Hartley-Asp B
Prostate. 1984;5(1):93-100. doi: 10.1002/pros.2990050109.
In growth proliferation experiments on two human prostatic carcinoma cell lines, DU 145 cells were found to be more sensitive to the cytotoxic effect of estramustine and nor-nitrogen mustard than PC-3 cells. Estramustine was, however, much more cytotoxic in both cell lines than nor-nitrogen mustard. Cytogenetic experiments revealed that estramustine produced a drastic increase of the mitotic index in both these cell lines. This increase could be accounted for by the arrest of cells in their first treatment-metaphase. The arrested metaphases exhibited all the characteristics commonly found for stathmokinetic agents such as colchicine and vinca-analogues. No mitotic arrest was found for nor-nitrogen mustard but chromosomal aberrations were found at toxic concentrations. Estradiol exhibited minimal toxicity and caused no mitotic arrest in these cell lines. The mitotic arrest induced by estramustine was found to be reversible on removal of the drug.
在对两种人前列腺癌细胞系进行的生长增殖实验中,发现DU 145细胞比PC - 3细胞对雌莫司汀和去甲氮芥的细胞毒性作用更敏感。然而,在这两种细胞系中,雌莫司汀的细胞毒性都比去甲氮芥大得多。细胞遗传学实验表明,雌莫司汀使这两种细胞系的有丝分裂指数急剧增加。这种增加可以通过细胞在首次处理的中期停滞来解释。停滞的中期表现出有丝分裂抑制剂(如秋水仙碱和长春花类似物)常见的所有特征。去甲氮芥未发现有丝分裂停滞,但在有毒浓度下发现了染色体畸变。雌二醇表现出最小的毒性,并且在这些细胞系中未引起有丝分裂停滞。发现去除药物后,雌莫司汀诱导的有丝分裂停滞是可逆的。