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Mutagenesis vol. 1 no. 5 pp. 375-380, 1986
© 1986 UK Environmental Mutagen Society/Oxford University Press

other

Evidence that the [3H]thymidine-induced adaptive response of human lymphocytes to subsequent doses of X-rays involves the induction of a chromosomal repair mechanism

John K. Wiencke, Veena Afzal, Gregorio Olivieri and Sheldon Wolff1

Laboratory of Radiobiology and Environmental Health, University of California San Francisco, CA 94143, USA

When human lymphocytes are treated with [3H]thymidine ([3H]dThd), the observed number of chromosomal aberrations induced by [3H]dThd and subsequent doses of X-rays is less than the number induced by X-rays alone. Experiments in which cells were examined at various times after exposure to the X-rays showed that this phenomenon, termed an adaptive response to the endogenous radiation from tritium, is not an artefact caused by radiation-induced mitotic delays, which could result in the sampling of metaphase cells that were irradiated in different parts of the G2 phase of the cell cycle, where sensitivity to X-rays changes dramatically. Reconstruction experiments in which labelled female cells were co-cultured with unlabelled male cells now show that labelled and unlabelled cells progress to metaphase equally, and therefore that the adaptive response is not the result of selection against a radiosensitive population of cells that have incorporated [3H]dThd. Measurements of chromosomal aberrations induced in the labelled female cells and unlabelled male cells that had been co-cultured show that the adaptive response is restricted to those cells exposed to radiation from the incorporation of [3H]dThd and that diffusible factors are not involved. The results are consistent with the proposal that this adaptive response is the result of the induction of a hitherto unknown chromosomal repair mechanism. It has now been found that this repair mechanism is induced at levels of radiation from [3H]dThd that in themselves are too low to induce any discernible chromosomal aberrations and that its activity is dependent on the enzyme poly(ADP-ribose) polymerase, because 3-aminobenzamide, an inhibitor of poly(ADP-ribosyl)ation, prevents the adaptive response.

1To whom correspondence should be addressed


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