Are allopurinol and metabolites found in HPRT deficient erythrocytes responsible for increased NAD synthesis?
نویسندگان
چکیده
Aim of this study was to ascertain whether allopurinol, usually administered to hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficient patients, or metabolites abnormally increased in HPRT deficient erythrocytes (NAD, PPribP) could be directly responsible for the reported increased activities of nicotinic acid phosphoribosyltransferase (NAPRT) and NADsynthetase (NADs) in these patients. No direct effect of the mentioned metabolites was demonstrated.
منابع مشابه
The renal phenotype of allopurinol-treated HPRT-deficient mouse
Excess of uric acid is mainly treated with xanthine oxidase (XO) inhibitors, also called uricostatics because they block the conversion of hypoxanthine and xanthine into urate. Normally, accumulation of upstream metabolites is prevented by the hypoxanthine-guanine phosphoribosyltransferase (HPRT) enzyme. The recycling pathway, however, is impaired in the presence of HPRT deficiency, as observed...
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ورودعنوان ژورنال:
- Nucleosides, nucleotides & nucleic acids
دوره 23 8-9 شماره
صفحات -
تاریخ انتشار 2004