Are allopurinol and metabolites found in HPRT deficient erythrocytes responsible for increased NAD synthesis?
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.
Micheli
V
V
Dip. Biologia Molecolare, Università di Siena, Siena, Italy.
Jacomelli
G
G
Sestini
S
S
Notarantonio
L
L
Cerboni
B
B
Peruzzi
L
L
Pompucci
G
G
D000493:Allopurinol / Q000097:blood* / Q000378:metabolism*; D019732:Amide Synthases / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004912:Erythrocytes / Q000201:enzymology / Q000378:metabolism*; D006801:Humans; D007041:Hypoxanthine Phosphoribosyltransferase / Q000097:blood* / Q000172:deficiency*; D009243:NAD / Q000378:metabolism; D010117:Oxypurinol / Q000378:metabolism; D010430:Pentosyltransferases / Q000378:metabolism
D004791:Enzyme Inhibitors; D009243:NAD; D000493:Allopurinol; D010430:Pentosyltransferases; D007041:Hypoxanthine Phosphoribosyltransferase; D019732:Amide Synthases; C038479:NAD+ synthase; C021864:nicotinate phosphoribosyltransferase; D010117:Oxypurinol