Mizushima Y, Morikage T, Yano S
First Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
Cancer Res. 1990 Mar 15;50(6):1847-52.
The toxicity effects of several anticancer drugs on normal mouse bone marrow (BM) were estimated using the in vitro proliferative responsiveness [( 3H]thymidine incorporation) of the treated BM cells to recombinant human granulocyte colony-stimulating factor (G-CSF) and recombinant human interleukin 2 (IL-2). From the response pattern of the treated BM cells to G-CSF and IL-2, the anticancer drugs were classified into three groups: (a) BM cells from cyclophosphamide- or nimustine hydrochloride-treated mice showed an increased responsiveness to G-CSF but a decreased responsiveness to IL-2; (b) BM cells from vindesine- or peplomycin-treated mice showed an increased responsiveness to both G-CSF and IL-2; and (c) BM cells from mitomycin C-treated mice showed a decreased responsiveness to both G-CSF and IL-2. These different response patterns may reflect qualitative differences in the myelotoxicity effects of these anticancer drugs.
使用经处理的骨髓细胞对重组人粒细胞集落刺激因子(G-CSF)和重组人白细胞介素2(IL-2)的体外增殖反应性[(3H)胸腺嘧啶核苷掺入],评估了几种抗癌药物对正常小鼠骨髓(BM)的毒性作用。根据经处理的骨髓细胞对G-CSF和IL-2的反应模式,将抗癌药物分为三组:(a)来自环磷酰胺或盐酸尼莫司汀处理小鼠的骨髓细胞对G-CSF的反应性增加,但对IL-2的反应性降低;(b)来自长春地辛或培洛霉素处理小鼠的骨髓细胞对G-CSF和IL-2的反应性均增加;(c)来自丝裂霉素C处理小鼠的骨髓细胞对G-CSF和IL-2的反应性均降低。这些不同的反应模式可能反映了这些抗癌药物骨髓毒性作用的质量差异。