very important diagnostic and prognostic factor of many multifactorial disorders. This review presented few clinical conditions which are not directly related to uric acid, but the concentrations of uric acid might have a great impact in observing, monitoring, prognosis and therapy of such disorders. Uric acid is recognized as a marker of oxidative stress. Production of the uric acid includes enzyme xanthine oxidase which is involved in producing of radical-oxigen species (ROS). As by-products ROS have a significant role in the increased vascular oxidative stress and might be involved in atherogenesis. Uric acid may inhibit endothelial function by inhibition of nitric oxide-function under conditions of oxidative stress. Down regulation of nitric oxide and induction of endothelial dysfunction might also be involved in pathogenesis of hypertension. The most important and well evidenced is possible predictive role of uric acid in predicting short-term outcome (mortality) in acute myocardial infarction (AMI) patients and stroke. Nephrolithiasis of uric acid origin is significantly more common among patients with the metabolic syndrome and obesity. On contrary to this, uric acid also acts is an "antioxidant", a free radical scavenger and a chelator of transitional metal ions which are converted to poorly reactive forms.
Highlights
Uric acid is a weak organic acid, the end product of purine nucleotides degradation [1]
Some studies showed that therapeutic use of allopurinol, xanthine oxidase inhibitor, which reduces serum levels of uric acid, show protective effects in situations associated with oxidative stress [27,30], because of decreasing of reactive oxygen species (ROS)
Hyperuricaemia is a significant predictor of disease state and progression of chronic heart failure [61]
Summary
Uric acid is a weak organic acid, the end product of purine nucleotides degradation [1]. Degradation of purine nucleotides (Figure 1) starts with nucleotidase activity in reaction which releases phosphate from nucleotides and produces nucleosides, adenosine and guanosine [3]. Adenosine is than deaminated into inosine in reaction catalyzed by adenosine deaminase. Purine nucleotide phosphorilase hydrolyses ribose group from inosine and guanosine to produce xypoxantine and guanine, respectively [3]. It oxidases hypoxantine to xsantine, and xantine to uric acid in the liver, gut, lung, kidney, heart, brain and plasma [4]. Deposition of monosodium urate monohydrate microcrystals or uric acid in various parts of the body leads to the development of gout, common painful rheumatic disease [6].
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