Results 211 to 220 of about 74,149 (232)
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Hypoxanthine Transport in Human Erythrocytes

1980
De novo synthesis of purines does not appear to take place in mature human erythrocytes because the enzymes for the pathway are absent1. Therefore purine bases should be normally have to be supplied exogenously to erythrocytes.
GIACOMELLO, Alessandro   +1 more
openaire   +4 more sources

Hypoxanthine transport in human erythrocytes

Biochimica et Biophysica Acta (BBA) - Biomembranes, 1967
Abstract Using rapid sampling by filtration, it has been possible to follow and describe the transport of hypoxanthine across the human red blood cell membrane. The dependence of the transport rate upon the concentration of hypoxanthine is complex, and suggests a two-component mechanism. The first is a “saturable carrier system” with a K m of 0.
Ulrik V. Lassen, Ulrik V. Lassen
openaire   +3 more sources

Automated Analysis of Hypoxanthine

Journal of Food Science, 1965
SUMMARYHypoxanthine concentration is a useful index of the quality of flesh foods. A rapid manual assay of the purine was automated by modifying commercially available proportioning and spectrophotometric equipment. Extracts are sampled serially and mixed with xanthine oxidase and buffer.
J. Murray, J. R. Burt, N. R. Jones
openaire   +2 more sources

An amperometric hypoxanthine biosensor based on Au@FeNPs for determination of hypoxanthine in meat samples

International Journal of Biological Macromolecules, 2013
A xanthine oxidase (XOD) from buttermilk was immobilized covalently onto boronic acid functionalized gold coated iron nanoparticles (Au@FeNPs) electrodeposited on pencil graphite (PG) electrode, via the boroester linkages, between free hydroxyl groups of boronic acid, α-COOH and -NH2 groups of enzyme.
Rooma Devi   +3 more
openaire   +3 more sources

Uptake of Hypoxanthine in Human Erythrocytes

1977
The concentration of oxypurines in the plasma is known to be rather low (10 – 40 μM) (6). Since the formation of purines is accomplished to a great extent by the liver (7, 8), a transport of purines by erythrocytes from liver to tissues with limited or no capacity of de novo purine synthesis has been postulated (1, 3).
G. Falkner, Mathias Müller
openaire   +3 more sources

Partial hypoxanthine–guanine phosphoribosyl transferase deficiency without elevated urinary hypoxanthine excretion

Molecular Genetics and Metabolism, 2007
Partial hypoxanthine-guanine phosphoribosyl transferase (HGPRT) deficiency, also known as the Kelley-Seegmiller syndrome, can give rise to a wide range of neurological symptoms, and renal insufficiency. Biochemically, it is characterized by high uric acid concentrations in blood, high uric acid and hypoxanthine excretion in urine, and decreased ...
O. P. van Diggelen   +5 more
openaire   +4 more sources

The Spectrum of Hypoxanthine-guanine Phosphoribosyltransferase Deficiency

QJM: An International Journal of Medicine, 1973
The spectrum of clinical manifestations of hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) deficiency is presented by reference to eight patients from five kindred. These patients illustrate the range of associated neurological findings, together with the variety of presentation and complications due to the associated over-production of urate.
Emmerson, B. T., Thompson, L.
openaire   +3 more sources

Hypoxanthine transport in normal and hypoxanthine guanine phosphoribosyltransferase (HGPRT) deficient diploid human lymphoblasts

Experimental Cell Research, 1977
Abstract We have examined the possible relation between hypoxanthine guanine phosphoribosyltransferase (EC 2.4.2.7., HGPRT) activity and hypoxanthine transport in the normal human lymphoblast line MGL8 and two HGPRT- mutant lines derived from it. The mutant line MGL8A29 (L8A29) had considerable amounts of material cross-reacting immunologically to ...
J. Epstein, J.W. Littlefield
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Salvage of circulating hypoxanthine by tissues of the mouse

Canadian Journal of Biochemistry and Cell Biology, 1983
Hypoxanthine is an inefficient precursor of purine nucleotides in mouse tissues. In vitro, mouse erythrocytes salvage <10% of hypoxanthine (10 μM) added to whole blood in 30 min of incubation at 37 °C. In vivo, circulating hypoxanthine is rapidly degraded (>90% in 10 min) to allantoin and uric acid. All tissues examined (other than erythrocytes)
J D Moyer, J F Henderson
openaire   +2 more sources

Mouse models of hypoxanthine phosphoribosyltransferase deficiency

Journal of Inherited Metabolic Disease, 1992
SummaryLesch‐Nyhan syndrome is an X‐linked disease caused by the deficiency of hypoxanthine phosphoribosyltransferase, an enzyme involved in the purine salvage pathways. It is characterized by severe gout, choreoathetosis, self‐mutilatory behaviour and mental retardation. The derivation of mice genetically deficient in this enzyme may help to elucidate
M. L. Hooper   +2 more
openaire   +3 more sources

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