| Evidence for Excision of Ultraviolet-Induced Pyrimidine Dimers from the DNA of Human Cells In Vitro Biophysical Journal, Volume 8, Issue 3, 1 March 1968, Pages 319-325 James D. Regan, James E. Trosko and William L. Carrier Abstract Within 12–24 hr after human cells were irradiated with ultraviolet light, approximately 50% of the ultraviolet-induced pyrimidine dimers were lost from the DNA. Pyrimidine dimers were found in the TCA-soluble fraction of ultraviolet-irradiated cells at 24 hr. Excess thymidine, caffeine, or hydroxyurea had no effect on the loss of pyrimidine dimers from the DNA of ultraviolet-irradiated cells. Abstract | PDF (358 kb) |
| Strand breaks and alkali-labile bonds induced by ultraviolet light in DNA with 5-bromouracil in vivo Biophysical Journal, Volume 24, Issue 3, 1 December 1978, Pages 657-664 F. Krasin and F. Hutchinson Abstract Supercircular gamma phage DNA with 10 bromouracils/100 thymine bases, irradiated with 313 nm light in Tris buffer and sedimented on alkaline and neutral gradients, showed 4.6 alkali-labile bonds per true single-strand break, in agreement with Hewitt and Marburger (1975 Photochem. Photobiol. 21:413). The same DNA irradiated in Escherichia coli host cells showed about the same number of breaks in alkaline gradients for equal fluence, but only 0.5 alkali-labile bond per true break. Similarly, E. coli DNA with bromouracil irradiated in the cells showed only 10--20% more breaks when denatured with 0.1 M NaOH than under neutral conditions with 9 M sodium perchlorate at 50 degrees C. These results show that true single-strand breaks occur more frequently than alkali-labile bonds after ultraviolet irradiation of DNA containing bromouracil in cells. Abstract | PDF (408 kb) |
| Enhancement of postreplication repair in ultraviolet-light-irradiated Chinese hamster cells by irradiation in G2 or S-phase Biophysical Journal, Volume 23, Issue 1, 1 July 1978, Pages 71-78 S.M. D'Ambrosio, P.M. Aebersold and R.B. Setlow Abstract Postreplication repair in synchronous Chinese hamster cells was determined after split doses of ultraviolet (UV) radiation. Repair was enhanced by irradiation of cells in G2 or S-phase with a small dose of UV radiation at least 1.5 h before a three-fold larger dose of UV. There was significantly greater enhancement when the first dose was given in G2 than when it was given in the S-phase 0.5–1.5 h before the test dose. These data indicate that enhancement of postreplication repair does not require active DNA replication and qualitatively is independent of when in the cell cycle the cells are irradiated. Abstract | PDF (405 kb) |
Copyright © 1974 The Biophysical Society. All rights reserved.
Biophysical Journal, Volume 14, Issue 3, 209-220, 1 March 1974
doi:10.1016/S0006-3495(74)85908-4
Articles
A.M. Rauth, M. Tammemagi and G. Hunter
The technique of alkaline sucrose gradient centrifugation was used to study newly synthesized DNA in control and ultraviolet light-irradiated mouse L, human HeLa, and Chinese hamster ovary cells. Nascent DNA molecular weight distributions did not appear to differ among the three cell lines for unirradiated cells. However, at short times after ultraviolet light irradiation, human HeLa cells appeared to synthesize more low molecular weight DNA than either mouse L or Chinese hamster ovary cells. Since this difference was not related to differences in either the rate of DNA synthesis or amount of ultraviolet damage in the irradiated cells it appeared to be a phenotypic characteristic of the cell lines tested. A parallel was noted for these three cell lines between an increase in the synthesis of low molecular weight DNA, detected on alkaline sucrose gradients, and cell killing as measured by the ability of irradiated cells to form colonies.