Molecular basis of oxidative stress in gouty arthropathy

Zamudio-Cuevas, Yessica; Hernández‐Díaz, Cristina; Pineda, Carlos; Reginato, Anthony M.; Cerna-Cortés, Jorge F.; Ventura‐Ríos, Lucio; López‐Reyes, Alberto

doi:10.1007/s10067-015-2933-y

Cited by 58 publications

(47 citation statements)

References 51 publications

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“…In the parallel, the antioxidant enzyme; glutathione peroxidase (GPx); helps in scavenging cellular free radicals. GPx prevents lipid peroxidation and maintain intracellular homeostasis [32]. In current study, hyperuricemia increased ROS due to the increase Fig.…”

Section: Discussionsupporting

confidence: 53%

Impact of Lesinurad and allopurinol on experimental Hyperuricemia in mice: biochemical, molecular and Immunohistochemical study

Alghamdi

Soliman

Nassan

2020

BMC Pharmacol Toxicol

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Background: Hyperuricemia is an abnormal increase in uric acid levels in the blood. It is the cause of gout that manifested by inflammatory arthritis and painful disable. Therefore, current study evaluated the potential ameliorative impact of Lesinurad and Allopurinol on the kidneys of hyperuricemic mice at the biochemical, molecular and cellular levels. Methods: Lesinurad and allopurinol alone or in combination were orally administered to hyperuricemic and control mice for seven consecutive days. Levels of uric acid and blood urea nitrogen, along with antioxidants and inflammatory cytokines (IL-1β and TNF-α) were measured in the serum. The mRNA expression of mouse urate anion transporter-1, glucose transporter 9, organic anion transporters, in renal tissues were examined using quantitative real time PCR. Simultaneously, the immunoreactivity of transforming growth factor-beta 1 was examined immunohistochemically. Results: Lesinurad and allopurinol administration resulted in significant decrease in serum levels of uric acid, blood urea nitrogen, xanthine oxidase activity, catalase, glutathione peroxidase and inflammatory cytokines (IL-1β and TNF-α) reported in hyperuricemic mice. Both partially reversed oxonate-induced alterations in renal mURAT-1, mGLUT-9, mOAT-1 and mOAT-3 expressions, as well as alterations in the immunoreactivity of TGF-β1, resulting in the increase of renal uric acid secretion and excretion. The combined administration of lesinurad and ALP restored all altered parameters in a synergistic manner, improving renal function in the hyperuricemic mouse model employed.Conclusion: This study confirmed synergistic ameliorative hypouricemic impact of both lesinurad and allopurinol in the treatment of hyperuricemia in mice at the biochemical, molecular and cellular levels.

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Section: Discussionsupporting

confidence: 53%

Impact of Lesinurad and allopurinol on experimental Hyperuricemia in mice: biochemical, molecular and Immunohistochemical study

Alghamdi

Soliman

Nassan

2020

BMC Pharmacol Toxicol

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“…It is a well-known risk factor for gout [1]. Moreover, a growing body of evidence suggests that high levels of serum UA are also biomarkers for cardiovascular disease (CVD) morbidity and mortality [2].…”

Section: Introductionmentioning

confidence: 99%

Fructose Intake, Serum Uric Acid, and Cardiometabolic Disorders: A Critical Review

et al. 2017

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There is a direct relationship between fructose intake and serum levels of uric acid (UA), which is the final product of purine metabolism. Recent preclinical and clinical evidence suggests that chronic hyperuricemia is an independent risk factor for hypertension, metabolic syndrome, and cardiovascular disease. It is probably also an independent risk factor for chronic kidney disease, Type 2 diabetes, and cognitive decline. These relationships have been observed for high serum UA levels (>5.5 mg/dL in women and >6 mg/dL in men), but also for normal to high serum UA levels (5–6 mg/dL). In this regard, blood UA levels are much higher in industrialized countries than in the rest of the world. Xanthine-oxidase inhibitors can reduce UA and seem to minimize its negative effects on vascular health. Other dietary and pathophysiological factors are also related to UA production. However, the role of fructose-derived UA in the pathogenesis of cardiometabolic disorders has not yet been fully clarified. Here, we critically review recent research on the biochemistry of UA production, the relationship between fructose intake and UA production, and how this relationship is linked to cardiometabolic disorders.

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“…High urate in gout is connected to increased oxidative stress. Early in the pathogenesis of gout along with infl ammation, crystals trigger oxidative stress by stimulating the production of ROS and NO radicals [26]. In turn ROS mediate various signaling pathways and induce apoptosis in endothelial and smooth muscle cells through ox-LDL [4].…”

Section: Discussionmentioning

confidence: 99%

Serum Oxidative Stress Markers are not Associated with Renal and Common Carotid Arteries Arteriosclerotic Vascular Changes in Patients with Gout

Gancheva

Kundurdjiev²,

Nikolova

et al. 2019

Acta Medica Bulgarica

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Objective: To establish the association between serum levels of reactive oxygen species (ROS) products, nitric oxide (NO) radicals and ascorbate radicals with renal resistive index (RRI), common carotid artery resistive index (CCARI) and intima-media thickness (IMT) in gout patients, and to find out whether the connection is more pronounced when tophi are present. Methods: A cross-sectional study including 71 consecutive gout patients, divided into two groups according to the presence of subcutaneous tophi. Serum concentrations of ROS products, NO radicals and ascorbate radicals were determined by ex vivo electron paramagnetic resonance (EPR) study. RRI was measured in both kidneys at the level of interlobar arteries with 3.5 MHz transducer. By applying ultrasound of the common carotid arteries, conducted with 10 MHz linear transducer CCARI and IMT were measured. Results: Gouty arthritis without tophi and gouty tophi subjects were age-matched. Serum uric acid and distribution of conventional cardiovascular risk factors was equal in the groups. However, in tophi patients CRP and the number of individuals who had suffered a cardiovascular event were higher. In the two stages of the disease serum levels of ROS products, NO radicals, ascorbate radicals, as well as RRI and CCARI were comparable but intima-media was thicker in gouty tophi. Serum concentrations of ROS products, NO radicals and ascorbate radicals did not correlate with RRI, CCARI and IMT. Among untreated and treated with Allopurinol or Febuxostat patients the means of ROS products, NO radicals, ascorbate radicals, RRI, CCARI and IMT were similar. Conclusions: In the earlier and advanced stage of the disease we found no difference in oxidative stress level but the degree of inflammation was higher in tophi subjects. No connection was established between serum ROS products, NO radicals and ascorbate radicals with renal and carotid arteries arteriosclerotic vascular changes. We suggest that in gout individuals intrinsic inflammation has a leading role in the process of atherogenesis.

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Molecular basis of oxidative stress in gouty arthropathy

Cited by 58 publications

References 51 publications

Impact of Lesinurad and allopurinol on experimental Hyperuricemia in mice: biochemical, molecular and Immunohistochemical study

Impact of Lesinurad and allopurinol on experimental Hyperuricemia in mice: biochemical, molecular and Immunohistochemical study

Fructose Intake, Serum Uric Acid, and Cardiometabolic Disorders: A Critical Review

Serum Oxidative Stress Markers are not Associated with Renal and Common Carotid Arteries Arteriosclerotic Vascular Changes in Patients with Gout

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