4-去甲氧基柔红霉素及其代谢产物4-去甲氧基-13-羟基柔红霉素对人急性髓性白血病细胞的细胞毒性和DNA损伤
Cytotoxicity and DNA damage caused by 4-demethoxydaunorubicin and its metabolite 4-demethoxy-13-hydroxydaunorubicin in human acute myeloid leukemia cells.
作者信息
Limonta M, Biondi A, Giudici G, Specchia G, Catapano C, Masera G, Barbui T, D'Incalci M
机构信息
Instituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
出版信息
Cancer Chemother Pharmacol. 1990;26(5):340-2. doi: 10.1007/BF02897289.
4-Demethoxydaunorubicin (4-DMDR) and its major metabolite 4-demethoxy-13-hydroxydaunorubicin (4-DMDRol) were investigated for their cytotoxicity and mode of action against human leukemic cells. The drug and its metabolite appeared to be equally potent as both inhibitors of cell proliferation and inducers of DNA double-strand breaks in the OCI AML-3 cell line and cells derived directly from patients with acute myeloid leukemia (AML). This suggests that 4-DMDRol plays an important role in the antileukemic activity of 4-DMDR.
对4-去甲氧基柔红霉素（4-DMDR）及其主要代谢产物4-去甲氧基-13-羟基柔红霉素（4-DMDRol）针对人白血病细胞的细胞毒性及其作用方式进行了研究。在OCI AML-3细胞系以及直接来自急性髓性白血病（AML）患者的细胞中，该药物及其代谢产物作为细胞增殖抑制剂和DNA双链断裂诱导剂似乎具有同等效力。这表明4-DMDRol在4-DMDR的抗白血病活性中发挥重要作用。
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