Myocardial xanthine oxidase/dehydrogenase
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Keywords:
Hypoxanthine
Allopurinol
Xanthine
Inosine
Xanthine dehydrogenase
CSF obtained for clinical purposes from newborn, children and adults has been analysed by high pressure liquid chromatography for hypoxanthine, xanthine, inosine, uridine and urate. Large rises in hypoxanthine and to a lesser extent xanthine occur for about 24 h after hypoxia. High concentrations were associated with later evidence of brain damage or subsequent death. Changes in CSF could be independent of those in plasma. Small or negligible rises were associated with localised and generalised infections including bacterial meningitis, fits, or both. Marked and rapid rises were found after death. These estimations may "predict" the extent of brain damage or brain death.
Hypoxanthine
Xanthine
Inosine
Hypoxia
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The present investigation was made to clarify the action of adrenalin on the formation of inosine, which was identified as antibody-promoting factor. The results obtained were as follows.Adrenalin displayed its action at two locations in the course of metabolic degradation of ATP and adenosine. At one location, it accelerated the degradation from ATP or adenosine to inosine and hypoxanthine, and at the other it inhibited the conversion from inosine and hypoxanthine to xanthine. Especially, when adrenalin and adenosine were used together, inosine and hypoxanthine were found to have increased about 1.7 times after incubation for 40-60 minutes, but xanthine did not behave in the same manner. The optimal rate of adrenalin was 100μg per ml of basic medium.
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Xanthine
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The existence of uric acid in mammalian brain was recently reported, but it has not yet become a consensus. The mammalian brain has been thought to lack xanthine oxidase, which catalyzes hypoxanthine to xanthine and xanthine to uric acid as the last steps of ATP degradation in other tissue. Using high-performance liquid chromatography, we performed assays for hypoxanthine, xanthine, and uric acid in rat brain after cerebral ischemia. It was confirmed that all three substances showed significant augmentation in the removed brains and that the chronological order of those increases corresponded to the order in the metabolic pathway. Allopurinol, a specific inhibitor of xanthine oxidase, significantly suppressed the increases in uric acid and xanthine, and a compensatory accumulation of hypoxanthine was observed. From these results, it was concluded that uric acid does exist in the brain, increases after ischemia, and is possibly the end product of purine degradation in the brain. Furthermore, it is suggested that xanthine oxidase exists in the brain and catalyzes the reaction from hypoxanthine to xanthine and then to uric acid. These reactions catalyzed by xanthine oxidase are considered to be a source of free radicals and may play important roles in the pathogenesis of cerebral ischemic injury. (Neurosurgery 25:613-617, 1989)
Hypoxanthine
Allopurinol
Xanthine
Xanthine dehydrogenase
Xanthine oxidase inhibitor
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Hypoxanthine
Xanthine dehydrogenase
Xanthine
Allopurinol
Purine metabolism
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Allopurinol
Hypoxanthine
Xanthine
Lesch–Nyhan syndrome
Purine metabolism
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Abstract Isocratic reverse-phase high performance liquid chromatography techniques were developed to resolve and quantitate the purine nucleosides adenosine (Ado) and inosine (Ino) and their metabolites hypoxanthine (Hyp), xanthine (Xan), and uric acid (UA) in the cerebrospinal fluid of the rat. The moving phase composition for resolving hypoxanthine, xanthine and uric acid was a 0.22 M, pH 5.8 phosphate buffer. The moving phase composition for resolving adenosine and inosine was a 0.22 M, pH 6.8 phosphate buffer, 7% methanol (v/v) and 2.5 mM tetrabutylammonium phosphate. The observed cerebrospinal fluid concentrations in the rat were: Ado = 35 ± 9 nM (s.e.m.), Ino = 359 ± 85 nM, Hyp = 243 ± 77 nM, Xan = 1340 ± 423 nM and UA = 6130 ± 678 nM.
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Inosine
Xanthine
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Inosine
Hypoxanthine
Xanthine
Purine metabolism
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We applied a sensitive, precise liquid-chromatographic method of analysis for inosine, hypoxanthine, and xanthine to the study of fructose metabolism in humans and in rats. In the rat, intravenous loading with fructose induced, within minutes, substantial increases in the concentrations of inosine, hypoxanthine, and xanthine in plasma and urine. In plasma, these concentrations peaked after 5 min, then practically disappeared within 10 min. As expected, the fructose-induced increase in hypoxanthine was greatly amplified by pretreating the rats with allopurinol, an inhibitor of xanthine oxidase. In a healthy human subject, intravenous administration of fructose also induced prompt, substantial, and rapidly reversing increases in the concentrations of these metabolites of adenine nucleotides in plasma. The finding that fructose induced almost-immediate increases in the plasma concentrations of inosine, hypoxanthine, and xanthine is consistent with previous studies in rats, in which parenteral administration of fructose induced almost-immediate decreases of total adenine nucleotides (ATP + ADP + AMP) in the liver, and increased concentrations of uric acid and allantoin in the plasma.
Hypoxanthine
Xanthine
Inosine
Allopurinol
Adenine nucleotide
Allantoin
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The present investigation was made to clarify the action of adrenalin on the formation of inosine, which was identified as antibody-promoting factor. The results obtained were as follows.Adrenalin displayed its action at two locations in the course of metabolic degradation of ATP and adenosine. At one location, it accelerated the degradation from ATP or adenosine to inosine and hypoxanthine, and at the other it inhibited the conversion from inosine and hypoxanthine to xanthine. Especially, when adrenalin and adenosine were used together, inosine and hypoxanthine were found to have increased about 1.7 times after incubation for 40-60 minutes, but xanthine did not behave in the same manner. The optimal rate of adrenalin was 100μg per ml of basic medium.
Hypoxanthine
Inosine
Xanthine
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Hypoxanthine
Xanthine dehydrogenase
Xanthine
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