Interaction between Radiation and Drug Damage in Mammalian Cells: IV. Radiation Response of Adriamycin-Resistant V79 Cells

1989 ◽  
Vol 119 (1) ◽  
pp. 88 ◽  
Author(s):  
James A. Belli
1989 ◽  
Vol 9 (3) ◽  
pp. 1277-1283 ◽  
Author(s):  
H Vrieling ◽  
M L Van Rooijen ◽  
N A Groen ◽  
M Z Zdzienicka ◽  
J W Simons ◽  
...  

The influence of DNA repair on the molecular nature of mutations induced by UV light (254 nm) was investigated in UV-induced hprt mutants from UV-sensitive Chinese hamster cells (V-H1) and the parental line (V79). The nature of point mutations in hprt exon sequences was determined for 19 hprt mutants of V79 and for 17 hprt mutants of V-H1 cells by sequence analysis of in vitro-amplified hprt cDNA. The mutation spectrum in V79 cells consisted of single- and tandem double-base pair changes, while in V-H1 cells three frameshift mutations were also detected. All base pair changes in V-H1 mutants were due to GC----AT transitions. In contrast, in V79 all possible classes of base pair changes except the GC----CG transversion were present. In this group, 70% of the mutations were transversions. Since all mutations except one did occur at dipyrimidine sites, the assumption was made that they were caused by UV-induced photoproducts at these sites. In V79 cells, 11 out of 17 base pair changes were caused by photoproducts in the nontranscribed strand of the hprt gene. However, in V-H1 cells, which are completely deficient in the removal of pyrimidine dimers from the hprt gene and which show a UV-induced mutation frequency enhanced seven times, 10 out of 11 base pair changes were caused by photoproducts in the transcribed strand of the hprt gene. We hypothesize that this extreme strand specificity in V-H1 cells is due to differences in fidelity of DNA replication of the leading and the lagging strand. Furthermore, we propose that in normal V79 cells two processes determine the strand specificity of UV-induced mutations in the hprt gene, namely preferential repair of the transcribed strand of the hprt gene and a higher fidelity of DNA replication of the nontranscribed strand compared with the transcribed strand.


1988 ◽  
Vol 7 (4) ◽  
pp. 337-341 ◽  
Author(s):  
D. Anderson ◽  
P. Fisher ◽  
P.C. Jenkinson ◽  
B.J. Phillips

In bacteria, there is evidence that a damage inducible repair response system known as the adaptive response exists since pretreatment with low doses of a simple monofunctional alkylating agent leads to a decrease in both the lethal and mutagenic effects of a subsequent challenge dose of the agent. The evidence for an analagous system in mammalian cells has proved to be inconsistent to date. The induction of chromosome repair mechanisms in human cells by low-dose radiation from tritiated thymidine has been shown to make the cells refractory to the induction of chromosome aberrations by X-rays. The present communication investigates the induction of an adaptive response in human lymphocytes from four donors and V79 cells using SCE and mutation as endpoints and MNNG and MNU for the adapting and challenging treatment. It is clear that a reproducible model of the adaptive response in human lymphocytes is difficult to establish because of the variability between different donors and different culture times. In V79 cells, assays with much larger cell numbers are required to detect a reproducible response with such small changes in mutant frequency. To demonstrate an adaptive response conclusively in mammalian cells will probably require the use of more sensitive experimental protocols and alternative methods of administration of adaptive doses of mutagen.


1973 ◽  
Vol 53 (1) ◽  
pp. 33 ◽  
Author(s):  
C. J. Koch ◽  
J. Kruuv ◽  
H. E. Frey

Radiology ◽  
1977 ◽  
Vol 123 (3) ◽  
pp. 771-772
Author(s):  
Saadoon Kadir ◽  
Fred W. Hetzel ◽  
Gerald M. Kolodny

1965 ◽  
Vol 25 (2) ◽  
pp. 359 ◽  
Author(s):  
M. M. Elkind ◽  
H. Sutton-Gilbert ◽  
W. B. Moses ◽  
T. Alescio ◽  
R. W. Swain

1990 ◽  
Vol 01 (01) ◽  
pp. 85-92 ◽  
Author(s):  
SHINJI MATSUMOTO ◽  
KANAME TSUCHIYA ◽  
REN CHIBA

PIXE analysis was successfully applied to the measurement of cellular elements of mammalian cells in relation to the study of hyperthermia. V79 cells were heated at 44.0°C for 30 min or 1 h and the following element releases or uptakes were determined with PIXE measurement of samples obtained after appropriate periods of incubation at 37°C. Linear relationships were confirmed between the produced X-ray yields of P, S, Cl, K and Ca and the cell numbers. The cellular contents P, S, and K decreased promptly after the heat treatment and recovered gradually in the following incubation. Changes in the contents of Cl and Ca did not show abrupt decreases. Curiously, the content of Ca increased after the treatment at 44.0°C for 30 min. The results suggest that various structural modifications were induced in the membrane by the heat treatment.


1983 ◽  
Vol 93 (1) ◽  
pp. 51 ◽  
Author(s):  
Shelagh D. Campbell ◽  
Jack Kruuv ◽  
James R. Lepock

1968 ◽  
Vol 41 (485) ◽  
pp. 390-391 ◽  
Author(s):  
James A. Belli ◽  
Alice Roach

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