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Allopurinol

Allopurinol is a xanthine oxidase inhibitor used to treat hyperuricemia and prevent gout attacks.
It works by reducing the production of uric acid, which can accumulate in the joints and cause painful inflammation.
Allopurinol is effective in lowering serum uric acid levels and reducing the frequency of gout flares.
It may also be used to prevent kidney stones associated with high uric acid levels.
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Most cited protocols related to «Allopurinol»

The data set was prepared based on an extensive literature survey taking IC50 values of in-vitro enzyme inhibition assays against XO and HMGR by various secondary metabolites. Based on IC50 values, sixteen plant- and fungus-based secondary metabolites (Tables 1 and 2) were chosen for the ligand-protein docking study. The docking study was performed against commercial drugs such as atorvastatin, simvastatin, lovastatin, and pravastatin for HMGR. On the other hand, commercial drugs such as allopurinol, febuxostat, topiroxostat, and probenecid were used for molecular docking studies with XO. The structures of the ligand molecules and the control drugs of both enzymes were retrieved from the PubChem database [38 (link)] and verified from SciFinder. The structures were retrieved in SDF format and were converted to PDB and MOL2 format using Discovery Studio Visualizer 4.0 software. The structure and complete chemical properties, torsional energy, van der Waals potential energy, electrostatic energy, weight, log P, total polar surface area (TPSA), donor atoms, and acceptor atoms of the ligands were listed (Supplementary Table 4S) by the help of MOE Module [39 (link)].
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Publication 2021
Allopurinol Atorvastatin chemical properties Electrostatics Enzyme Assays Enzymes Febuxostat Fungi Ligands Lovastatin Molecular Structure Pharmaceutical Preparations Plants Pravastatin Probenecid Proteins Psychological Inhibition Simvastatin Tissue Donors topiroxostat
Thirty-seven dogs with clinical leishmaniosis were enrolled at the time of their diagnosis from January 2014 to May 2015. The dogs were treated at different Catalonian veterinary centers: Fundació Hospital Clínic Veterinari (Bellaterra, Barcelona), Hospital Ars Veterinaria (Barcelona), Hospital Mediterrani Veterinaris (Reus, Tarragona) and Consultori Montsant (Falset, Tarragona). The diagnosis of canine leishmaniosis (day 0) was made based on the results of a physical examination, a complete blood count (System Siemens Advia 120), a biochemical profile including creatinine, urea, total proteins, ALT and total cholesterol (Analyzer Olympus AU 400), serum electrophoresis (Hydrasys), urianalysis with urinary protein creatinine ratio (UPC) and quantitative serology for the detection of L. infantum-specific antibodies by means of an in-house diagnostic ELISA [11 (link)]. All dogs presented medium to high antibody levels [11 (link)]. Cytological or histological evaluations with Leishmania immunohistochemistry of cutaneous or other lesions were also performed when needed [19 (link)]. Dogs were classified into clinical stages at the time of diagnosis as previously described [2 (link)]. Dogs were treated with a daily subcutaneous injection of meglumine antimoniate (80–100 mg/kg) for a month and 10 mg/kg BID of oral allopurinol for 12 months. The dogs were followed up at days 30 (n = 36), 180 (n = 37) and 365 (n = 29) during treatment. A full physical examination and laboratory tests described above were also performed during treatment monitoring visits. A signed informed consent was obtained from all owners. Residual samples from blood EDTA tube and serum were used in this study. Therefore, ethical approval was not needed.
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Publication 2016
Allopurinol Antibodies BLOOD Canis familiaris Cholesterol Complete Blood Count Creatinine Diagnosis Edetic Acid Electrophoresis Enzyme-Linked Immunosorbent Assay Immunoglobulins Immunohistochemistry Leishmania Leishmaniasis Meglumine Antimoniate Physical Examination Proteins Serum Subcutaneous Injections Urea Urine
All reagents were high grade and were purchased from Sigma with the following exceptions. RPMI, DMEM, Calcein and ethidium homodimer and other culture reagents were purchased from Invitrogen Inc (Grand Island, NY, USA) and the UCSF cell culture facility (UCSF, San Francisco, CA). Fetal bovine Serum Defined (FBS) was purchased from Hyclone Laboratories (Logan, UT, USA). PD98059, a MEK inhibitor; SP600 125, a JNK inhibitor; wortmanin an inhibitor of PI3 kinase and pyrrolidinecarbodithoic acid (PDTC), a NF-κB inhibitor); AG490, a JAK2-STAT inhibitor were purchased from Calbiochem (San Diego, CA). LPS (Escherichia coli, O26:B6), aminoguandine, apocynin, allopurinol, minocycline, N(omega)-hydroxy-L-arginine (NOHA), indomethacin and amino-3-morpholinyl-1,2,3-oxadiazolium chloride (SIN-1) were purchased from Sigma (St Louis, MO). Drugs were dissolved in DMSO or ethanol and stored at -20°C and either used (final concentration of vehicle 0.1% (v/v or dried down and resuspended in PBS/0.1% bovine serum albumin (BSA). Mitogen activated kinase (MAPK) Anti-phospho-ERK monoclonal antibody (mAb), anti-ERK polyclonal antibody (#4370), anti-phospho-p38 MAPK mAb (# 4631), anti-phospho-JNK/SAPK mAb (#4668) were from Cell Signaling Technology (Danvers, MA); anti-NF-κBp65 (# SC-8008), anti-IκBα (# SC-1643) and respective horseradish peroxidase-coupled secondary antibodies were purchased from Santa Cruz (Santa Cruz, CA) and. Antibodies against iNOS ( # 61043), iNOS positive control lysates (#611473) were from BD Biosciences (BD Biosciences, Lexington, KY).
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Publication 2011
1-Phosphatidylinositol 3-Kinase acetovanillone Acids AG-490 Allopurinol alpha, NF-KappaB Inhibitor Antibodies Antibodies, Anti-Idiotypic Arginine Cell Culture Techniques Chlorides Escherichia coli Ethanol ethidium homodimer fluorexon Horseradish Peroxidase I-kappa B Proteins Indomethacin JAK2 protein, human Minocycline Mitogens Monoclonal Antibodies NOS2A protein, human PD 98059 Pharmaceutical Preparations Phosphotransferases prolinedithiocarbamate Serum Albumin, Bovine Sulfoxide, Dimethyl
ARIC is a population-based cohort study of 15,792 individuals recruited in 1987–89 from 4 US communities (Washington County, Maryland; Forsyth County, North Carolina; Jackson, Mississippi; Minneapolis, Minnesota; Figure 2). The institutional review board of the participating institutions (Johns Hopkins University, University of Mississippi, Wake Forest University, University of Minnesota, Baylor University, University of Texas, and University of North Carolina) approved the ARIC study protocol and study participants provided written informed consent. This study consisted of 1 baseline visit (visit 1) and 3 followup visits (visits 2, 3, and 4) administered 3 years apart. Importantly, there was a surveillance component to ARIC throughout the followup period. When a participant was hospitalized within the catchment area of the participating institutions, all of the corresponding discharge diagnoses were recorded.
Our study population consisted of men and women who self-reported their gout status at visit 4. Notably, at ARIC visit 4 each participant was asked, “Has a doctor ever told you that you had gout?”. Participants who answered “Yes” were considered to have a self-reported, physician-diagnosed case of gout. If a participant was recorded through surveillance as having a hospital discharge summary that listed an International Classification of Diseases (ICD)-9 code for gout (274.0, 274.1, 274.8, or 274.9), then they were considered to have gout based on this assignment of a gout discharge diagnosis. Therefore, if a participant attended visit 4 and the date of the gout-related hospitalization was prior to the visit 4 date, they were considered to be a gout case for the assessment of sensitivity. In addition, at each of the 4 ARIC visits, all medications used within the preceding month were recorded. We defined gout medications as colchicine, probenecid, and allopurinol. If a participant reported the use of any of these 3 medications at any study visit, they were considered to be a gout case. In our study, the gold standard for a diagnosis of gout was defined as either a hospital discharge diagnosis of gout or use of gout medication at any cohort visit. Although a prescription for these medications does not mean with absolute certainty that the ARIC participant has gout, in a random sample of 4 US communities, a prescription for colchicine, allopurinol, or probenecid is most likely issued to treat gout.
The gold standard gout definition was applied to all participants who attended visit 4. We calculated the sensitivity of a self-report of physician-diagnosed gout. Sensitivity was defined as the percentage of gold standard gout cases with a corresponding affirmative self-report of gout on the visit 4 questionnaire. Next, we conducted a stratified analysis for the sensitivity of a self-report of physician-diagnosed gout by sex, race, education, and hyperuricemia (serum urate level > 7.0 mg/dl at either visit 1 or 2) categories.
Additionally, we performed a sensitivity analysis to assess whether the sensitivity of a report of gout at visit 4 depended upon the definition of the gold standard. Specifically, we calculated sensitivity, separately, for participants with a hospital discharge diagnosis of gout as well as for those using gout medications. All analyses were performed in SAS, version 9.1 (SAS Institute, Cary, NC, USA).
Publication 2010
Allopurinol Colchicine Diagnosis Ethics Committees, Research Forests Gold Gout Hospitalization Hypersensitivity Hyperuricemia Patient Discharge Pharmaceutical Preparations Physicians Probenecid Serum Urate Woman
The MIC of allopurinol against P. aeruginosa PAO1 and C. violaceum CV026 were determined by the broth microdilution method according to the Clinical Laboratory and Standards Institute Guidelines (CLSI, 2015) [6 (link),26 (link)]. Several dilutions of allopurinol (32, 16, 8, 4, 2, 1, 0.5, and 0.25 mg/mL) were prepared in Mueller–Hinton broth by two-fold serial dilution. Aliquots of 100 µl of allopurinol dilutions were delivered into the wells of microtiter plates. Then, aliquots of 100 µl of bacterial suspension in MH broth with an approximate cell density of 1 × 106 CFU/mL were added to the wells. After overnight incubation of the microtiter plate at 37 °C, the growth was observed in the wells and the MIC was detected as the least concentration of allopurinol that inhibited observable growth.
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Publication 2021
Allopurinol Bacteria Clinical Laboratory Services Pseudomonas aeruginosa Technique, Dilution

Most recents protocols related to «Allopurinol»

Example 5

FIG. 16 illustrates (A) a biosynthetic scheme for conversion of L-tyrosine to bisBlAs and (B) yeast strains engineered to biosynthesize bisBlAs, in accordance with embodiments of the invention. In particular, FIG. 16 illustrates (A) a pathway that is used to produce bisBlAs berbamunine and guattegaumerine. FIG. 16 provides the use of the enzymes ARO9, aromatic aminotransferase; ARO10, phenylpyruvate decarboxlase; TyrH, tyrosine hydroxylase; DODC, DOPA decarboxylase; NCS, norcoclaurine synthase; 6OMT, 6-O-methyltransferase; CNMT, coclaurine N-methyltransferase; CYP80A1, cytochrome P450 80A1; CPR, cytochrome P450 NADPH reductase. Of the metabolites provided in FIG. 16, 4-HPA, 4-HPP, and L-tyrosine are naturally synthesized in yeast. Other metabolites that are shown in FIG. 16 are not naturally produced in yeast.

In examples of the invention, a bisBIA-producing yeast strain, that produces bisBlAs such as those generated using the pathway illustrated in (A), is engineered by integration of a single construct into locus YDR514C. Additionally, FIG. 16 provides (B) example yeast strains engineered to synthesize bisBlAs. Ps6OMT, PsCNMT, PsCPR, and BsCYP80A1 were integrated into the yeast genome at a single locus (YDR514C). Each enzyme was expressed from a constitutive promoter. The arrangement and orientation of gene expression cassettes is indicated by arrows in the schematic. These strains convert (R)- and (S)-norcoclaurine to coclaurine and then to N-methylcoclaurine. In one example, the strains may then conjugate one molecule of (R)—N-methylcoclaurine and one molecule of (S)—N-methylcoclaurine to form berbamunine. In another example, the strains may conjugate two molecules of (R)—N-methylcoclaurine to form guattegaumerine. In another example, the strains may conjugate one molecule of (R)—N-methylcoclaurine and one molecule of (S)-coclaurine to form 2′-norberbamunine. In another embodiment, the strain may be engineered to supply the precursors (R)- and (S)-norcoclaurine from L-tyrosine, as provided in FIG. 5.

The construct includes expression cassettes for P. somniferum enzymes 6OMT and CNMT expressed as their native plant nucleotide sequences. A third enzyme from P. somniferum, CPR, is codon optimized for expression in yeast. The PsCPR supports the activity of a fourth enzyme, Berberis stolonifera CYP80A1, also codon optimized for expression in yeast. The expression cassettes each include unique yeast constitutive promoters and terminators. Finally, the integration construct includes a LEU2 selection marker flanked by loxP sites for excision by Cre recombinase.

A yeast strain expressing Ps6OMT, PsCNMT, BsCYP80A1, and PsCPR is cultured in selective medium for 16 hours at 30° C. with shaking. Cells are harvested by centrifugation and resuspended in 400 μL breaking buffer (100 mM Tris-HCl, pH 7.0, 10% glycerol, 14 mM 2-mercaptoethanol, protease inhibitor cocktail). Cells are physically disrupted by the addition of glass beads and vortexing. The liquid is removed and the following substrates and cofactors are added to start the reaction: 1 mM (R,S)-norcoclaurine, 10 mM S-adenosyl methionine, 25 mM NADPH. The crude cell lysate is incubated at 30° C. for 4 hours and then quenched by the 1:1 addition of ethanol acidified with 0.1% acetic acid. The reaction is centrifuged and the supernatant analyzed by liquid chromatography mass spectrometry (LC-MS) to detect bisBlA products berbamunine, guattegaumerine, and 2′-norberbamunine by their retention and mass/charge.

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Patent 2024
2-Mercaptoethanol 3-phenylpyruvate Acetic Acid Allopurinol Anabolism Barberry Base Sequence berbamunine Buffers Cells Centrifugation coclaurine Codon Cre recombinase Culture Media Cytochrome P450 Dopa Decarboxylase enzyme activity Enzymes Ethanol Gene Expression Genome Glycerin guatteguamerine higenamine Liquid Chromatography Mass Spectrometry Methyltransferase NADP NADPH-Ferrihemoprotein Reductase norcoclaurine synthase Plants Protease Inhibitors Retention (Psychology) S-adenosyl-L-methionine coclaurine N-methyltransferase S-Adenosylmethionine Saccharomyces cerevisiae Strains Transaminases Tromethamine Tyrosine Tyrosine 3-Monooxygenase
We considered five kidney-related phenotypes: eGFRcrea (based on creatinine, UKB field 30,700, instance 0), eGFRcys (based on cystatin C, UKB field 30720, instance 0), UACR (UKB fields 30,500 and 30,510), serum urate (UKB field 30,880, instance 0), and urea (UKB field 30,670, instance 0). eGFRcrea and eGFRcys were calculated using the CKD-EPI equations41 (link) and winsorized to 15 and 200 ml/min/1.73 m2. To calculate UACR, values for urinary albumin below the detection limit were set to the detection limit value. All phenotypes were inverse-normal transformed.
We fitted linear regression models to the phenotypes, adjusting for sex, age, and the first 40 genetic principal components, as provided by the UK Biobank. For secondary analyses, the same models were additionally adjusted for 639 SNPs for eGFR28 (link), 63 SNPs for UACR9 (link), and 184 SNPs for urate18 (link) to account for the potential effect of common variants.
CKD and gout were defined using ICD10 codes from hospital inpatient records (N18.*, M10.*, UKB field 41270). Microalbuminuria was defined as UACR > 30 mg/g. ExWAS were carried out for these clinically relevant outcomes and used to annotate the findings for continuous kidney markers with respect to the direction and significance of their association with disease. To further characterize the risk allele carriers of selected trait-associated variants, kidney disease was additionally defined by ICD codes for acute kidney injury (N17.9), CKD (N18.3, N18.4, N18.5, N18.9), polycystic kidney disease (Q61.2, Q61.3), and another kidney (N28.1) or ureter (N39.0) disease. Information on allopurinol treatment was obtained from a verbal interview on medication usage.
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Publication 2023
Albumins Alleles Allopurinol Creatinine Gene Components Gout Inpatient Kidney Kidney Diseases Kidney Injury, Acute Pharmaceutical Preparations Phenotype Polycystic Kidney Diseases Post-gamma-Globulin Serum Single Nucleotide Polymorphism Urate Urea Ureter Urine
The Wuling San (capsule) and allopurinol were purchased from Jiangxi Pinxin Pharmaceutical Co., Ltd. (Xinyu, China) and Shanghai Xinyi Wanxiang Pharmaceutical Co., Ltd. (Shanghai, China), respectively. Potassium oxonate (PO) and sodium carboxymethyl cellulose (CMC-Na) were purchased from Yuanye Biological Co., Ltd. (Shanghai, China). Yeast extract was bought from OXOID Ltd. (Basingstoke, UK). UA content detection kit was purchased from BioSino Bio-Technology & Science Inc. (Beijing, China). Catalase (CAT) assay kit, total antioxidant capacity (T-AOC) assay kit, malondialdehyde (MDA) assay kit, superoxide dismutase (SOD) assay kit, creatinine (Cr) assay kit, and blood urea nitrogen (BUN) assay kit were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China). The kits for the detection of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were bought from Neobioscience Technology Co., Ltd. (Shenzhen, China).
Publication 2023
Allopurinol Antioxidants Biological Assay Biopharmaceuticals Capsule Catalase Creatinine Interleukin-6 Malondialdehyde Pharmaceutical Preparations potassium oxonate Sodium Carboxymethylcellulose Superoxide Dismutase TNF protein, human Urea Nitrogen, Blood Yeast, Dried
Forty Specific Pathogen-Free (SPF) Sprague-Dawley (SD) male rats were purchased from SPF (Beijing) Biotechnology Co., Ltd (laboratory animal license number: SCXK (Jing) 2020–0033). Before the experiments, the rats were acclimated for one week to the experimental conditions (temperature: 22 ± 2°C; 12h dark-light cycle; humidity 50 ±10%) and were fed a standard diet with free access to water. The Ethics Committee of Beijing University of Chinese Medicine approved all proposals involving animals (BUCM-4-2022022802-1026) and the experimental procedures were carried out in accordance with the Guidelines on the Care and Use of Laboratory Animal issued by the Chinese Council on Animal Research and the Guidelines of Animal Care.
The rats were randomly divided into five groups (each group of 8): blank control (BC) group; model control (MC) group; Allopurinol (ALL) group (10mg/kg/d); Wuling San high-dose group (WLS-HD, 630mg/kg/d); Wuling San low-dose group (WLS-LD, 315mg/kg/d). Potassium oxonate, Allopurinol, and Wuling San (capsule) were suspended in the 0.5% CMC-Na solution, respectively. The yeast extract was dissolved in pure water. In order to induce HUA, all groups except the BC group were intragastrically given PO (750 mg/kg /d) for 14 days. The model group was given 0.5% CMC-Na, the ALL group was given allopurinol treatment, and the WLS groups were given different WLS treatments via gavage, respectively. In contrast, the BC group received 0.5% CMC-Na in comparable volumes. In order to simulate the purine metabolism disorder caused by human consumption of high-purine food and increase UA levels, all groups except the BC group were intragastrically given yeast extract (10g/kg/d) on the same day; meanwhile, the BC group received pure water in comparable volumes.
Publication 2023
Allopurinol Animals Animals, Laboratory Capsule Chinese Diet Ethics Committees Food Homo sapiens Humidity Males Metabolic Diseases Pharmaceutical Preparations potassium oxonate purine Rats, Sprague-Dawley Rattus norvegicus Specific Pathogen Free Tube Feeding Yeast, Dried
The sensitivity of individual B. burgdorferi strains including the WT 5A18NP1, Tn:0556 mutant, the entire operon deletion as well as its complement to H2O2 was determined using an outgrowth assay similar to one previously described [23 (link)]. Cells were grown for 3 days in BSK-II. The cell density of the cultures was determined using dark-field microscopy, and the cultures were diluted to a concentration of 2×107 ml−1 and grown overnight. Spirochetes were again counted under darkfield microscopy and 8.75×107 cells were exposed to 125 µM or 185 µM H2O2 for 4 h at 32 °C. The concentration of H2O2 for each experiment was chosen to result in approximately 50 % survival of the parental strain, which varied between bottles of H2O2. At the end of the stress exposure, the cells were diluted fivefold in BSK-II. Cell density was quantified after 3 days, when the cell density of the untreated control reached ~1×108 ml−1. A percent outgrowth was determined for each strain by enumerating cell numbers using dark-field microscopy and then comparing the treated samples to the untreated controls. For experiments using allopurinol or uric acid, strains were exposed to the treatment (1 mM allopurinol, 300 nM uric acid) or DMSO control for 2 h and washed twice prior to counting and exposure to H2O2.
Publication 2023
Allopurinol Biological Assay Cell Culture Techniques Deletion Mutation Hypersensitivity Microscopy Operon Parent Peroxide, Hydrogen Spirochetes Strains Sulfoxide, Dimethyl Uric Acid

Top products related to «Allopurinol»

Sourced in United States, Germany, United Kingdom, Italy, France, Japan, Sao Tome and Principe
Allopurinol is a laboratory reagent used in the study of purine metabolism. It functions as an inhibitor of the enzyme xanthine oxidase, which is involved in the breakdown of purines. The core function of Allopurinol is to facilitate the investigation of purine-related metabolic processes in research settings.
Sourced in United States, Germany, Italy, Spain, Poland, China, Japan, Sao Tome and Principe
Xanthine is a laboratory equipment product manufactured by Merck Group. It is a chemical compound used as a reagent in various analytical and research applications. Xanthine serves as a core functional component in these laboratory procedures, but a detailed description of its intended use is not available within the scope of this request.
Sourced in United States, Germany, Japan, Spain, Italy, Sao Tome and Principe, Macao, Chile, Poland, China
Xanthine oxidase is a lab equipment product used for the detection and quantification of xanthine and hypoxanthine levels. It catalyzes the oxidation of xanthine to uric acid, a key step in purine metabolism. The enzyme can be used in various biochemical and analytical applications to measure these purine metabolites.
Sourced in United States, China
Potassium oxonate is a chemical compound used in laboratory settings. It is a white, crystalline powder that serves as a precursor for the synthesis of other chemical compounds. The core function of potassium oxonate is to provide a source of the potassium and oxonate ions for various chemical reactions and applications.
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Uric acid is a laboratory reagent used in the quantitative determination of uric acid levels in biological samples, such as blood or urine. It is a chemical compound that serves as a diagnostic tool for various medical conditions, including gout, kidney disorders, and metabolic disorders. The core function of uric acid is to provide an analytical measurement of this substance in the body, which can help healthcare professionals assess and monitor a patient's health status.
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
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Quercetin is a natural compound found in various plants, including fruits and vegetables. It is a type of flavonoid with antioxidant properties. Quercetin is often used as a reference standard in analytical procedures and research applications.
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DPPH is a chemical compound used as a free radical scavenger in various analytical techniques. It is commonly used to assess the antioxidant activity of substances. The core function of DPPH is to serve as a stable free radical that can be reduced, resulting in a color change that can be measured spectrophotometrically.
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Apocynin is a chemical compound used in laboratory settings. It functions as an inhibitor of the enzyme NADPH oxidase, which plays a role in the production of reactive oxygen species. Apocynin is commonly utilized in research applications to investigate the involvement of oxidative stress in various biological processes.
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Hypoxanthine is a purine base that is an intermediate in the metabolism of purines. It is a colorless, crystalline compound that is used as a cellular nutrient in cell culture media and as a reference standard in analytical chemistry.

More about "Allopurinol"

Allopurinol is a powerful xanthine oxidase inhibitor that is widely used to treat hyperuricemia and prevent gout attacks.
This medication works by reducing the production of uric acid, which can accumulate in the joints and cause painful inflammation.
By lowering serum uric acid levels, allopurinol is effective at reducing the frequency of gout flares.
Xanthine, a purine metabolite, is the primary substrate for the enzyme xanthine oxidase.
This enzyme catalyzes the oxidation of xanthine to uric acid, the end product of purine metabolism.
Inhibiting xanthine oxidase, as allopurinol does, decreases the amount of uric acid produced and can help prevent the formation of painful uric acid crystals in the joints.
In addition to its use in treating gout, allopurinol may also be prescribed to prevent kidney stones associated with high uric acid levels.
The medication can help dissolve existing stones and reduce the risk of new stone formation.
Researchers can leverage the power of PubCompare.ai's AI-driven platform to easily locate and compare research protocols for allopurinol from a variety of sources, including scientific literature, preprints, and patents.
This optimization tool can help scientists make more informed decisions and streamline their studies, unlocking the future of protocol optimization today.
Other compounds that may be of interest in the context of allopurinol and uric acid metabolism include potassium oxonate, a uricase inhibitor; DMSO, a solvent with anti-inflammatory properties; quercetin, a natural flavonoid with antioxidant effects; DPPH, a free radical scavenging compound; and apocynin, an NADPH oxidase inhibitor.
Exploring the interactions and mechanisms of these related substances can provide valuable insights into the complex pathways involved in uric acid production and gout pathogenesis.