Redox-active ferrocene-modified pyrimidines and adenine as antitumor agents: structure, separation of enantiomers, and inhihibition of the DNA synthesis in tumor cells

2013 ◽  
Vol 62 (9) ◽  
pp. 2056-2064 ◽  
Author(s):  
L. V. Snegur ◽  
S. I. Zykova ◽  
A. A. Simenel ◽  
Yu. S. Nekrasov ◽  
Z. A. Starikova ◽  
...  
2013 ◽  
Vol 59 (5) ◽  
pp. 498-513 ◽  
Author(s):  
O.Yu. Abakumova ◽  
O.V. Podobed ◽  
P.A. Karalkin ◽  
L.I. Kondakova ◽  
N.N. Sokolov

We have studied dose- and time-dependent antitumor and cytotoxic effects of Erwinia carotovora L-asparaginase (ECAR LANS) and Escherichia coli L-asparaginase (MEDAC) on human leukemic cells and human and animal solid tumor cells. We determined the sensitivity of tumor cells to L-asparaginases, as well the effect L-asparaginases on cell growth rate, protein and DNA synthesis per se and with addition of different cytostatics. The data obtained demonstrated that ECAR LANS L-asparaginase suppressed growth of all tested solid tumor cells. Evaluation of leukemic cell number after treatment with L-asparaginases for 24, 48 and 72 h demonstrated that asparagine deficiency did not kill cells but stopped normal cell division and had no effect on protein and DNA synthesis. Cytofluorometric study of solid and leukemic cells demonstrated that the treatment with L-asparaginase for 72 h did not change cell cycle phase distribution and did not increase the number of apoptotic cells. The HL-60 cell line was only exemption. At the same time, cells treatment with L-asparaginase and doxorubicin combination leaded to increase of apoptotypical cell number to 60% for MCF7 cells, to 40% for Jurkat cells and to 99% for HL-60 cells. We have excluded apoptosis as main reason for tumor cell death after asparaginase treatment because multi resistant Jurkat/A4 cells have been asparaginase sensitive. We have not found ECAR LANS L-asparaginase effect on normal human fibroblasts growth ability and we had come to conclusion that enzyme cytotoxcisity related only with asparagine deficiency.


1977 ◽  
Vol 13 (10) ◽  
pp. 1195-1196 ◽  
Author(s):  
K. Rothbarth ◽  
G. Maier ◽  
E. Schöpf ◽  
D. Werner

2013 ◽  
Vol 86 (4) ◽  
pp. 458-468 ◽  
Author(s):  
Hideaki Yamaguchi ◽  
Yumi Kidachi ◽  
Katsuyoshi Kamiie ◽  
Toshiro Noshita ◽  
Hironori Umetsu ◽  
...  

1964 ◽  
Vol 22 (2) ◽  
pp. 341-350 ◽  
Author(s):  
Joseph Post ◽  
Joseph Hoffman

The replication time and pattern have been investigated in hepatoma cells induced by feeding 3'Me-DAB to male rats for 5 months. With the use of tritiated thymidine as a DNA label along with autoradiography, mitotic nuclear labeling has been studied 0.5 to 72 hours after the administration of the label. The following time intervals have been estimated: replication time, 31 hours; DNA synthesis, 17 hours; G2 plus Mitosis, 2 hours; G1, 12 hours. Only about 8 per cent of the tumor cell (interphase) population is "flash" labeled, following a single dose of 50 µC of H3TDR. This group of cells has been followed through three cycles of division. The repeated rhythmic passage of tumor cells through cell division is similar to that previously reported for normal liver cells in the growing rat. However, tumor cells have longer replication and DNA synthesis times. In addition, the several time intervals studied vary more in the tumor cell population than they do in the growing normal cell population.


1983 ◽  
Vol 96 (3) ◽  
pp. 1289-1291 ◽  
Author(s):  
A. A. Pekhov ◽  
O. S. Zhukova ◽  
T. P. Ivanova ◽  
V. A. Zanin ◽  
T. T. Berezov ◽  
...  
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