| Autor: |
Foray, N., Priestley, A., Alsbeih, G., Badie, C., Capulas, E. P., Arlett, C. F., Malaise, E. P. |
| Předmět: |
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| Zdroj: |
International Journal of Radiation Biology; Sep97, Vol. 72 Issue 3, p271-283, 13p |
| Abstrakt: |
Abstract. We have studied the intrinsic radiosensitivity, repair of potentially lethal damage (PLD) and the repair rate of radiation-induced DNA double-strand breaks (DSB) in 11 nontransformed human fibroblast cell lines, four of which were homozygous for the A-T mutation and two that were heterozygous (A-TH). All the experiments were done on cells in plateau phase of growth (97-99% of cells in G0/G1). With a dose of 30 Gy delivered at 4 C, the A-T cell lines had faster repair rates of up to 6 h, after which the repair curve crossed that of the control so that the residual damage at 24 h was higher in the A-T cells. Irradiation at 37 C at low dose rate (1 cGy.min -1) produced even more marked differences between the A-T cells and controls: the residual DSB level was always higher in A-T cells than controls at doses of 5-40 Gy, due to defective repair of a small fraction of DSB in A-T cells. The two protocols showed DSB repair rates for the A-TH cell lines that were intermediate between those of the A-T and control cells. There was a quantitative relationship between the residual DSB after irradiation at 37 C and the intrinsic radiosensitivity, and with the extent of PLD repair. There were very few apoptotic cells in the non-transformed control and A-T cell lines, both before and after irradiation. In combination, these results support the contention that the defective repair of DSB is a mechanism of the hypersensitivity linked to the A-T mutation. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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