Gulonolactone Oxidase

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Studies on microsomal phospholipids that inhibit gulonolactone oxidase.

Fractions of rat liver microsomal phospholipid that inhibit gulonolactone oxidase are described. The inhibition was shown to be complete and occurs rapidly after the reaction has proceeded at the control rate for 20 to 30 min. It could be totally reversed by the addition of tocopherol, Mn++, Co++, or ethylenediaminetetraacetate. The inhibitory activity of the phospholipid was lost by enzymic cl...

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A kinetic study of the mechanism of action of L-gulonolactone oxidase.

The mechanism of action of L-gulonolactone oxidase has been studied by enzyme kinetic methods. Techniques have been developed for determining initial reaction rates above 1 atm lof oxygen pressure. The data are consistent with the following sequence of reactions: (a) combination of the enzyme with L-gulono-ylactone; (b) reduction of the enzyme to produce ascorbic acid; (c) combination of the re...

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Evaluation of gene expression profiling in a mouse model of L-gulonolactone oxidase gene deficiency.

Humans and guinea pigs are species which are unable to synthesize ascorbic acid (vitamin C) because, unlike rodents, they lack the enzyme L-gulonolactone oxidase (Gulo). Although the phenotype of lacking vitamin C in humans, named scurvy, has long been well known, information on the impact of lacking Gulo on the gene expression profiles of different tissues is still missing. This knowledge coul...

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Formation of malonaldehyde in vitamin E deficiency and its relation to the inhibition of gulonolactone oxidase.

The impairment of synthesis in vitro of ascorbic acid by liver extracts from animals deprived of vitamin E (1, 2) is due to the inhibition of the enzyme(s) located in the microsomes (3) which catalyzes the oxidation of n-gulonolactone to L-ascorbic acid. This enzyme or enzymic complex will be termed gulonolactone oxidase. Concurrent with the inhibition of gulonolactone oxidase, a material is fo...

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Gulonolactone Addition to Human Hepatocellular Carcinoma Cells with Gene Transfer of Gulonolactone Oxidase Restores Ascorbate Biosynthesis and Reduces Hypoxia Inducible Factor 1

Humans are unable to synthesise ascorbate (Vitamin C) due to the lack of a functional gulonolactone oxidase (Gulo), the enzyme that catalyses the final step in the biosynthesis pathway. Ascorbate is a vital micronutrient required for many biological functions, including as a cofactor for metalloenzymes that regulate the transcription factor hypoxia-inducible factor-1 (HIF-1), which governs cell...

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ژورنال

عنوان ژورنال: Journal of Biological Chemistry

سال: 1969

ISSN: 0021-9258

DOI: 10.1016/s0021-9258(18)83447-0