Delayed Initiation of DNA Synthesis in Irradiated Human Diploid Cells

Nature ◽  
1968 ◽  
Vol 218 (5146) ◽  
pp. 1064-1065 ◽  
Author(s):  
JOHN B. LITTLE
Keyword(s):  
Dna Synthesis ◽  
Delayed Initiation ◽  
Human Diploid Cells ◽  
Diploid Cells

scholarly journals ASYNCHRONY OF DNA SYNTHESIS IN CHROMOSOMES OF HUMAN DIPLOID CELLS

1963 ◽  
Vol 16 (1) ◽  
pp. 202-209 ◽  
Author(s):  
P. S. Moorhead ◽  
Vittorio Defendi
Keyword(s):  
Dna Synthesis ◽  
Human Diploid Cells ◽  
Diploid Cells

scholarly journals Oxygen-sensitive stages of the cell cycle of human diploid cells.

1978 ◽  
Vol 78 (2) ◽  
pp. 390-400 ◽  
Author(s):  
A K Balin ◽  
D B Goodman ◽  
H Rasmussen ◽  
V J Cristofalo
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Oxygen Tension ◽  
Cycle Growth ◽  
Partial Pressures ◽  
Oxygen Sensitive ◽  
Oxygen Tensions ◽  
Human Diploid Cells ◽  
Diploid Cells

We had established that growth of human diploid WI-38 cells is reversibly inhibited by elevated partial pressures of oxygen (PO2) and we were interested in determining where in the cell cycle growth was delayed. A technique combining cytospectrophotometry and autoradiography was used to determine cell cycle parameters. Confluent cells that were subcultivated and exposed to a PO2 of 365 +/- 8 mm Hg were delayed primarily after DNA synthesis but before metaphase. At a PO2 of 590 +/- 35 mm Hg, most cells did not initiate DNA synthesis, and the few that did, failed to complete the process. When exponentially growing cells that had already begun DNA synthesis were exposed to a PO2 of 590 p 35 mm Hg, they accumulated after completing DNA synthesis but before initiating mitosis. The rate at which (3H)thymidine was incorporated into DNA was inversely correlated with oxygen tension (PO2 of 135--590 mm Hg). These results suggest that the process most sensitive to oxygen causes cells to be delayed after DNA synthesis but before metaphase. Slightly higher PO2's were needed to inhibit the initiation of DNA synthesis. Further, the rate of DNA synthesis is decreased by elevated oxygen tensions.

Senescent Human Diploid Cells in Culture: Survival, DNA Synthesis and Morphology

1979 ◽  
Vol 34 (3) ◽  
pp. 328-334 ◽  
Author(s):  
T. Matsumura ◽  
Z. Zerrudo ◽  
L. Hayflick
Keyword(s):  
Dna Synthesis ◽  
Cells In Culture ◽  
Human Diploid Cells ◽  
Diploid Cells

Reinitiation of host DNA synthesis in senescent human diploid cells by infection with simian virus 40

1983 ◽  
Vol 143 (2) ◽  
pp. 343-349 ◽  
Author(s):  
Toshinori Ide ◽  
Yoshiaki Tsuji ◽  
Sadahiko Ishibashi ◽  
Youji Mitsui
Keyword(s):  
Dna Synthesis ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Human Diploid Cells ◽  
Diploid Cells

scholarly journals Evidence for endogenous polypeptide-mediated inhibition of cell-cycle transit in human diploid cells.

1982 ◽  
Vol 94 (1) ◽  
pp. 187-192 ◽  
Author(s):  
G C Burmer ◽  
C J Zeigler ◽  
T H Norwood
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Dna Synthesis ◽  
Tritiated Thymidine ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Human Diploid Fibroblasts ◽  
Senescent Phenotype ◽  
Human Diploid Cells ◽  
Diploid Cells

Previous studies have shown that the senescent phenotype is dominant with respect to DNA synthesis in fusions between late passage and actively replicating human diploid fibroblasts. Brief postfusion treatments with the protein synthesis inhibitor cycloheximide (CHX) or puromycin have been found to significantly delay (by 24-48 h) the inhibition of entry into DNA synthesis of young nuclei in heterokaryons after fusion with senescent cells. A significant fraction of the senescent nuclei incorporated tritiated thymidine in CHX-treated heterokaryons. The optimal duration of exposure to CHX was 1-3 h immediately after fusion, although treatments beginning as late as 9 h after fusion elevated the heterokaryon labeling index. Prefusion treatments with CHX were without a significant effect. These results are consistent with the interpretation that regulatory cell cycle inhibitor(s) which are dependent upon protein synthesis may be present in heterokaryons between senescent and actively replicating cells.

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