Urate oxidate

Uricase Tissues of mammals except primates 100,000 — 0.056 1 -1- Urate oxidation (MS)... 

It was quite recently reported that La can be electrodeposited from chloroaluminate ionic liquids [25]. Whereas only AlLa alloys can be obtained from the pure liquid, the addition of excess LiCl and small quantities of thionyl chloride (SOCI2) to a LaCl3-sat-urated melt allows the deposition of elemental La, but the electrodissolution seems to be somewhat Idnetically hindered. This result could perhaps be interesting for coating purposes, as elemental La can normally only be deposited in high-temperature molten salts, which require much more difficult experimental or technical conditions. Furthermore, La and Ce electrodeposition would be important, as their oxides have interesting catalytic activity as, for instance, oxidation catalysts. A controlled deposition of thin metal layers followed by selective oxidation could perhaps produce cat-alytically active thin layers interesting for fuel cells or waste gas treatment. 

A remaining crucial technological milestone to pass for an implanted device remains the stability of the biocatalytic fuel cell, which should be expressed in months or years rather than days or weeks. Recent reports on the use of BOD biocatalytic electrodes in serum have, for example, highlighted instabilities associated with the presence of 02, urate or metal ions [99, 100], and enzyme deactivation in its oxidized state [101]. Strategies to be considered include the use of new biocatalysts with improved thermal properties, or stability towards interferences and inhibitors, the use of nanostructured electrode surfaces and chemical coupling of films to such surfaces, to improve film stability, and the design of redox mediator libraries tailored towards both mediation and immobilization. 

Electrochemical biosensors based on detection of hydrogen peroxide at platinized electrodes were found to be more versatile allowing a decrease in detection limit down to 1 i,mol L 1 [109]. However, all biological liquids contain a variety of electrochemically easily oxidizable reductants, e.g. ascorbate, urate, bilirubin, catecholamines, etc., which are oxidized at similar potentials and dramatically affect biosensor selectivity producing parasitic anodic current [110]. 

Another free radical, which is supposedly formed in biological systems is the nitric dioxide N02. This radical is much more reactive than nitric oxide its rate constants with thiols, urate, and Trolox C are about 107—10s lmol-1 s 1 [88,89] (Table 21.1). It has been proposed [88] that thiols are dominant acceptors of N02 in cells and tissues while urate is a major scavenger... 

In the last decade numerous studies were dedicated to the study of biological role of nonenzymatic free radical oxidation of unsaturated fatty acids into isoprostanes. This task is exclusively difficult due to a huge number of these compounds (maybe many hundreds). Therefore, unfortunately, the study of several isoprostanes is not enough to make final conclusions even about their major functions. F2-isoprostanes were formed in plasma and LDL after the treatment with peroxyl radicals [98], It is interesting that their formation was observed only after endogenous ascorbate and ubiquinone-10 were exhausted, despite the presence of other antioxidants such as urate or a-tocopherol. LDL oxidation was followed by... 

Flavonoids exhibit protective action against LDL oxidation. It has been shown [145] that the pretreatment of macrophages and endothelial cells with tea flavonoids such as theaflavin digallate diminished cell-mediated LDL oxidation probably due to the interaction with superoxide and the chelation of iron ions. Quercetin and epicatechin inhibited LDL oxidation catalyzed by mammalian 15-lipoxygenase, and are much more effective antioxidants than ascorbic acid and a-tocopherol [146], Luteolin, rutin, quercetin, and catechin suppressed copper-stimulated LDL oxidation and protected endogenous urate from oxidative degradation [147]. Quercetin was also able to suppress peroxynitrite-induced oxidative modification of LDL [148],... 

In 1998, Schlotte et al. [259] showed that uric acid inhibited LDL oxidation. However, subsequent studies showed that in the case of copper-initiated LDL oxidation uric acid behaves itself as prooxidant [260,261]. It has been suggested that in this case uric acid enhances LDL oxidation by the reduction of cupric into cuprous ions and that the prooxidant effect of uric acid may be prevented by ascorbate. On the other hand, urate radicals formed during the interaction of uric acid with peroxyl radicals are able to react with other compounds, for example, flavonoids [262], and by that participate in the propagation of free radical damaging reactions. In addition to the inhibition of oxygen radical-mediated processes, uric acid is an effective scavenger of peroxynitrite [263]. 

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. 

Purine metabolism in some mammals is characterized by a further oxidation of uric acid to al-lantoin by the enzyme urate oxidase. Allantoin is significantly more water soluble than uric acid and is also freely excreted via the renal route. 

Similarly, 5-methyl-2-furaldehyde was converted into 3,4,6-tri-deoxy-DL-hex-3-enopyranosides. 4,4,5,5-Tetramethyl-2-(5-methyl-2-furyl)-l,3-dioxolane was oxidized with bromine-water, and the unsat-urated dioxolane resulting was immediately reduced with sodium borohydride, to give a mixture of DL-2-(l,4-dihydroxy-cts-pentenyl)-4,4,5,5-tetramethyl-l,3-dioxolane. Methanolysis gave the known methyl 3,4-6-trideoxy-a-DL-threo- and -en/f/iro-hex-3-enopyranosides, identified by H-n.m.r. spectroscopy.24 ... 

Dietary purines are not an important source of uric acid. Quantitatively important amounts of purine are formed from amino acids, formate, and carbon dioxide in the body. Those purine ribonucleotides not incorporated into nucleic acids and derived from nucleic acid degradation are converted to xanthine or hypoxanthine and oxidized to uric acid (Figure 36-7). Allopurinol inhibits this last step, resulting in a fall in the plasma urate level and a decrease in the size of the urate pool. The more soluble xanthine and hypoxanthine are increased. 

Gout is caused by the deposition of crystals of monosodium urate hydrate which are ingested by leucocyctes and trigger the inflammatory response. The biosynthesis of uric acid involves the oxidation of the more soluble compound xanthine (2,6-dihydroxypurine) by xanthine oxidase, and this enzyme is inhibited by allopurinol (187). The treatment of gout also relies on uricosuric drugs to accelerate urinary excretion of uric acid and antiinflammatory drugs to ease the pain and inflammation. 

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