Topic
Xanthine
About: Xanthine is a research topic. Over the lifetime, 4046 publications have been published within this topic receiving 129820 citations. The topic is also known as: Xanthine.
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TL;DR: Xanthine oxidase (XO) inhibitors were isolated from the flowers and buds of Daphne genkwa SIEB and were identified as genkwanin (1), apigenin (2), luteolin 7-methyl ether (3) and lutenolin (4).
Abstract: Xanthine oxidase (XO) inhibitors were isolated from the flowers and buds of Daphne genkwa SIEB. et ZUCC. (Thymelaeaceae) and were identified as genkwanin (1), apigenin (2), luteolin 7-methyl ether (3) and luteolin (4). Compounds 2 and 4 showed particularly strong inhibitory activity against XO. The modes of inhibition by 2 and 4 with respect to xanthine as a substrate were of mixed type. This is the first report of isolation of 3 and 4 from these flowers and buds.
169 citations
TL;DR: Under isocratic conditions all compounds could be eluted with reasonable resolution and retention time and Quantitation by peak height for several of the compounds was used to the 10-ng level.
167 citations
TL;DR: It is demonstrated that chronic XOR inhibition restores cardiac structure and function and offsets alterations in fetal gene expression/Ca2+ handling pathways, supporting the idea that inhibiting XOR-derived oxidative stress substantially improves the HF phenotype.
Abstract: Increased reactive oxygen species (ROS) generation is implicated in cardiac remodeling in heart failure (HF). As xanthine oxidoreductase (XOR) is 1 of the major sources of ROS, we tested whether XO...
167 citations
TL;DR: This review discusses the mechanism of uric acid homeostasis and alterations, updated prevalence, therapeutic outcomes, and molecular pathophysiology of hyperuricemia-related diseases, and summarize current discoveries in the development of new XOR inhibitors.
Abstract: Uric acid is the final oxidation product of purine metabolism in humans. Xanthine oxidoreductase (XOR) catalyzes oxidative hydroxylation of hypoxanthine to xanthine to uric acid, accompanying the production of reactive oxygen species (ROS). Uric acid usually forms ions and salts known as urates and acid urates in serum. Clinically, overproduction or under-excretion of uric acid results in the elevated level of serum uric acid (SUA), termed hyperuricemia, which has long been established as the major etiologic factor in gout. Accordingly, urate-lowering drugs such as allopurinol, an XOR-inhibitor, are extensively used for the treatment of gout. In recent years, the prevalence of hyperuricemia has significantly increased and more clinical investigations have confirmed that hyperuricemia is an independent risk factor for cardiovascular disease, hypertension, diabetes, and many other diseases. Urate-lowering therapy may also play a critical role in the management of these diseases. However, current XOR-inhibitor drugs such as allopurinol and febuxostat may have significant adverse effects. Therefore, there has been great effort to develop new XOR-inhibitor drugs with less or no toxicity for the long-term treatment or prevention of these hyperuricemia-related diseases. In this review, we discuss the mechanism of uric acid homeostasis and alterations, updated prevalence, therapeutic outcomes, and molecular pathophysiology of hyperuricemia-related diseases. We also summarize current discoveries in the development of new XOR inhibitors.
166 citations
TL;DR: In this paper, the presence and significance of xanthine oxidase-mediated free radical generation in the isolated rat heart was investigated and shown to be a significant source of the oxidative injury which occurs upon reperfusion of the ischemic rat heart.
163 citations