Pérignon J L, Thuillier L, Hamet M, Houllier A M, Cartier P H
Int J Immunopharmacol. 1986;8(4):427-31. doi: 10.1016/0192-0561(86)90127-x.
The intermediary metabolism of pyrimidine nucleosides was studied in a line of human B lymphoblasts (Raji) in which pyrimidine de novo synthesis deficiency was pharmacologically induced by pyrazofurin. It was found that Raji cells are cytidine deaminase deficient that cytidine has a synergistic effect on the toxicity of pyrazofurin towards these cytidine deaminase deficient cells, affecting both the proliferation and the viability of the cells. Indirect evidences suggest that this synergistic toxicity is not mediated by an effect on nucleoside diphosphate reductase nor on the first steps of pyrimidine de novo synthesis.
在人B淋巴母细胞系（拉吉细胞）中研究了嘧啶核苷的中间代谢，在该细胞系中，通过吡唑呋林药理学诱导嘧啶从头合成缺陷。发现拉吉细胞缺乏胞苷脱氨酶，胞苷对吡唑呋林对这些缺乏胞苷脱氨酶的细胞的毒性具有协同作用，影响细胞的增殖和活力。间接证据表明，这种协同毒性不是由对核苷二磷酸还原酶或嘧啶从头合成的第一步的作用介导的。
