Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.17.3.2 (xanthine oxidase)
 8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with juvenile gout and partial deficiency of HGPRT is presented. In this subject, hepatic xanthine oxidase activity showed a twelve-fold increase. Xanthine oxidase is a readily induced enzyme and this increased activity is probably correlated with the increased availability of hypoxanthine observed in such patients.
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PMID:Xanthine oxidase activity in a gouty patient with partial deficiency of HGPRT. 85 14

The genetic toxicity of active oxygen species produced during the enzymic oxidation of xanthine has been investigated using Chinese hamster ovary (CHO) cells. Incubation of cells with xanthine plus xanthine oxidase resulted in extensive chromosome breakage and sister-chromatid exchange and gave a small increase in frequency of thioguanine-resistant cells (HGPRT test). Inclusion of superoxide dismutase or catalase in the xanthine/xanthine oxidase system inhibited chromosome breakage, whereas only catalase prevented SCE and mutant induction. It is concluded that hydrogen peroxide is responsible for most of the genetic effects observed in CHO cells exposed to xanthine/xanthine oxidase but that superoxide plays a key role in chromosome breakage.
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PMID:Genetic damage in CHO cells exposed to enzymically generated active oxygen species. 632

The results of animal experiments and clinical observations concerning the pathological role of hyperuricaemia and the effect of allopurinol treatment in acute metabolic disturbances and critically ill patients is reported. In uricase enzyme blocked rats treated by oxonic acid, urate nephropathy could be elicited by endogenous purine catabolism in shock. Hyperuricaemia aggravated the shock, while allopurinol increased the survival time. In shock resistant rats hyperuricaemia did not develop when shock was elicited. Allopurinol prevented hyperuricaemia and increased the physical performance of swimming rats, while in experimental DIC allopurinol reduced markedly the hyperuricaemia and the kidney damage. In clinical studies a close correlation was observed between the degree of hyperuricaemia and the severity of illness. Serum uric acid values were lowered in cases treated by peritoneal dialysis. In randomized control studies of newborns with IRDS the survival rate was improved by allopurinol treatment. In critically ill patients with various illnesses allopurinol prevented the progression of the pathological process and improved the clinical condition. The effect of allopurinol in acute clinical metabolic disturbances may be due to its protection against the renal damage by hyperuricaemia and against purine loss by inhibition of xanthine oxidase during the hypoxic stress and the enhancement of hypoxanthine salvage by HGPRT. Allopurinol reduced the production of superoxide radicals and thus the effect of injury may also be moderated by xanthine oxidase blockade.
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PMID:Role of hyperuricaemia in critically ill patients especially newborns. 638 36

The molecular and biochemical aspects of purine nucleotide biosynthesis through de novo and salvage pathways, the production of uric acid, and their regulation mechanisms are reviewed for further understanding of hyperuricemia and gout. The metabolic rate of purine nucleotide biosynthesis is chiefly determined by the regulation of the de novo pathway, especially amidophosphoribosyltransferase and PRPP synthetase, and the accumulation of uric acid results from the acceleration of de novo biosynthesis and catabolism of purine nucleotide or the decrease in urinary excretion of uric acid. Moreover, several enzyme mutations of purine nucleotide metabolism are also clinically important including gout with hyperactive HPRT and the deficiency of HPRT (Lesch-Nyhan syndrome), adenylosuccinate lyase, xanthine oxidase, APRT, PNP, or ADA (SCID) with gene therapy.
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PMID:[Metabolism of purine nucleotides and the production of uric acid]. 897 90

Objectives. Hyperuricemia (HUA) is a disease caused by increased production of uric acid (UA) or reduced excretion of UA in the body. Results of an epidemiological survey show that 60% of patients with HUA have hyperlipidemia (HPA). Dendrobium officinalis (DOF) six nostrum (DOS) is based on the theory of traditional Chinese medicine for the transformation of the traditional Chinese nostrum Si Miao Wan. In this article, we aim to discuss the efficacy and mechanism of DOS in reducing UA and regulating lipid metabolism. The rat model of HUA with HPA was induced by potassium oxonate (PO) combined with high-fat sorghum feed. We monitored the serum UA and blood lipids. Liver xanthine oxidase (XOD), adenosine deaminase (ADA), lipoprotein lipase (LPL), and fatty acid-binding protein (FABP1) activities were measured by enzyme-linked immunosorbent assay (ELISA) after the last administration of DOS. We performed a histopathological examination of rat kidney and intestine. Immunohistochemistry (IHC) was used to detect the expression of renal inflammatory proteins NLRP3 / Caspase-1 and intestinal inflammatory proteins TLR4 / NLRP3. We used western blot for measurement of liver hypoxanthine-guanine phosphoribosyl transferase (HPRT1) protein expression and renal PDZ domain protein kidney 1 (PDZK1) protein expression. DOS administration significantly reduced serum UA, total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-c) level, and improved liver steatosis in the model rat. At the same time, DOS treatment effectively inhibited liver XOD and ADA, increased the level of liver HPRT1, and reduced the production of UA. Additional studies had shown that DOS can restore normal UA excretion function in the intestine and kidney and regulated liver lipids metabolism. IHC and histopathological sections showed that DOS reduced the level of kidney, intestinal inflammatory body (NLRP3, Caspase-1, and TLR4), improved inflammation of the kidney and intestinal tract in rats. DOS is a promising drug that can effectively reduce serum UA and lipid level in the model rat. The mechanism of action may be related to inhibition of UA production, promotion of UA excretion, regulation of lipids metabolism, and anti-inflammatory response.
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PMID:Effects and Mechanisms of Dendrobium officinalis Six Nostrum for Treatment of Hyperuricemia with Hyperlipidemia. 3230 2