Schmalbach T K, Borch R F
Department of Pharmacology, University of Rochester School of Medicine and Dentistry, New York 14642.
Cancer Res. 1990 Oct 1;50(19):6218-21.
Sodium diethyldithiocarbamate (DDTC) has been shown to modulate the myelosuppression that commonly occurs following treatment with anticancer drugs in mice. In order to investigate the mechanism of action of this myeloprotector, murine long-term bone marrow cultures were treated with DDTC alone or were preceded by the anticancer drug cis-diammine(cyclobutanedicarboxylato)platinum(II) (CBDCA), and the granulocyte/macrophage colony-stimulating activity of the supernatants was measured. The supernatants harvested from DDTC-treated cultures enhanced proliferation of granulocyte/macrophage progenitor cells almost 4-fold compared to cultures treated with no drug or with CBDCA alone. Pretreatment of cultures with CBDCA neither enhanced nor inhibited DDTC-induced colony-stimulating activity. Similar results were obtained by using marrow stromal cell cultures free of hematopoietic cells. Thus, DDTC may hasten bone marrow recovery by augmenting stromal cell production of a factor(s) with hematopoietic colony-stimulating activity.
二乙基二硫代氨基甲酸钠（DDTC）已被证明可调节小鼠接受抗癌药物治疗后常见的骨髓抑制。为了研究这种骨髓保护剂的作用机制，对小鼠长期骨髓培养物单独用DDTC处理，或先用抗癌药物顺式二氨（环丁烷二羧酸根）铂（II）（CBDCA）处理，然后测量上清液的粒细胞/巨噬细胞集落刺激活性。与未用药或仅用CBDCA处理的培养物相比，从用DDTC处理的培养物中收获的上清液使粒细胞/巨噬细胞祖细胞的增殖增强了近4倍。用CBDCA预处理培养物既不增强也不抑制DDTC诱导的集落刺激活性。使用不含造血细胞的骨髓基质细胞培养物也得到了类似的结果。因此，DDTC可能通过增强具有造血集落刺激活性的因子的基质细胞产生来加速骨髓恢复。
