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Thymidine, in the absence of hypoxanthine, failed to protect normal mice from the acute toxicity of methotrexate, though tumor-bearing animals could be protected with thymidine alone, probably as a result of the availability of DNA degradation products released from drug-sensitive tumor cells. Although metrotrexate induced an early purine deficiency in gut cells, this effect was not detected in bone marrow. Later, purine deficiency became apparent in the gut and bone marrow of methotrexate-treated animals.


Journal article


J Natl Cancer Inst

Publication Date





91 - 95


Animals Bone Marrow/drug effects/metabolism Bone Marrow Cells DNA/biosynthesis Drug Interactions Drug Therapy, Combination Hypoxanthines/pharmacology Intestines/drug effects/metabolism Leucovorin/pharmacology Leukemia L1210/drug therapy Male Methotrexate/therapeutic use/*toxicity Mice Mice, Inbred C57BL Purines/metabolism Pyrimidines/metabolism Thymidine/pharmacology