A naphthalimide-based novel “Turn-On” fluorescence approach for the determination of uric acid and monitoring of xanthine oxidase activity

2019 ◽  
Vol 11 (32) ◽  
pp. 4190-4196 ◽  
Author(s):  
Jagpreet Singh Sidhu ◽  
Shilpa Sharma ◽  
Ashutosh Singh ◽  
Neha Garg ◽  
Navneet Kaur ◽  
...  
Keyword(s):  
Uric Acid ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Fluorescence Emission ◽  
Turn On ◽  
Xanthine Oxidase Activity

Fluorescence emission of the receptor enhanced upon its binding with uric acid due to the cancellation of the PET phenomenon.

Determination of human plasma xanthine oxidase activity by high-performance liquid chromatography

1996 ◽  
Vol 681 (2) ◽  
pp. 395-400 ◽  
Author(s):  
Tetsuya Yamamoto ◽  
Yuji Moriwaki ◽  
Sumio Takahashi ◽  
Zennta Tsutsumi ◽  
Jun-ichi Yamakita ◽  
...  
Keyword(s):  
High Performance Liquid Chromatography ◽  
Liquid Chromatography ◽  
Xanthine Oxidase ◽  
Human Plasma ◽  
Oxidase Activity ◽  
High Performance ◽  
Xanthine Oxidase Activity

Decreased hepatosplanchnic antioxidant uptake during hepatic ischaemia/reperfusion in patients undergoing liver resection

2008 ◽  
Vol 114 (8) ◽  
pp. 553-560 ◽  
Author(s):  
Marcel C. G. van de POLL ◽  
Cornelis H. C. Dejong ◽  
Marc A. J. G. Fischer ◽  
Aalt Bast ◽  
Ger H. Koek
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Liver Resection ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Ischaemic Preconditioning ◽  
Xanthine Oxidase Activity ◽  
Ischaemia Reperfusion ◽  
Plasma Antioxidant Capacity ◽  
Plasma Antioxidant

Oxidative stress mediates cell injury during ischaemia/reperfusion. On the other hand, experimental findings suggest that ROS (reactive oxygen species) induce processes leading to ischaemic preconditioning. The extent and source of oxidative stress and its effect on antioxidant status in the human liver during intermittent ischaemia and reperfusion remains ill-defined. Therefore the aim of the present study was to investigate the occurrence of oxidative stress in humans undergoing liver resection. Liver biopsies, and arterial and hepatic venous blood samples were taken from ten patients undergoing hepatectomy with an intermittent Pringle manoeuvre. Plasma MDA (malondialdehyde) and hepatic GSSG levels were measured as markers of oxidative stress and plasma uric acid as a marker of xanthine oxidase activity. In addition, changes in hepatosplanchnic consumption of plasma antioxidants and hepatic levels of carotenoids and glutathione (GSH) were measured. After ischaemia, hepatosplanchnic release of MDA and increased hepatic GSSG levels were found. This was accompanied by the release of uric acid, reflecting xanthine oxidase activity. During reperfusion, ongoing oxidative stress was observed by further increases in hepatic GSSG content and hepatosplanchnic MDA release. Uric acid release was minimal during reperfusion. A gradual decrease in plasma antioxidant capacity and net hepatosplanchnic antioxidant uptake was observed upon prolonged cumulative ischaemia. Oxidative stress occurs during hepatic ischaemia in man mainly due to xanthine oxidase activity. Interestingly, the gradual decline in plasma antioxidant capacity and net hepatosplanchnic antioxidant uptake during prolonged cumulative ischaemia, preserved both hydrophilic and lipophilic hepatic antioxidant levels. Decreasing plasma levels and net hepatosplanchnic uptake of plasma antioxidants may warrant antioxidant supplementation, although it should be clarified to what extent limitation of oxidative stress compromises ROS-dependent pathways of ischaemic preconditioning.

8-Azaguanine, 3, 3' -4, 4' -tetrahydroxy-chalcone and purine in experimental shock in the rat

1960 ◽  
Vol 198 (3) ◽  
pp. 501-506
Author(s):  
Aaron Janoff ◽  
B. W. Zweifach
Keyword(s):  
Uric Acid ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Traumatic Injury ◽  
Traumatic Shock ◽  
Iron Release ◽  
Xanthine Oxidase Activity ◽  
Experimental Shock ◽  
Elevate Plasma

Two substances, 8-azaguanine (8AG) and 3, 3' -4, 4' -tetrahydroxy-chalcone (THC), believed to be nonoxidized in vivo inhibitors of xanthine oxidase in the rat, were used in an attempt to depress iron-release mechanisms during shock. Purine, a substrate of xanthine oxidase, was administered during shock as a means of stimulating these same mechanisms. No protection was obtained with 8AG and subsequent tests revealed that 8AG failed to depress the release of iron and uric acid both in shocked and untreated rats. The data point, instead, to inhibition of uricase by 8AG in the intact rat and not to inhibition of xanthine oxidase activity. Despite occasional depression of xanthine oxidase activity, THC exacerbated the course of traumatic shock in rats, possibly as a result of interference with pressor amine mechanisms. Purine loads were administered to normal rats and to rats primed with thorotrast. Although purine is known to elevate plasma iron in other species, rats treated with this metabolite were not unusually susceptible to lethal traumatic injury.

scholarly journals Eggshell Membrane Ameliorates Hyperuricemia by Increasing Urate Excretion in Potassium Oxonate-Injected Rats

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3323
Author(s):  
Yoon-Young Sung ◽  
Dong-Seon Kim
Keyword(s):  
Uric Acid ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Glucose Transporter ◽  
Organic Anion ◽  
Gouty Arthritis ◽  
Eggshell Membrane ◽  
Acid Uptake ◽  
Xanthine Oxidase Activity ◽  
Potassium Oxonate

Hyperuricemia is the primary cause of gouty arthritis and other metabolic disorders. Eggshell membrane (EM) is an effective and safe supplement for curing pain and stiffness connected with osteoarthritis. However, the effect of EM on hyperuricemia is unclear. This study determines the effects of EM on potassium oxonate-injected hyperuricemia. Uric acid, creatinine, blood urea nitrogen concentrations in the serum, and xanthine oxidase activity in the liver are measured. Protein levels of renal urate transporter 1 (URAT1), organic anion transporters 1 (OAT1), glucose transporter 9 (GLUT9), and ATP-binding cassette transporter G2 (ABCG2) in the kidney are determined with renal histopathology. The results demonstrate that EM reduces serum uric acid levels and increases urine uric acid levels in hyperuricemic rats. Moreover, EM downregulates renal URAT1 protein expression, upregulates OAT1 and ABCG2, but does not change GLUT9 expression. Additionally, EM does not change xanthine oxidase activity in the liver or the serum. EM also decreases uric acid uptake into oocytes expressing hURAT1. Finally, EM markedly reduces renal inflammation and serum interleukin-1β levels. These findings suggest that EM exhibits antihyperuricemic effects by promoting renal urate excretion and regulating renal urate transporters. Therefore, EM may be useful in the prevention and treatment of gout and hyperuricemia.

scholarly journals Weight Loss Mediated Reduction in Xanthine Oxidase Activity and Uric Acid Clearance in Adolescents with Severe Obesity

2016 ◽  
Vol 12 (4) ◽  
pp. 286-291 ◽  
Author(s):  
Harrison K. Tam ◽  
Aaron S. Kelly ◽  
Claudia K. Fox ◽  
Brandon M. Nathan ◽  
L'Aurelle A. Johnson
Keyword(s):  
Weight Loss ◽  
Uric Acid ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Severe Obesity ◽  
Xanthine Oxidase Activity ◽  
Acid Clearance ◽  
Uric Acid Clearance ◽  
Mediated Reduction

Changes in xanthine oxidase in ischemic rat brain

1989 ◽  
Vol 71 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Yuji Kinuta ◽  
Mieko Kimura ◽  
Yoshinori Itokawa ◽  
Masatsune Ishikawa ◽  
Haruhiko Kikuchi
Keyword(s):  
Uric Acid ◽  
Free Radicals ◽  
Cerebral Ischemia ◽  
Xanthine Oxidase ◽  
Rat Brain ◽  
Oxidase Activity ◽  
High Performance ◽  
Vessel Occlusion ◽  
Content Type ◽  
Xanthine Oxidase Activity

✓ Xanthine oxidase activity in the rat brain was measured by means of high-performance liquid chromatography with electrochemical detection of uric acid. Cerebral ischemia was produced by a four-vessel occlusion method. In the control rat, the enzyme activity was 0.87 ± 0.13 nmol/gm wet weight/min at 25°C (mean ± standard deviation), of which 92.4% was associated with the nicotinamide adenine dinucleotide (NAD)-dependent dehydrogenase form and only 7.6% with the oxygen-dependent superoxide-producing oxidase form. However, the ratio of the latter form increased to 43.7% after 30 minutes of global ischemia, despite the total xanthine oxidase activity remaining the same. Thus, it was revealed that uric acid can be synthesized in the rat brain and that cerebral ischemia induced the conversion of xanthine oxidase from an NAD-dependent dehydrogenase to an oxygen-dependent superoxide-producing oxidase. Although the xanthine oxidase pathway has been proposed as a source of oxygen-derived free radicals in various ischemic organs other than brain, the results of the present study suggest the involvement of the oxygen free radicals generated from this pathway in the pathogenesis of the ischemic injury of the rat brain.

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