Further characterization of the growth inhibitory effect of rotenone on in vitro cultured Ehrlich ascites tumour cells
Further characterization of the growth inhibitory effect of rotenone on in vitro cultured Ehrlich ascites tumour cells
复制标题
鱼藤酮对体外培养的艾氏腹水肿瘤细胞生长抑制作用的进一步表征
DOI：
--
复制
发表时间：
1982
影响因子：
4.3
通讯作者：
F. Schneider
中科院分区：
文献类型：
--
作者：
Monika Löffler;F. Schneider
Summaryas是一种更好地理解鱼藤酮对哺乳动物细胞的作用方式的方法。抑制剂。在异步细胞上的示例显示，通过增加的糖酵解速率，氧气消耗降低，DNA含量中等增加以及蛋白质的蛋白质含量和RNA培养物的公平增加，从而迅速停止了细胞分裂。在细胞周期的G2和M相中的细胞积累。和有丝分裂过程 - 使用离心液的Ehrlich腹水肿瘤细胞对细胞周期不同阶段的细胞进行了对细胞周期的影响。在存在2,5 AM的Rotenone中培养的不同部分表明，除了观察到的G2中的积累和细胞的有丝分裂停滞之外，细胞周期的进程在G1期延迟。呼吸链。S相细胞似乎以与控制的速率继续进行几个小时。对烤烤烤烤龙甲酮处理的无抑制剂培养基中的异步细胞进行了重新培养的实验证实，某些细胞可以重新启动DNA合成必须得出结论，在循环的所有阶段，细胞都受藤酮的影响，但是一旦废除有丝分裂的急性阻滞，细胞代谢的损害就会显现，并致命，并且细胞重新进入周期。
SummaryAs an approach for a better understanding of the mode of action of rotenone on mammalian cells we have studied the proliferation properties, metabolism and basic cell composition of Ehrlich ascites tumour cells cultured in vitro in the presence of 2,5 µM rotenone and after removal of the inhibitor.Experiments on asynchronous cells showed a rapid cessation of cell division accompanied by increased glycolytic rate, reduced oxygen consumption, moderate increase in DNA content and a fair increase in protein and RNA content of the cultures. DNA histograms obtained by flow-cytometry revealed an accumulation of cells in the G2 and M phase of the cell cycle. Electron micrographs taken after a 24 h treatment of cells illustrated the formation of giant mitochondria and fragmented nuclei.In order to elucidate the dual effect of rotenone — inhibition of mitochondrial energy metabolism and of mitotic processes — the influence on cells of rotenone at different stages of the cell cycle was tested using Ehrlich ascites tumour cells enriched in G1, S and G2 by centrifugal elutriation. DNA histograms and [3H]thymidine labelling index curves of cells from the different fractions cultured in the presence of 2,5 AM rotenone indicated that in addition to the observed accumulation in G2 and mitotic arrest of cells, the cell cycle progression is delayed in G1 phase. This may be explained by an effect of the inhibitor on the respiratory chain. S phase cells seemed to continue the cycle for several hours at a rate comparable to that of controls.Recultivation experiments on rotenone-treated asynchronous cells in inhibitor-free medium confirmed that some cells reinitiate DNA synthesis without preceeding cell division.Thus it must be concluded that cells at all stages of the cycle are affected by rotenone, but the impairment of cellular metabolism becomes manifest and lethal as soon as the acute block at mitosis is abolished and cells reenter the cycle.