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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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Journal ArticleDOI
TL;DR: It is demonstrated that in vitro and in vivo, uric acid can stimulate basal COX-2 expression and thereby provide insight into previous epidemiological evidence linking elevated serum uric levels with systemic hypertension and increased mortality from cardiovascular diseases.
Abstract: Xanthine oxidoreductase (XOR) is the enzyme responsible for the final step in purine degradation resulting in the generation of uric acid. Here we have generated mice deficient in XOR. As expected, these animals lack tissue XOR activity and have low to undetectable serum levels of uric acid. Although normal at birth, XOR/ mice fail to thrive after 10 to 14 days, and most die within the first month. The cause of death appears to be a form of severe renal dysplasia, a phenotype that closely resembles what has been observed previously in cyclooxygenase-2 (COX-2)- deficient mice. We further demonstrate that in the first month of life, a period in which the mouse kidney is undergoing rapid maturation and remodeling, wild-type mice exhibit an 30-fold increase in renal XOR activity, with a corresponding induction of COX-2 expression. In contrast, during this same period, XOR/ animals fail to augment renal COX-2 expression. Finally, we show that in vitro and in vivo, uric acid can stimulate basal COX-2 expression. These results demonstrate that XOR activity is an endogenous physiological regulator of COX-2 expression and thereby provide insight into previous epidemiological evidence linking elevated serum uric levels with systemic hypertension and increased mortality from cardiovascular diseases. In addition, these results suggest a novel molecular link between cellular injury and the inflammatory response. (Circ Res. 2004;95:1118-1124.)

89 citations

Journal ArticleDOI
TL;DR: The data supported the presumption of increased oxidative stress in Down syndrome and suggested increased conversion of hypoxanthine and xanthine to uric acid with subsequent free radical-dependent oxidation of uric Acid to allantoin, mechanisms potentiated by the oxidative Stress in DS.

89 citations

Journal ArticleDOI
TL;DR: P-Iodonitrotetrazolium was reduced to a water-soluble product with an absorbance maxima at about 505 nm (reddish pink) by superoxide anion (O2-.) generated by xanthine/xanthine oxidase.

89 citations

Journal ArticleDOI
TL;DR: The use of the coupling capillary electrophoresis with wall-jet amperometric detection for the separation and detection of compounds present in human plasma samples was reported.

89 citations

Journal ArticleDOI
TL;DR: It is suggested that uric acid decreased eNOS activity and NO production through reducing the binding between eN OS and CaM in EC and this result may provide molecular mechanism by which uric Acid induces endothelial dysfunction.

88 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202361
2022108
202157
202060
201961
201869