Xanthine oxidoreductase-catalyzed reactive species generation: A process in critical need of reevaluation

Cantú‐Medellín, Nadiezhda; Kelley, Eric E.

doi:10.1016/j.redox.2013.05.002

Cited by 185 publications

(164 citation statements)

References 49 publications

(19 reference statements)

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“…Its oxidase form is responsible for converting hypoxanthine to xanthine and xanthine to acid uric [33]. The purine cycle generates superoxide, hydrogen peroxide, and the reactive hydroxyl molecule [34], but uric acid itself is a potent non-enzymatic antioxidant [25]. Formed in the liver from hypoxanthine, it is released to the blood and either excreted or taken up by muscle, where it scavenges hydroxyl radical [35].…”

Section: Discussionmentioning

confidence: 99%

Anaerobic exercise affects the saliva antioxidant/oxidant balance in high-performance pentathlon athletes

Sant’Anna¹,

Casimiro-Lopes²,

Boaventura³

et al. 2018

Hum Mov.

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Purpose. Investigate free radical production and antioxidant buffering in military pentathletes' saliva after their performance of a standardized, running-based anaerobic sprint test (RAST). Methods. Seven members of the Brazilian Navy pentathlon team were recruited to perform a running-based anaerobic test (~90 sec). The participants provided samples of saliva before and after the test that were analyzed for biomarkers of oxidative stress such as lipid peroxidation, total antioxidant capacity and the quantity of two specific antioxidants, glutathione and uric acid. Results. The lipid peroxidation increased ~2 fold after RAST, despite an increase in total antioxidant capacity (46%). The concentration of reduced glutathione did not change, while the uric acid concentration increased by 65%. Conclusions. The evaluation in saliva following a sprint test that lasted no more than 90 sec was sensitive enough to reveal changes in redox state.

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Section: Discussionmentioning

confidence: 99%

Anaerobic exercise affects the saliva antioxidant/oxidant balance in high-performance pentathlon athletes

Sant’Anna¹,

Casimiro-Lopes²,

Boaventura³

et al. 2018

Hum Mov.

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“…For example, the required doses of allopurinol and oxypurinol are higher than the theoretical doses, and a pharmacological inhibitor may exert antioxidative effects [21]. In addition, studies have demonstrated that xanthine oxidase has several functions, including nitrate reductase activity, which increases production of nitric oxide [19, 20, 22]. The production of nitric oxide can minimize ischemia-reperfusion injury by stimulating vasodilation and inhibiting inflammatory responses.…”

Section: Mechanisms Of Xanthine Oxidase Induction Of Oxidative Stressmentioning

confidence: 99%

Current Mechanistic Concepts in Ischemia and Reperfusion Injury

Yiang

Liao

et al. 2018

Cell Physiol Biochem

978

728

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Ischemia-reperfusion injury is associated with serious clinical manifestations, including myocardial hibernation, acute heart failure, cerebral dysfunction, gastrointestinal dysfunction, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. Ischemia-reperfusion injury is a critical medical condition that poses an important therapeutic challenge for physicians. In this review article, we present recent advances focusing on the basic pathophysiology of ischemia-reperfusion injury, especially the involvement of reactive oxygen species and cell death pathways. The involvement of the NADPH oxidase system, nitric oxide synthase system, and xanthine oxidase system are also described. When the blood supply is re-established after prolonged ischemia, local inflammation and ROS production increase, leading to secondary injury. Cell damage induced by prolonged ischemia-reperfusion injury may lead to apoptosis, autophagy, necrosis, and necroptosis. We highlight the latest mechanistic insights into reperfusion-injury-induced cell death via these different processes. The interlinked signaling pathways of cell death could offer new targets for therapeutic approaches. Treatment approaches for ischemia-reperfusion injury are also reviewed. We believe that understanding the pathophysiology ischemia-reperfusion injury will enable the development of novel treatment interventions.

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“…Not only transporters, but also transcriptional factors, signaling receptors, enzymes are involved in serum UA level. Table 1 shows association between life-style related diseases and UA metabolism [16][17][18][19][20][21][22][23][24] . Distinguishing cause and effect is difficult; some diseases raise SUA level, but UA affect disease onset or progression.…”

Section: Factors That Define Serum Uric Acid Levelsmentioning

confidence: 99%

Linking uric acid metabolism to diabetic complications

Kushiyama

Tanaka

Hara

et al. 2014

WJD

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Hyperuricemia have been thought to be caused by the ingestion of large amounts of purines, and prevention or treatment of hyperuricemia has intended to prevent gout. Xanthine dehydrogenase/xanthine oxidase (XDH/ XO) is rate-limiting enzyme of uric acid generation, and allopurinol was developed as a uric acid (UA) generation inhibitor in the 1950s and has been routinely used for gout prevention since then. Serum UA levels are an important risk factor of disease progression for various diseases, including those related to lifestyle. Recently, other UA generation inhibitors such as febuxostat and topiroxostat were launched. The emergence of these novel medications has promoted new research in the field. Lifestyle-related diseases, such as metabolic syndrome or type 2 diabetes mellitus, often have a common pathological foundation. As such, hyperuricemia is often present among these patients. Many in vitro and animal studies have implicated inflammation and oxidative stress in UA metabolism and vascular injury because XDH/XO act as one of the major source of reactive oxygen species Many studies on UA levels and associated diseases implicate involvement of UA generation in disease onset and/or progression. Interventional studies for UA generation, not UA excretion revealed XDH/XO can be the therapeutic target for vascular injury and renal dysfunction. In this review, the relationship between UA metabolism and diabetic complications is highlighted.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Uric acid; Xanthine dehydrogenase/xanthine oxidase; Diabetes mellitus; Diabetic complications; Xanthine oxidase inhibitor; Metabolism Core tip: Uric acid (UA) is derived from essential metabolism, and UA metabolism is becoming a novel risk and interventional factor of lifestyle-related diseases in this obesity-prone era. The relationship between UA metabolism and diabetic complications is highlighted in this review and supposed molecular mechanisms are mentioned.Kushiyama A, Tanaka K, Hara S, Kawazu S. Linking uric acid metabolism to diabetic complications. World J Diabetes 2014; 5(6): 787-795 Available from:

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Xanthine oxidoreductase-catalyzed reactive species generation: A process in critical need of reevaluation

Cited by 185 publications

References 49 publications

Anaerobic exercise affects the saliva antioxidant/oxidant balance in high-performance pentathlon athletes

Anaerobic exercise affects the saliva antioxidant/oxidant balance in high-performance pentathlon athletes

Current Mechanistic Concepts in Ischemia and Reperfusion Injury

Linking uric acid metabolism to diabetic complications

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