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Purines perform many important functions in the cell, being the formation of the monomeric precursors of nucleic acids DNA and RNA the most relevant one. Purines which also contribute to modulate energy metabolism and signal transduction, are structural components of some coenzymes and have been shown to play important roles in the physiology of pl...
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... are further converted to purine base hypoxanthine and gua- nine, respectively, by purine nucleoside phosphorylase (PNP). Hypoxan- thine is then oxidized to form xanthine by xanthine-oxidase (XO), and guanine is deaminated to form xanthine by guanine deaminase. Xan- thine is again oxidized by xanthine oxidase to form the final product, uric acid. Fig. 1 shows the enzymatic pathway for the purines degrada- tion. At physiologic pH, uric acid is a weak acid with a pKα of 5.8. Uric acid exists majorly as urate, the salt of uric acid. As urate concentration increases in blood, uric acid crystal formation increases. The normal ref- erence interval of uric acid in human blood is 1.5 to 6.0 ...Context 2
... are further converted to purine base hypoxanthine and gua- nine, respectively, by purine nucleoside phosphorylase (PNP). Hypoxan- thine is then oxidized to form xanthine by xanthine-oxidase (XO), and guanine is deaminated to form xanthine by guanine deaminase. Xan- thine is again oxidized by xanthine oxidase to form the final product, uric acid. Fig. 1 shows the enzymatic pathway for the purines degrada- tion. At physiologic pH, uric acid is a weak acid with a pKα of 5.8. Uric acid exists majorly as urate, the salt of uric acid. As urate concentration increases in blood, uric acid crystal formation increases. The normal ref- erence interval of uric acid in human blood is 1.5 to 6.0 ...Similar publications
Objective: To examine the effects of oral sucrose on procedural pain and biochemical markers of adenosine triphosphate utilization and oxidative stress in preterm neonates with mild to moderate respiratory distress.
Study design: Preterm neonates with a clinically required heel lance that met study criteria (n = 49) were randomized into three group...
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High-performance liquid chromatographic methods for directly determining products of nucleic acid and purine catabolism in urine and blood plasma of sheep were developed. Urine and plasma samples were diluted 1:3 with deionized water. Fractionation and quantification of allantoin, uric acid, hypoxanthine and xanthine were performed using two Nova-P...
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The authors describe a fluorescent “turn-on” assay for detection of uric acid (UA) based on the use of graphene quantum dots coated with a shell of silver (GQD@Ag). The fluorescence of the GQDs is quenched by the silver shell. However, if the silver shell was removed via etching with H2O2 (which is produced by uricase catalyzed oxidation of UA), th...
Citations
... Hyperuricemia (HUA) is a chronic metabolic disease due to excessive production or impaired excretion of uric acid in the body (Maiuolo et al., 2016), and has been associated with adverse health outcomes such as hypertension, diabetes, chronic kidney disease, and other chronic diseases, as well as higher rates of hospital admissions and longer hospital stays (Li et al., 2021;Maiuolo et al., 2016). A recent meta-analysis showed that the pooled prevalence of HUA in China during 2000-2019 was estimated at 16.4% in general population, 20.5% in those aged 60 years or over, and 24.9% in those aged over 70 years (Li et al., 2021). ...
... Hyperuricemia (HUA) is a chronic metabolic disease due to excessive production or impaired excretion of uric acid in the body (Maiuolo et al., 2016), and has been associated with adverse health outcomes such as hypertension, diabetes, chronic kidney disease, and other chronic diseases, as well as higher rates of hospital admissions and longer hospital stays (Li et al., 2021;Maiuolo et al., 2016). A recent meta-analysis showed that the pooled prevalence of HUA in China during 2000-2019 was estimated at 16.4% in general population, 20.5% in those aged 60 years or over, and 24.9% in those aged over 70 years (Li et al., 2021). ...
Previous studies have related single toxic metals (TMs) to hyperuricemia (HUA) among the general population, however, the association of the TM mixture with HUA, especially in older adults, remains poorly understood. We aimed to examine the relationships between individual TMs and their mixture and HUA in Chinese rural older adults. This study consisted of 2075 rural older adults aged 60 years or over. Blood concentrations of aluminum (Al), arsenic (As), barium (Ba), cadmium (Cd), cesium (Cs), gallium (Ga), mercury (Hg), lead (Pb), thallium (Tl), and uranium (U) were detected using inductively coupled plasma mass spectrometry. The associations of single TMs with HUA were assessed using logistic regression and restricted cubic spline (RCS) models, and the association of TM mixture with HUA was explored using the elastic net with environmental risk score (ENET-ERS), quantile g-computation (QGC), and Bayesian kernel machine regression (BKMR) models, respectively. Adjusted logistic regression model showed that Cs (OR = 1.65, 95% CI 1.37–1.99) and Pb (OR = 1.46, 95% CI 1.28–1.67) were positively related to HUA, and RCS model exhibited a positive linear association of Cs and Pb with HUA. ENET-ERS and QGC models quantified a positive correlation between the TM mixture and the odds of HUA, with estimated ORs of 1.15 (95% CI 1.11–1.19) and 1.84 (95% CI 1.37–2.47), respectively, and Cs and Pb had the most weight. BKMR model demonstrated a significant linear association between the TM mixture and increased odds of HUA, with the posterior inclusion probabilities (PIPs) of both Cs and Pb being 1.00. Moreover, we observed a positive interaction between Cs and Pb on HUA. The TM mixture is associated with increased odds of HUA in rural older adults, which may mainly be driven by Cs and Pb. Subsequent studies are warranted to confirm these findings and clarify the mechanisms linking multiple TMs with HUA.
... [5][6][7] Recently, a few studies have demonstrated that elevated levels of uric acid (UA) and high-sensitivity C-reactive protein (hs-CRP) may contribute to CCB. 8,9 UA, which is produced as a result of purine metabolism with the help of xanthine oxidase, has been extensively studied for its association with cardiovascular diseases (CVD). 10,11 Epidemiological evidence consistently suggests that hyperuricemia (HUA), characterized by elevated UA levels, is a risk factor for various cardiovascular conditions. 11,12 UA levels are positively correlated with hs-CRP levels, which are proteins produced following inflammation, infection, or tissue damage and are associated with chronic diseases. ...
Objective
This study aimed to explore the impact of a combination of hyperuricemia (HUA) and excessive high-sensitivity C-reactive protein (hs-CRP) levels on the likelihood of developing cardiac conduction block (CCB). Additionally, it sought to assess whether the influence of uric acid (UA) on CCB is mediated by hs-CRP.
Methods
A prospective study was executed utilizing data from the Kailuan cohort, including 81,896 individuals initially free from CCB. The participants were categorized into four groups depending on the existence of HUA and low-grade inflammation (hs-CRP>3 mg/L). Cox regression analysis was employed to ascertain hazard ratios (HRs) and 95% confidence intervals (CIs) for the risk of incident CCB. A mediation analysis was performed to determine if hs-CRP functioned as a mediator in the connection between UA levels and the incidence of CCB.
Results
During a median observation period of 11.8 years, we identified 3160 cases of newly occurring CCB. Compared with the low UA/low CRP group, the combination of HUA and low-grade inflammation elevated the CCB risks (HR:1.56, 95% CI:1.22–1.99), atrioventricular block (AVB) (HR:1.88, 95% CI:1.27–2.77), and right bundle branch block (HR:1.47, 95% CI:1.02–2.12), respectively. Mediation analysis revealed that in the HUA group, compared with the non-HUA group, the risk of CCB elevated by 14.0%, with 10.3% of the increase mediated through hs-CRP.
Conclusion
HUA combined with elevated hs-CRP increased the risk of CCB, especially AVB. The connection between UA and the CCB risk was partly mediated by hs-CRP.
... Results from CU therapy was comparable with antibiotics available in the market such as ofloxacin, ciprofloxacin, ampicillin, chloramphenicol, nalidixic acid, rifampicin, tetracycline, streptomycin, cefpodoxime and gentamycin. The CU is reported similar antimicrobial action with minimum or no side effects which is commonly observed in case of commercial antibiotics [1,5,17,23,91,152,157,159,160]. ...
The use of cow urine (CU) in treating a variety of illness can be traced back to ancient ages. It has been referred as an important and integral component of Cowpathy – an age-old practice in Indian sub-continent since the Vedic period (1500 BC – 600 BC). The CU contains several important compounds that are essential in maintaining a balance between the well-being of human and the nature. It is composed of about 95 % water and other useful ingredients such as urea, hormones, lyase enzyme, and salts containing Fe, Ca, P, Mn, S, N, and K. In addition, it also contains lactose, cytokine, and amino acid which are the fundamental building blocks of protein. Researchers have developed various processes for the green synthesis of CU concentrate and evaluated its usefulness in treating various diseases owing to its antibacterial and antifungal properties. Further, CU has also shown promising immunity boosting and anti-oxidant characteristics. Even though human civilization has benefited from the use of CU in treating various types illness but the modern scientific understanding of the cause-effect relationships was partly developed in the last few decades. There exists a huge knowledge gap and a comprehensive study on exploring the science and application of CU hasn’t been reported. This paper reviews the historical perspective, compositional analysis, processing, applications, knowledge gap, and future research required in the field of therapeutic usage of CU.
... In general, the reference interval of serum UA is 1.5 to 6.0 mg/dl in women and 2.5 to 7.0 mg/dl in men. Hyperuricemia is defined as a serum UA level greater than 6.0 mg/dL in women and 7.0 mg/dL in men [29]. Only suitable concentrations of serum UA may have a protective effect. ...
Background
Serum uric acid (UA) and the neutrophil-to-lymphocyte ratio (NLR) have been reported to be associated with outcomes in acute ischemic stroke (AIS). However, whether UA is related to the prognosis of AIS patients undergoing intravenous thrombolysis (IVT) remains inconclusive. We sought to explore the combined effect of UA and NLR on the prognosis of AIS treated with IVT.
Methods
A total of 555 AIS patients receiving IVT treatment were enrolled. Patients were categorized into four groups according to the levels of UA and NLR: LNNU (low NLR and normal UA), LNHU (low NLR and high UA), HNNU (high NLR and normal UA), and HNHU (high NLR and high UA). Multivariable logistic regression analysis was used to evaluate the value of serum UA level and NLR in predicting prognosis. The primary outcomes were major disability (modified Rankin scale (mRS) score 3–5) and death within 3 months.
Results
After multivariate adjustment, a high NLR (≥ 3.94) increased the risk of 3-month death or major disability (OR, 2.23; 95% CI, 1.42 to 3.55, p < 0.001). However, there was no statistically significant association between a high UA level (≥ 313.00 µmol/L) and clinical outcome. HNHU was associated with a 5.09-fold increase in the risk of death (OR, 5.09; 95% CI, 1.31–19.83; P value = 0.019) and a 1.98-fold increase in the risk of major disability (OR, 1.98; 95% CI 1.07–3.68; P value = 0.030) in comparison to LNNU.
Conclusions
High serum UA levels combined with high NLR were independently associated with 3-month death and major disability in AIS patients after IVT.
... Quail, similar to humans, lack uricase in their UA synthesis and metabolism processes. The nucleic acids produced from nucleotide proteolytic hydrolysis are degraded into purine substances, which are then converted into UA by XOD and excreted as UA (99,100). An animal experiment in quail, involving a model of endogenous gout induced by a high-purine diet, examined administration of rutin for 10 days. ...
The present review expounds the advancements in the application and mechanisms of flavonoids in gouty arthritis, highlighting their significance in managing the disease. Gouty arthritis is among the most common and severe inflammatory diseases, caused by hyperuricemia and the deposition of sodium urate crystals in the joints and surrounding tissues, posing a serious threat to human life and health. Flavonoids, extracted from various herbs, have attracted significant attention due to their efficacy in improving gouty arthritis. The present study systematically reviews the in vivo studies and in vitro animal studies on flavonoids from herbal medicines for the treatment of gouty arthritis that have been previously published in the PubMed, ScienceDirect, Google Scholar and China National Knowledge Infrastructure databases between 2000 and 2023. The review of the literature indicated that flavonoids can improve gouty arthritis through multiple mechanisms. These include lowering xanthine oxidase activity, inhibiting uric acid (UA) synthesis, regulating UA transporters to promote UA excretion, reducing the inflammatory response and improving oxidative stress. These mechanisms predominantly involve regulating the NOD‑like receptor 3 inflammasome, the Toll‑like receptor 4/myeloid differentiation factor 88/nuclear factor‑κB signaling pathway, and the levels of UA transporter proteins, namely recombinant urate transporter 1, glucose transporter 9, organic anion transporter (OAT)1 and OAT3. Various flavonoids used in traditional Chinese medicine hold therapeutic promise for gouty arthritis and are anticipated to pave the way for novel pharmaceuticals and clinical applications.
... Abnormal purine metabolism may directly affect the metabolic function of liver. The liver is one of the main sites of purine synthesis and uric acid production, and the disorder of purine metabolism may lead to excessive production or insufficient excretion of uric acid, and then cause hyperuricemia (Maiuolo et al., 2016). In addition, oxidative stress and inflammation in the liver may also be exacerbated by abnormal purine metabolism, which together affect liver function and aggravate the condition of type 2 diabetes . ...
Our previous study revealed that red kidney bean polysaccharides (RKB) exhibit a pronounced hypoglycemic effect on type 2 diabetic rats, while simultaneously exerting a significant ameliorative impact on hepatic damage in these animals. However, the precise mechanism underlying the effects of RKB on diabetes and liver metabolism remains unproven. In this study, we utilized a mouse model of type 2 diabetes induced by a high‐fat diet combined with streptozotocin to investigate the impact of RKB. We administered a combined intervention involving antibiotics, fexaramine, and RKB to elucidate the mechanism underlying RKB's effects. Our findings demonstrated that RKB significantly ameliorated liver function indices and histopathological injuries. Nevertheless, when antibiotics and fexaramine were introduced as interventions, they hindered the beneficial effects of RKB on liver function in type 2 diabetic mice. Furthermore, our nontargeted metabolomics analysis revealed that antibiotics and fexaramine exerted their inhibitory actions on RKB efficacy through modulation of distinct metabolites involved in glycerophospholipid and purine metabolic pathways.
... Introduction Hyperuricemia (HUA) is a metabolic disease. Purine metabolism disorder in the body decreased excretion or increased production of serum uric acid (SUA), which developed into HUA [1]. The prevalence and incidence of HUA in the world population have been continuously rising over the past four decades [2,3], which has been considered as an emerging public health concern over the world. ...
Background
The relationship between physical activity and hyperuricemia (HUA) remains inconsistent, and the dose-response association between moderate-to- vigorous physical activity (MVPA) level and HUA still unclear. In this study, we aimed to investigate the dose-response association of MVPA with HUA, and to explore an appropriate range of MVPA level for preventing HUA.
Methods
Data from the US National Health and Nutrition Examination Survey (NHANES) 2007–2018 were used, including 28740 non-gout adult Americans. MVPA level was self-reported using the Global Physical Activity Questionnaire and serum uric acid was measured using timed endpoint method. The dose-response relationship between MVPA level and HUA was modeled with restricted cubic spline analysis. Logistic regression analysis were applied to estimate odd ratios (ORs) and 95% confidence intervals (CIs) of the relationships between MVPA level and HUA.
Results
A total of 28740 adults were included in the study (weighted mean age, 47.3 years; 46.5% men), with a prevalence rate of HUA was 17.6%. The restricted cubic spline functions depicted a general U-shaped relationship between MVPA level and HUA. The MVPA level of 933 and 3423 metabolic equivalent (MET) -min/wk were the cut-off discriminating for the risk of HUA. Participants with MVPA levels in the range of 933–3423 MET-min/wk had lower risk of HUA and they had the lowest risk when MVPA levels at around 1556 MET-min/wk. Compared with the moderate-activity group (600–2999 Met-min/wk), the low-activity group (< 600 Met-min/wk) had a greater risk of HUA (OR, 1.13 [95%CI, 1.02–1.26]) after fully adjusting for potential confounders.
Conclusions
Compared with the moderate MVPA level, the low MVPA level was associated with the higher risk of HUA. And there may be a U-shaped dose-response relationship between MVPA level and HUA. When MVPA level was approximately 933–3423 MET-min/wk, the risk of HUA may at a lower level and the risk reached the lowest when MVPA level at around 1556 MET-min/wk.
... 32,33 The majority of uric acid undergoes glomerular filtration, with its reabsorption and secretion predominantly occurring at the proximal tubule, where approximately 90% of it is reabsorbed into the bloodstream. 34 In our study, we enrolled healthy subjects unaffected by factors such as impaired kidney function or consumption of purine-rich foods or medications. ...
Pioglitazone is class of thiazolidinediones that activates peroxisome proliferator‐activated receptors (PPARs) in adipocytes to improve glucose metabolism and insulin sensitivity and has been used as a treatment for type 2 diabetes. However, the underlying mechanisms of associated pioglitazone‐induced effects remain unclear. Our study aimed to investigate endogenous metabolite alterations associated with pioglitazone administration in healthy male subjects using an untargeted metabolomics approach. All subjects received 30 mg of pioglitazone once daily in the assigned sequence and period. Urine samples were collected before pioglitazone administration and for 24 h after 7 days of administration. A total of 1465 compounds were detected and filtered using a coefficient of variance below 30% and 108 metabolites were significantly altered upon pioglitazone administration via multivariate statistical analysis. Fourteen significant metabolites were identified using authentic standards and public libraries. Additionally, pathway analysis revealed that metabolites from purine and beta‐alanine metabolisms were significantly altered after pioglitazone administration. Further analysis of quantification of metabolites from purine metabolism, revealed that the xanthine/hypoxanthine and uric acid/xanthine ratios were significantly decreased at post‐dose. Pioglitazone‐dependent endogenous metabolites and metabolic ratio indicated the potential effect of pioglitazone on the activation of PPAR and fatty acid synthesis. Additional studies involving patients are required to validate these findings.
... UA is the ultimate by-product of the breakdown of purine. An imbalance involving excessive UA production, diminished excretion or amalgamation of both factors can lead to hyperuricaemia, which is distinguished by elevated UA levels [8,9]. Gout is caused by excessive UA production, diminished excretion or a combination of both. ...
Uric acid (UA) levels in blood serum have been associated with hypertension, indicating a potential causal relationship between high serum UA levels and the progression of hypertension. Therefore, the reduction of serum UA level is considered a potential strategy for lowering and mitigating blood pressure. If an individual is at risk of developing or already manifesting elevated blood pressure, this intervention could be an integral part of a comprehensive treatment plan. By addressing hyperuricaemia, practitioners may subsidize the optimization of blood pressure regulation, which illustrates the importance of addressing UA levels as a valuable strategy within the broader context of hypertension management. In this analysis, we outlined the operational principles of effective xanthine oxidase inhibitors for the treatment of hyperuricaemia and hypertension, along with an exploration of the contribution of nanotechnology to this field.
... Previous research revealed that the enzymatic activities and expression levels of xanthine oxidase (XOD) and adenosine deaminase (ADA) in the livers of goslings infected with GAstV are significantly elevated, showing a clear difference compared to those in the livers of uninfected control goslings. This increase in enzymatic activity directly leads to a significant surge in uric acid production in goslings, which is considered a key factor in the development of hyperuricemia and gout [25,26]. Notably, uric acid is primarily excreted through the kidneys, and during this process, organic anion transporters, multidrug resistance-associated protein 4 (MRP4), sodium-dependent phosphate transport protein 1, and sodium-potassium pumps play crucial roles, collectively forming the main mechanism of uric acid transport in poultry [27,28]. ...
The goose astrovirus (GAstV), a key pathogen causing visceral gout and high mortality in geese, has spread widely in China, with frequent outbreaks in recent years. Outbreaks and transmissions of this virus have been reported across China, causing considerable economic losses to the goose industry worldwide, with losses exceeding tens of billions in China alone. However, there is still no effective prevention strategy against this virus. Therefore, continuous monitoring of the genetic diversity of dominant GAstV strains is crucial for developing targeted vaccines and appropriate therapeutics. As a crucial region for goose breeding in China, Hebei Province has previously lacked reports on the epidemiology of GAstV. Hence, investigating the epidemiology of GAstV in Hebei Province is highly important. From January 2019 to December 2021, 474 samples suspected of having a GAstV infection were collected in Hebei Province in this study. Through detailed histological observations, pathological examinations, virus isolation and identification, and genetic diversity analysis, we found that GAstV-2 has become the predominant circulating genotype. However, the presence of GAstV-1 and mixed infections cannot be ignored and should receive increased attention. The findings of this study not only deepened our understanding of GAstV in waterfowl in China but also provided scientific evidence for developing effective prevention and control measures, thereby promoting the healthy development of the goose industry in China.
