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Alloxanthin

Anti-gout Drugs. Figure 1 Xanthine oxidase-catalyzed reactions. Xanthine oxidase converts hypoxanthine to xanthine and xanthine to uric acid, respectively. Hypoxanthine and xanthine are more soluble than uric acid. Xanthine oxidase also converts the uricostatic drug allopurinol to alloxanthine. Allopurinol and hypoxanthine are isomers that differ from each other in the substitution of positions 7 and 8 of the purine ring system. Although allopurinol is converted to alloxanthine by xanthine oxidase, allopurinol is also a xanthine oxidase inhibitor. Specifically, at low concentrations, allopurinol acts as a competitive inhibitor, and at high concentrations it acts as a noncompetitive inhibitor. Alloxanthine is a noncompetitive xanthine oxidase inhibitor. XOD xanthine oxidase. [Pg.135]

Allopurinol is an analog of hypoxanthine and is converted to alloxanthine by XOD. Both allopurinol and hypoxanthine inhibit XOD (Fig. 1). Alloxanthine is a noncompetitive inhibitor of XOD as is allopurinol at high concentrations. At low concentrations, allopurinol is a competitive inhibitor of XOD. As a result of XOD inhibition, the formation of the poorly soluble... [Pg.137]

Xanthine oxidase (XOD) is the key enzyme in purine catabolism. XOD catalyses the conversion ofhypoxan-thine to xanthine and of xanthine to uric acid, respectively. The uricostatic drug allopurinol and its major metabolite alloxanthine (oxypurinol) inhibit xanthine oxidase. [Pg.1323]

South, Y. and Whittick, H., Introduction to Phycology. Blackwell, New York, 1987. Cheng, J.Y., Don Raul, M., and Antia, N.J., Isolation of an unusually stable cis isomer of alloxanthin from a bleached autolysed culture of Chroomonas salina grown pho-toheterotrophically on glycerol observation on cis trans isomerization of alloxanthin,... [Pg.422]

Very recently (84) this specific binding of alloxanthine-like compounds to active xanthine oxidase has been made the basis of a method of separating the active from the inactivated enzyme, using a pyrazolo-(3,4) pyrimidine attached to agarose. [Pg.125]

We have not so far mentioned the Phase III increase in the Rapid signal (Fig. 5). It seems (67) that Phase II represents over reduction of molybdenum to Mo(IV), possibly by substrate radicals (see Section V H). The system then comes towards thermodynamic equilibrium by interaction between reduced active enzyme molecules and oxidized inactive ones (67, cf. 64). As Mo(IV) of the former is oxidized to Mo(V), during Phase III, so iron or flavin of the inactive enzyme is reduced. Later, in Phase IV, molybdenum of the inactive enzyme is reduced also to give the Slow signed. Alloxanthine, which as noted above, forms a stable complex with Mo(IV), seems to abolish both the slow phase in the 450 nm bleaching of the enzyme by xanthine and the Phase III increase in Rapid signal (91). [Pg.131]

Finally, in the case of inhibitory substrate analogues such as allo-xanthine, strong evidence has recently been presented that these bind to molybdenum in reduced xanthine oxidase (33). If the enzyme is reduced with xanthine, then treated anaerobically with alloxanthine and finally exposed to air, catalytic activity is lost. Though flavin and iron in the final product are in the oxidized state, there are significant spectral differences between it and the native enzyme. These are believed (33) due to reduction of molybdenum from Mo(VI) to Mo(IV) and complexing of... [Pg.134]

The answer is c. (Hardman, pp 649—650.) Acute hyperuricemia, which often occurs in patients who are treated with cytotoxic drugs for neoplasic disorders, can lead to the deposition of urate crystals in the kidneys and their collecting ducts. This can produce partial or complete obstruction of the collecting ducts, renal pelvis, or ureter. Allopurinol and its primary metabolite, alloxanthine, are inhibitors of xanthine oxidase, an enzyme that catalyzes the oxidation of hypo xanthine and xanthine to uric acid. The use of allopurinol in patients at risk can markedly reduce the likelihood that they will develop acute uric acid nephropathy. [Pg.216]

Fig. 2.124. HPLC absorbance chromatograms of phytoplankton samples collected from the study site on 24 November 2000 (a), 25 November 2000 (b) and 1 December 2000 (c). Peak identification 1 = chlorophyll-a 2 = chlorophyll-b 3 = chlorophyll-c2 4 = peridin 5 = fucoxanthin 6 = neoxanthin 7 = 19 -hexanoylfucoxanthin 8 = diadinoxanthin 9 = alloxanthin 10 = lutein 11 = zeaxanthin 12 = /1-carotene. Reprinted with permission from C. K. Wong et al. [282],... Fig. 2.124. HPLC absorbance chromatograms of phytoplankton samples collected from the study site on 24 November 2000 (a), 25 November 2000 (b) and 1 December 2000 (c). Peak identification 1 = chlorophyll-a 2 = chlorophyll-b 3 = chlorophyll-c2 4 = peridin 5 = fucoxanthin 6 = neoxanthin 7 = 19 -hexanoylfucoxanthin 8 = diadinoxanthin 9 = alloxanthin 10 = lutein 11 = zeaxanthin 12 = /1-carotene. Reprinted with permission from C. K. Wong et al. [282],...
Per = peridinin But-fuco = 19 -butanoyloxyfucoxanthin fuco = fucoxanthin Hex-fuco = 19 -hexanoyloxyfucoxanthin Neo = neoxanthin Viol = violaxanthin Alio = alloxanthin Zea = zeaxanthin Chi b = chlorophyll-b DV chi a = divinyl chlorophyll-a. [Pg.293]

After oral intake it is absorbed relatively rapidly. It is converted to alloxanthine which is active and non competitive inhibitor. [Pg.94]

Allopurinol is approximately 80% absorbed after oral administration and has a terminal serum half-life of 1-2 hours. Like uric acid, allopurinol is itself metabolized by xanthine oxidase, but the resulting compound, alloxanthine, retains the capacity to inhibit xanthine oxidase and has a long enough duration of action so that allopurinol is given only once a day. [Pg.816]

If the inherited defect involves certain enzymes then an enzyme inhibitor could also be effective. Allopurinol is a xanthine oxidase inhibitor, or purine antagonist, which can reduce the level of uric acid in organs and tissues. Its primary metabolite, alloxanthine, is also active which extends its half-life in the body (half-life of allopurinol is 2-3 hours, for alloxanthine is 18-30 hours). The drug is well-tolerated with few side... [Pg.61]

Murexide [3051-09-0] M 284.2, m >300 , Xmax 520nm (e 12,000). The sample may be grossly contaminated with uramil, alloxanthine, etc. Difficult to purify. It is better to synthesise it from pure alloxanthine [Davidson JACS 58 1821 1936], Crystd from water. [Pg.279]

Another alteration of unsaturated fatty acids is the formation of acetylenic groups (-OC-). This apparently occurs by dehydrogenation of -CH=CH- Examples of naturally occurring acetylenes are crepenynic acid (p. 381), alloxanthin (p. 1240), and the following remarkable hydrocarbon from the common cornflower Centaurea cyanusm ... [Pg.1195]

Other algal carotenoids contain acetylenic triple bonds. For example, alloxanthin has the following structure at both ends of the symmetric molecule. The symmetric carotenoids canthaxanthin and astaxan-thin have oxo groups at both ends ... [Pg.1240]


See other pages where Alloxanthin is mentioned: [Pg.304]    [Pg.19]    [Pg.76]    [Pg.63]    [Pg.402]    [Pg.1230]    [Pg.130]    [Pg.131]    [Pg.135]    [Pg.132]    [Pg.289]    [Pg.295]    [Pg.299]    [Pg.300]    [Pg.451]    [Pg.451]    [Pg.451]    [Pg.316]    [Pg.7]    [Pg.876]    [Pg.999]    [Pg.1240]    [Pg.334]    [Pg.335]    [Pg.886]    [Pg.661]    [Pg.15]    [Pg.387]   
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Alloxanthine

Alloxanthine, complex with xanthine

Alloxanthine, complex with xanthine oxidase

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