Lobova T G, Zharkov S A, Preobrazhenskaia M N, Garin A M
Eksp Onkol. 1985;7(3):63-5.
Administration of ribamidyl (Rb) prior to Ara-C to intact mice or mice with implanted tumours enhanced Ara-C toxicity. The growth of tumours (plasmacytoma MOPC-21, adenocarcinoma of the small intestine (strain AKATON), mammary adenocarcinoma 755 (Ca 755) resistant to Ara-C or Rb was inhibited after coadministration of these drugs. The augmentation of toxic and antitumour effects of Ara-C by Rb is similar to the described effect of high doses of thymidine. This is in accordance with the enhancement of the intracellular pool of thymidine phosphates under the action of Rb. The toxicity of methotrexate in vivo was increased by coadministration with Rb. This effect may be connected with a decrease in purine precursors pool under the action of Rb.
在给完整小鼠或植入肿瘤的小鼠注射阿糖胞苷（Ara-C）之前给予核糖氨咪（Rb）可增强阿糖胞苷的毒性。在联合使用这些药物后，肿瘤（浆细胞瘤MOPC-21、小肠腺癌（AKATON品系）、对阿糖胞苷或Rb耐药的乳腺腺癌755（Ca 755））的生长受到抑制。Rb增强阿糖胞苷的毒性和抗肿瘤作用与高剂量胸苷所描述的作用相似。这与Rb作用下细胞内胸苷磷酸池的增加一致。与Rb联合给药可增加甲氨蝶呤在体内的毒性。这种作用可能与Rb作用下嘌呤前体池的减少有关。
