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At least 721 records · Page 40Linked to original sources
PubMed1976

Uric acid catabolism in the woolly monkey.

The degradation and excretion of 2-14C-uric acid were examined in three adult woolly monkeys (Lagothrix lagothrichia) to determine the basis for the relatively high serum and urinary uric acid concentrations previously reported in this species. Like man and the great apes which lack uricase, but in distinction to most other mammals, these animals converted very little urate to allantoin. Uric acid turnover, as has been reported for other New World monkeys, was several times that of normal man. Renal urate excretion as well as disposition by extrarenal mechanisms may protect Lagothrix vrom hyperuricemia. The capacity to convert urate to allantoin appears to have been lost late in the evolution of New World monkeys. The woolly monkey deserves further study as a primate model for investigations of enzyme replacement strategies.

Animals↗
PubMed1994

Hypouricemic and uricosuric actions of AA-193 in a hyperuricemic rat model.

In normal rats, consecutive administrations of AA-193 for 7 days maintained the dose-dependent uricosuric activity without significant changes of the plasma urate level. In clearance studies, AA-193 produced an increase in the fractional excretion of urate (FEua) namely an inhibition of the net urate reabsorption in the nephron, which was probably dependent on the plasma concentration of the agent. During in vitro studies, 1 mmol/L AA-193 had no effect on liver uricase activity and 0.2 mmol/L AA-193 did not inhibit xanthine dehydrogenase activity. Therefore, it is unlikely that AA-193 at physiologic doses has a significant effect on either the production or degradation of urate. To assess the hypouricemic effect of AA-193 derived from its uricosuric effect, we used uricase-inhibited rats produced by oxonate feeding. In the hyperuricemic rat model, consecutive administrations of AA-193 for 7 days increased urate excretion and decreased the plasma urate level. We conclude that AA-193 has a hypouricemic effect caused by increases in urate excretion in hyperuricemic rats.

Animals↗
PubMed1989

Hyperuricemia and locomotor activity in developing rats.

This research was motivated by the previous finding that serum uric acid levels correlate with symptoms of hyperactivity in normal children. We attempted, therefore, to investigate this relationship in an animal model. Dose and time relationships between allantoxanamide-induced heightened serum uric acid and locomotor activity were investigated. A dose- and time-dependent relationship was shown between serum uric acid levels and allantoxanamide. Those doses of allantoxanamide which elevated serum uric acid produced time-dependent changes in locomotor activity. In the first two hours following injection, activity increased relative to controls, in the next two-hour block activity decreased, only to rise again above control levels in the third two-hour period. The possible role of uric acid and allantoxanamide are discussed in relation to these complex changes in activity.

Animals↗
PubMed1994

Chromium toxicity in Neurospora crassa.

A comparative study has been made on the mechanisms of toxicities of trivalent and hexavalent forms of chromium in Neurospora crassa. Of the two forms, Cr6+ is more toxic than Cr3+. The toxicity of Cr3+ was found to be due to its specific antagonism with iron uptake. Fe3+ was found to be very effective in reversing the toxicity of Cr3+ by concomitantly suppressing its uptake. That the Cr3+ toxicity caused a conditional intracellular iron deficiency was indicated by the decrease in the activities of catalase and uricase and a progressive increase in the excretion of iron binding compound into the medium. The toxicity of Cr6+ (as Cr2O7(2-)) was found to be due to its specific antagonism of sulfate uptake. Methionine was found to be more effective in reversing dichromate toxicity than sulfate, probably by repressing the synthesis of sulfate permeases responsible for dichromate (Cr6+) uptake. Maximal uptake of Cr6+ was nearly tenfold lower and Vmax much higher than that of Cr3+. Evidence has been adduced to show that Cr6+ and Cr3+ were toxic by themselves and that interconversion between the tri- and hexavalent forms of chromium did not occur to any detectable extent.

Biological Transport↗
PubMed1989

Cloning of rabbit uricase cDNA reveals a conserved carboxy-terminal tripeptide in three species.

cDNA clones encoding uricase have been isolated from a rabbit liver cDNA library. The nucleotide sequences of the cDNAs have been determined and those of the rat uricase cDNA have been revised. In all three uricases, the carboxy-terminal tripeptides are Ser-Arg/Lys-Leu sequences, which have recently been suggested as an essential element of peroxisomal targetting signals for many but not all peroxisomal proteins.

Amino Acid Sequence↗
PubMed1983

Effects of dietary di(2-ethylhexyl)phthalate on the structure and function of rat hepatocytes.

The effect of the plasticizer di(2-ethylhexyl)phthalate on the intracellular membranes of hepatocytes was investigated. Supplementation of the diet with 2% plasticizer resulted in the appearance of a large number of peroxisomes, and the number of mitochondria was also greatly increased. No significant change in the amount or appearance of the endoplasmic reticulum was detected. The oxidation of palmitoyl-CoA in peroxisomes and the activities of carnitine-acyltransferases are increased to a great extent in both mitochondria and peroxisomes. Intact respiratory control and oxidative phosphorylation indicated that mitochondrial integrity was maintained during the induction. In microsomes, cytochrome P-450 and NADPH-cytochrome c reductase are elevated. The increased incorporation of glycerol into phospholipids indicated an increased rate of synthesis. The induction of peroxisomal and mitochondrial membranes and enzymes, but not of the membranes of the endoplasmic reticulum, by phthalate esters is an unusual and valuable induction pattern not seen with other inducers.

Animals↗
PubMed1985

Studies on antigenicity of the polyethylene glycol (PEG)-modified uricase.

The purified uricase (urate: oxygen oxidoreductase, EC 1.7.3.3) from Candida utilis was modified to varying degrees with monomethoxypolyethylene glycol (PEG) of different molecular weights using cyanuric chloride as the coupling reagent. The PEG-uricase conjugates were examined on their immunological properties by means of ring test and passive cutaneous anaphylaxis (PCA). As increasing amounts of PEG were attached to uricase, it showed decreasing ability to elicit antibody production in rabbits. When sufficient polymers were attached, the modified uricase was devoid of the capacity to combine in vivo and in vitro with antibodies from guinea pigs injected with the unmodified uricase, however, were still able to react with antibodies to PEG-uricase conjugate. Antibodies against PEG-uricase conjugates also reacted with PEG modified superoxide dismutase (superoxide: superoxide oxidoreductase, EC 1.15.1.1). These results indicate that the coupling of PEG to uricase resulted in the loss of original antigenicity and immunogenicity, but in the appearance of new antigenicity and immunogenicity which never showed any cross-reactions against the native uricase.

Animals↗
PubMed1977

Purine degradation in Pseudomonas aeruginosa and Pseudomonas testosteroni.

1. Adenine, hypoxanthine, xanthine and guanine are broken down in Pseudomonas aeruginosa and Pseudomonas testosteroni to allantoin by the concerted action of the enzymes adenine deaminase, guanine deaminase, NAD+-dependent xanthine dehydrogenase and uricase. 2. Uric acid is broken down by an unstable, membrane-bound uricase with an unusually low pH optimum. 3. In both strains adenine inhibits growth and xanthine dehydrogenase. A second type of inhibition is manifest only in Ps. testosteroni and concerns the regulation of the biosynthesis of amino acids of the aspartate family. Enzymic studies showed that in this strain aspartate kinase is inhibited by AMP.

Adenine↗
PubMed1992

Quantitative separation of uric acid and allantoin from rat liver tissue.

A simple procedure is described for the assay of liver uric acid and allantoin and their specific radioactivity after administration of a radioactive precursor. Uric acid was quantified by the uricase reaction in liver trichloroacetic acid (TCA) extracts. The 'true' allantoin content of the liver could be estimated only after precipitation with Hg-acetate, a step by which the standard allantoin was also quantitatively recovered. Crude extracts lead to the evaluation of 'apparent' allantoin. For the determination of specific radioactivity, the Hg-acetate precipitate was further purified by ion-exchange chromatography. The purity of the two metabolites was confirmed by ultraviolet absorbance spectra, HPLC, constancy of specific radioactivity and the absence of amino acids. The incorporation of [14C]formate into uric acid and allantoin in the liver was studied by this procedure. The radioactivity in allantoin was several-fold higher than that in uric acid up to 60 min after administration of the precursor. This quite unexpected result is not easily explained on the basis of current knowledge.

Allantoin↗