The biochemical evidence against incorporation of the purine analogues, allopurinol and oxipurinol, into nucleic acids is reviewed. Cytological experiments have been carried out to investigate the possibility that chromosomal damage might result from exposure of human lymphocytes to these drugs. Lymphocytes from 19 patients receiving allopurinol and one receiving oxipurinol were examined for th...

Allopurinol (ALP) hypersensitivity is a major cause of severe cutaneous adverse reactions and is strongly associated with the HLA-B*58:01 allele. However, it can occur in the absence of this allele with identical clinical manifestations. The immune mechanism of ALP-induced severe cutaneous adverse reactions is poorly understood, and the T cell-reactivity pattern in patients with or without the ...

The land 7-ribosyl 5’-phosphates of oxipurinol [4,6dihydroxypyrazolo(3,4 d)pyrimidine] were enzymatically synthesized. These nucleotides, 3-xanthosine S’-phosphate, and the 1-ribosyl 5’-phosphate of allopurinol [4-hydroxypyrazolo(3,4-d)pyrimidine] were characterized by spectral, chromatographic, and enzymatic procedures. The oxipurinol nucleotides were found to be potent competitive inhibitors ...

Combination treatment with low-dose thiopurine and allopurinol (AP) has successfully been used in patients with inflammatory bowel disease with a so called skewed thiopurine metabolite profile. In red blood cells in vivo, it reduces the concentration of methylated metabolites and increases the concentration of the phosphorylated ones, which is associated with improved therapeutic efficacy. This...

We demonstrate that purine restriction is associated with a decreased excretion of a number of uv-absorbing compounds-including uric acid, hypoxanthine, xanthine, adenine, pseudouridine, and 5-acetylamino-6-amino-3methyluracil-indicating that these compounds originate, at least partly, exogenously. Administration of allopurinol and oxipurinol is associated with a decreased excretion of uric aci...

Myocardial dysfunction and heart failure perturb cardiovascular homeostatic signaling pathways as well as initiate a program of molecular, biochemical, and structural modifications to remodel the failing ventricle. Accumulating evidence suggests that the cardiovascular redox state plays an integral role in these processes. In fact, in the failing heart, elevated levels of reactive oxygen specie...