Defective removal of DNA cross-links in a repair-deficient mutant of Chinese hamster cells

R. E. Meyn, S. F. Jenkins, L. H. Thompson

Research output: Contribution to journalArticle

90 Citations (Scopus)

Abstract

To further understand the relationships between DNA damage, DNA repair, and cellular end points such as survival and mutation, the repair capacity of a DNA repair-deficient mutant (strain UV-20) of Chinese hamster ovary cells was characterized in response to DNA cross-linking agents. This mutant, previously shown to be hypersensitive to killing by both ultraviolet light and the cross-linking agent mitomycin C, was also found to be extremely sensitive to cis-diamminedichloroplatinum, another DNA cross-linking agent. The efficiency of DNA cross-link removal after treatment with mitomycin C or cis-diamminedichloroplatinum was measured using the technique of alkaline elution and compared in wild-type Chinese hamster ovary cells and strain UV-20. Wild-type cells removed 80 or 95% of the cross-links within 24 hr after treatment with cis-diamminedichloroplatinum or mitomycin C, respectively. In contrast, UV-20 cells, which were equally as susceptible to cross-link damage as were wild-type cells, removed only a small proportion of the cross-links made by either agent. These results emphasize the importance of DNA repair processes in modulating the cytotoxic effects of chemicals that produce DNA cross-link damage and suggest that cross-link repair in Chinese hamster ovary cells is controlled by a pathway that also repairs damage from ultraviolet radiation.

Original languageEnglish (US)
Pages (from-to)3106-3110
Number of pages5
JournalCancer Research
Volume42
Issue number8
StatePublished - 1982
Externally publishedYes

Fingerprint

Cricetulus
DNA
Mitomycin
Cisplatin
Ovary
DNA Repair
DNA Repair-Deficiency Disorders
Ultraviolet Rays
DNA Damage
Radiation
Mutation

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Meyn, R. E., Jenkins, S. F., & Thompson, L. H. (1982). Defective removal of DNA cross-links in a repair-deficient mutant of Chinese hamster cells. Cancer Research, 42(8), 3106-3110.

Defective removal of DNA cross-links in a repair-deficient mutant of Chinese hamster cells. / Meyn, R. E.; Jenkins, S. F.; Thompson, L. H.

In: Cancer Research, Vol. 42, No. 8, 1982, p. 3106-3110.

Research output: Contribution to journalArticle

Meyn, RE, Jenkins, SF & Thompson, LH 1982, 'Defective removal of DNA cross-links in a repair-deficient mutant of Chinese hamster cells', Cancer Research, vol. 42, no. 8, pp. 3106-3110.
Meyn, R. E. ; Jenkins, S. F. ; Thompson, L. H. / Defective removal of DNA cross-links in a repair-deficient mutant of Chinese hamster cells. In: Cancer Research. 1982 ; Vol. 42, No. 8. pp. 3106-3110.
@article{f14b1ad08e67445083a533699ec63af7,
title = "Defective removal of DNA cross-links in a repair-deficient mutant of Chinese hamster cells",
abstract = "To further understand the relationships between DNA damage, DNA repair, and cellular end points such as survival and mutation, the repair capacity of a DNA repair-deficient mutant (strain UV-20) of Chinese hamster ovary cells was characterized in response to DNA cross-linking agents. This mutant, previously shown to be hypersensitive to killing by both ultraviolet light and the cross-linking agent mitomycin C, was also found to be extremely sensitive to cis-diamminedichloroplatinum, another DNA cross-linking agent. The efficiency of DNA cross-link removal after treatment with mitomycin C or cis-diamminedichloroplatinum was measured using the technique of alkaline elution and compared in wild-type Chinese hamster ovary cells and strain UV-20. Wild-type cells removed 80 or 95{\%} of the cross-links within 24 hr after treatment with cis-diamminedichloroplatinum or mitomycin C, respectively. In contrast, UV-20 cells, which were equally as susceptible to cross-link damage as were wild-type cells, removed only a small proportion of the cross-links made by either agent. These results emphasize the importance of DNA repair processes in modulating the cytotoxic effects of chemicals that produce DNA cross-link damage and suggest that cross-link repair in Chinese hamster ovary cells is controlled by a pathway that also repairs damage from ultraviolet radiation.",
author = "Meyn, {R. E.} and Jenkins, {S. F.} and Thompson, {L. H.}",
year = "1982",
language = "English (US)",
volume = "42",
pages = "3106--3110",
journal = "Journal of Cancer Research",
issn = "0099-7013",
publisher = "American Association for Cancer Research Inc.",
number = "8",

}

TY - JOUR

T1 - Defective removal of DNA cross-links in a repair-deficient mutant of Chinese hamster cells

AU - Meyn, R. E.

AU - Jenkins, S. F.

AU - Thompson, L. H.

PY - 1982

Y1 - 1982

N2 - To further understand the relationships between DNA damage, DNA repair, and cellular end points such as survival and mutation, the repair capacity of a DNA repair-deficient mutant (strain UV-20) of Chinese hamster ovary cells was characterized in response to DNA cross-linking agents. This mutant, previously shown to be hypersensitive to killing by both ultraviolet light and the cross-linking agent mitomycin C, was also found to be extremely sensitive to cis-diamminedichloroplatinum, another DNA cross-linking agent. The efficiency of DNA cross-link removal after treatment with mitomycin C or cis-diamminedichloroplatinum was measured using the technique of alkaline elution and compared in wild-type Chinese hamster ovary cells and strain UV-20. Wild-type cells removed 80 or 95% of the cross-links within 24 hr after treatment with cis-diamminedichloroplatinum or mitomycin C, respectively. In contrast, UV-20 cells, which were equally as susceptible to cross-link damage as were wild-type cells, removed only a small proportion of the cross-links made by either agent. These results emphasize the importance of DNA repair processes in modulating the cytotoxic effects of chemicals that produce DNA cross-link damage and suggest that cross-link repair in Chinese hamster ovary cells is controlled by a pathway that also repairs damage from ultraviolet radiation.

AB - To further understand the relationships between DNA damage, DNA repair, and cellular end points such as survival and mutation, the repair capacity of a DNA repair-deficient mutant (strain UV-20) of Chinese hamster ovary cells was characterized in response to DNA cross-linking agents. This mutant, previously shown to be hypersensitive to killing by both ultraviolet light and the cross-linking agent mitomycin C, was also found to be extremely sensitive to cis-diamminedichloroplatinum, another DNA cross-linking agent. The efficiency of DNA cross-link removal after treatment with mitomycin C or cis-diamminedichloroplatinum was measured using the technique of alkaline elution and compared in wild-type Chinese hamster ovary cells and strain UV-20. Wild-type cells removed 80 or 95% of the cross-links within 24 hr after treatment with cis-diamminedichloroplatinum or mitomycin C, respectively. In contrast, UV-20 cells, which were equally as susceptible to cross-link damage as were wild-type cells, removed only a small proportion of the cross-links made by either agent. These results emphasize the importance of DNA repair processes in modulating the cytotoxic effects of chemicals that produce DNA cross-link damage and suggest that cross-link repair in Chinese hamster ovary cells is controlled by a pathway that also repairs damage from ultraviolet radiation.

UR - http://www.scopus.com/inward/record.url?scp=0019986881&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019986881&partnerID=8YFLogxK

M3 - Article

C2 - 6807537

AN - SCOPUS:0019986881

VL - 42

SP - 3106

EP - 3110

JO - Journal of Cancer Research

JF - Journal of Cancer Research

SN - 0099-7013

IS - 8

ER -