Abstract
A comparison was made of the ability of either X-radiation or a DNA-specific ligand (the vital bis-benzimidazole dye; Hoechst 33342) to induce: cell killing, inhibition of de novo DNA synthesis, DNA strand breakage and the delay of cell division in human colon adenocarcinoma cells in vitro. Unlike radiation-induced cell killing, ligand-induced cytotoxicity appeared to be positively correlated with the extent of inhibition of de novo DNA synthesis-a feature consistent with the persistent binding of ligand molecules to nuclear DNA. Ligand-induced DNA strand-breaks disappeared slowly although ligand-treated cells retained apparently normal capacities to repair discrete radiogenic DNA strand-breaks. Pre-treatment of cells with Hoechst 33342 resulted in a dose-modifying enhancement of radiation resistance not associated with altered dosimetry for strand-break induction. However, radioresistance was accompanied by the protracted retention of cells in the G/sub 2/ phase of the cell cycle. We suggest that the results provide direct evidence that the retention of cells in G/sub 2/ phase is a sparing phenomenon and is triggered by the responses of chromatin domains to the presence of DNA damage.
Citation Formats
Smith, P J, and Anderson, C O.
Modification of the radiation sensitivity of human tumour cells by a bis-benzimidazole derivative.
United Kingdom: N. p.,
1984.
Web.
doi:10.1080/09553008414551511.
Smith, P J, & Anderson, C O.
Modification of the radiation sensitivity of human tumour cells by a bis-benzimidazole derivative.
United Kingdom.
https://doi.org/10.1080/09553008414551511
Smith, P J, and Anderson, C O.
1984.
"Modification of the radiation sensitivity of human tumour cells by a bis-benzimidazole derivative."
United Kingdom.
https://doi.org/10.1080/09553008414551511.
@misc{etde_5607182,
title = {Modification of the radiation sensitivity of human tumour cells by a bis-benzimidazole derivative}
author = {Smith, P J, and Anderson, C O}
abstractNote = {A comparison was made of the ability of either X-radiation or a DNA-specific ligand (the vital bis-benzimidazole dye; Hoechst 33342) to induce: cell killing, inhibition of de novo DNA synthesis, DNA strand breakage and the delay of cell division in human colon adenocarcinoma cells in vitro. Unlike radiation-induced cell killing, ligand-induced cytotoxicity appeared to be positively correlated with the extent of inhibition of de novo DNA synthesis-a feature consistent with the persistent binding of ligand molecules to nuclear DNA. Ligand-induced DNA strand-breaks disappeared slowly although ligand-treated cells retained apparently normal capacities to repair discrete radiogenic DNA strand-breaks. Pre-treatment of cells with Hoechst 33342 resulted in a dose-modifying enhancement of radiation resistance not associated with altered dosimetry for strand-break induction. However, radioresistance was accompanied by the protracted retention of cells in the G/sub 2/ phase of the cell cycle. We suggest that the results provide direct evidence that the retention of cells in G/sub 2/ phase is a sparing phenomenon and is triggered by the responses of chromatin domains to the presence of DNA damage.}
doi = {10.1080/09553008414551511}
journal = []
volume = {46:4}
journal type = {AC}
place = {United Kingdom}
year = {1984}
month = {Oct}
}
title = {Modification of the radiation sensitivity of human tumour cells by a bis-benzimidazole derivative}
author = {Smith, P J, and Anderson, C O}
abstractNote = {A comparison was made of the ability of either X-radiation or a DNA-specific ligand (the vital bis-benzimidazole dye; Hoechst 33342) to induce: cell killing, inhibition of de novo DNA synthesis, DNA strand breakage and the delay of cell division in human colon adenocarcinoma cells in vitro. Unlike radiation-induced cell killing, ligand-induced cytotoxicity appeared to be positively correlated with the extent of inhibition of de novo DNA synthesis-a feature consistent with the persistent binding of ligand molecules to nuclear DNA. Ligand-induced DNA strand-breaks disappeared slowly although ligand-treated cells retained apparently normal capacities to repair discrete radiogenic DNA strand-breaks. Pre-treatment of cells with Hoechst 33342 resulted in a dose-modifying enhancement of radiation resistance not associated with altered dosimetry for strand-break induction. However, radioresistance was accompanied by the protracted retention of cells in the G/sub 2/ phase of the cell cycle. We suggest that the results provide direct evidence that the retention of cells in G/sub 2/ phase is a sparing phenomenon and is triggered by the responses of chromatin domains to the presence of DNA damage.}
doi = {10.1080/09553008414551511}
journal = []
volume = {46:4}
journal type = {AC}
place = {United Kingdom}
year = {1984}
month = {Oct}
}