scholarly journals The effect of chayote leaves (Sechium edule)’s flavonoid fraction on the reduction of the serum uric acid levels through the inhibition of xanthine oxidase activity

10.5219/1667 ◽  
2021 ◽  
Vol 15 ◽  
pp. 1049-1055
Author(s):  
Diah Pitaloka Putri ◽  
Aulia Putri Wahyuningtyas ◽  
Ahmad Ni'matullah Al-Baarri ◽  
Nani Maharani
Keyword(s):  
Body Weight ◽  
Uric Acid ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Sprague Dawley ◽  
Xanthine Oxidase Activity ◽  
Sechium Edule ◽  
Sprague Dawley Rats ◽  
Flavonoid Fraction ◽  
Potassium Oxonate

Uric acid is the final product of purine metabolism and is categorized as hyperuricemia when it reaches >6.0 mg.dL-1 for women and >7.0 mg.dL-1 for men. The chayote leaves (Sechium edule) contain a high amount of flavonoid and might be used as an alternative to reduce hyperuricemia. The purpose of this study is to analyze the effect of chayote leaves (Sechium edule)’s flavonoid fraction on the level of uric acid and the activity of xanthine oxidase (XO) in Sprague Dawley Rats. The flavonoid fraction (FF) was obtained by extracting the chayote leaves, fractionating with n-hexane, hydrolyzing with HCl, and finally re-fractionating with ethyl acetate. Thirty male Sprague Dawley rats were induced for hyperuricemia by potassium oxonate and broth block for 21 days, and the interventions were given orally for 14 days. The rats were divided randomly into five groups: normal control (K-), hyperuricemia control (K+), hyperuricemia with FF dose 50 mg.200g-1 body weight (P1), hyperuricemia with FF dose 100 mg.200g-1 body weight (P2) and hyperuricemia with allopurinol 1.8 mg.200g-1 body weight. Xanthine oxidase activity was measured by CheKineTM Xanthine Oxidase Assay Kit, with simple colorimetry methods. The statistical analysis for XO activity was done using Kruskal-Wallis followed by Mann Whitney. The results showed that chayote leaves (Sechium edule)’s flavonoid fraction contains apigenin, apigenin o-glucoside, and luteolin. It also has antioxidant activity with 98.45% inhibition.  There was a significant reduction in xanthine oxidase activity in groups treated with FF (p <0.005). The best dose of FF affecting XO activity was 100 mg.200g-1 body weight. The combination of FF and allopurinol can be more effective in decreasing uric acid levels by inhibiting XO activity.

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 PENGHAMBATAN KSANTIN OKSIDASE OLEH KOMBINASI EKSTRAK TEMPUYUNG (Sonchus Arvensis) DAN SALAM (Syzygium Polyanthum) PADA MENCIT HIPERURISEMIA

Biomedika ◽  
2012 ◽  
Vol 5 (1) ◽  
Author(s):  
Dr. Muhtadi . ◽  
Idi Retnani ◽  
Nurcahyanti Wahyuningtyas
Keyword(s):  
Uric Acid ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Xanthine Oxidase Activity ◽  
Group I ◽  
Sonchus Arvensis ◽  
Potassium Oxonate

Tempuyung (Sonchus arvensis) and salam (Syzygium polyanthum) leaves can lower uric acid levels were studied. The purpose of this research was to determine mechanism of combined o f tempuyung and salam extracts to reduce uric acid levels by inhibiting xanthine oxidase in hyperuricemic mice. This research used completely randomized design using mice. Fifteen mice were made hiperuricemic by 250 mg/kgBW potassium oxonate p.o then the mice were divided into 3 groups. Group I induced 10 mg/kgBW allopurinol p.o as positive control, group II induced tempuyung-salam p.o each 100 mg/kgBW as the treatment group, group th III induced 0.5 mL/20 gBW distilled water p.o as negative control. Liver was taken 4 day after 2 hours induced potassium oxonate. Data inhibition xanthine oxidase activity was tested with Mann-Whitney. The result showed that the combination of tempuyung-salam extract each 100 mg/kgBW could inhibit xanthine oxidase activity of 51,16%±2,76%, while allopurinol 90,20%±0,16% (p = 0.000).Keyword: Hyperuricemia, Xanthine Oxidase, Sonchus arvensis, Syzygium polyanthum

Hypouricemic and Nephroprotective Effects of Emodinol in Oxonate-Induced Hyperuricemic Mice are Mediated by Organic Ion Transporters and OIT3

Planta Medica ◽  
2015 ◽  
Vol 82 (04) ◽  
pp. 289-297 ◽  
Author(s):  
Wu Hui ◽  
Yuan Yongliang ◽  
Chen Yongde ◽  
Lu Guo ◽  
Lan Li ◽  
...  
Keyword(s):  
Uric Acid ◽  
Renal Dysfunction ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Glucose Transporter ◽  
Organic Anion ◽  
Organic Anion Transporter ◽  
Xanthine Oxidase Activity ◽  
Anion Transporter ◽  
Potassium Oxonate

AbstractEmodinol, 1β,3β,23-trihydroxyolean-12-en-28-acid, as the main active ingredient firstly extracted from the rhizomes of Elaeagus pungens by our research group, has been demonstrated to exhibit uricosuric activity by our previous study. The aim of this study was to evaluate the uricosuric and nephroprotective effects of emodinol and explore its possible mechanisms in potassium oxonate-induced hyperuricemic mice with renal dysfunction. Mice were orally administrated 250 mg/kg of potassium oxonate once daily for 7 consecutive days to induce hyperuricemia with renal dysfunction. Emodinol was given at doses of 25, 50, and 100 mg/kg on the same day 1 h after oxonate treatment, and allopurinol (10 mg/kg) was given as a positive control. After 1 week, serum uric acid, serum creatinine, urine uric acid, urine creatinine, blood urea nitrogen, and hepatic xanthine oxidase activity were determined. The mRNA and protein levels of urate transporter 1, glucose transporter 9, ATP-binding cassette subfamily G member 2, organic anion transporter 1, oncoprotein-induced transcript 3, and organic cation/carnitine transporters in the kidney were detected by real-time polymerase chain reaction and Western blot analysis. In addition, urinary and renal Tamm-Horsfall glycoprotein concentrations were examined by ELISA assays. Emodinol significantly reduced serum urate levels, increased urinary urate levels and fractional excretion of uric acid, and inhibited hepatic xanthine oxidase activity in hyperuricemic mice. Moreover, potassium oxonate administration led to dys expressions of renal urate transporter 1, glucose transporter 9, ATP-binding cassette subfamily G member 2, organic anion transporter 1, and oncoprotein-induced transcript 3 as well as alternations of uromodulin concentrations, which could be reversed by emodinol. On the other hand, treatment of emodinol caused upregulated expressions of organic cation/carnitine transporters, resulting in an improvement of renal function characterized by decreased serum creatinine and blood urea nitrogen levels. Emodinol exhibited hypouricemic and nephroprotective actions by inhibiting xanthine oxidase activity and regulating renal ion transporters and oncoprotein-induced transcript 3, which may be a potential therapeutic agent in hyperuricemia and renal dysfunction.

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 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

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.

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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