The action of chronic irradiation (dose rate 2.9 Gy/day) on human lymphocyte culture was investigated. Whole blood was irradiated at 37 degrees C. Aliquots (0.2 ml) of whole blood were cultivated by the standard method. A medium containing phytohemagglutinin was added immediately after irradiation. All structural chromosome- and chromatid-type changes were recorded. The experimental data showed that the conditions of irradiation of lymphocytes affected neither the background level of chromosome damage nor their radiosensitivity. The obtained dose-response curve of chromosome aberrations was described by a linear regression, which then became a plateau. There is no statistically significant difference between the results for the low doses (10-50 cGy) of chronic and acute radiation.

The combined influence of various doses of chronic irradiation (0.029 Gy/day) followed by acute irradiation at doses of 4 and 6 Gy (0.47 Gy/min) on the frequency of chromosomal aberrations in rat bone-marrow cells was studied. A pronounced adaptive response was observed at all doses of chronic irradiation followed by acute irradiation.

Supersensitivity of Chinese hamster cells to low doses of gamma-radiation (dose range 5 to 50 cGy) was revealed by means of the cytokinesis-block micronucleus test. Treating these cells with caffeine (repair inhibitor) and mercaptoethylamine (radioprotector) and exposing them to secondary radiation emitted by protons with an energy of 70 GeV showed that this supersensitivity is associated with the absence of cytogenetic repair. When cells at the G(2) phase received preliminary doses of 30 and 75 cGy before being irradiated at 150 cGy, the incidence of cytogenetic damage decreased, i.e., an adaptive cell response resulting from a radiation-induced mitotic delay was observed.

A model of formation of radiation-induced cytogenetic damage is proposed on the basis of our own and literature data. The model postulates that localization of DNA damage and repair process play an important role in the final effect.

Phenylmethylsulfonyl fluoride, a chromatin proteinase inhibitor, caused a nearly twofold diminution of the cytogenetic injury and a twofold increase in the rate of DNA repair in gamma-irradiated (3-15 Gy) Chinese hamster fibroblasts. The effect of the inhibitor was mainly exhibited by a rapidly repaired (for 15-20 min) component of the cytogenetic damage. A simultaneous treatment with phenylmethylsulfonyl fluoride and nicotinamide did not influence the effect of the proteinase inhibitor under study. The results obtained are indicative of poly (ADP-ribosylation)-independent contribution of chromatin proteinases to radiation-induced chromosome mutagenesis.

: Nicotinamide (NA) was shown to increase the yield of chromosome aberrations in irradiated Chinese hamster cells. The effect was observed with all doses used (1-4 Gy) and in all phases of the cell cycle; it was maximum as cells transferred from S to G1 phase. The modification of radiation-induced aberrations was more pronounced in the chromatid deletions and in exchanges. The combined action of NA and caffeine showed a synergism. It is assumed that NA inhibits reparation in a different way than caffeine does.

The cell culture of a Chinese hamster was irradiated on a Serpuchov proton synchrotron at a dose of 0.5-4 Gy and a dose rate of 1 Gy/min and by gamma-irradiation at dose 1-5 Gy and dose rate 1.2-1.4 Gy/min. The effect of radiation on the cell culture was judged from chromosomal aberrations in G2-stage of cell cycle and micronuclear test. The relative biological efficience of the secondary radiation was approximately 3. Modifying effect of caffeine on the cells irradiated by secondary radiation of synchrotron was not observed. In the presence of caffeine the effect of gamma-irradiation practically is increased up to the level observed upon secondary irradiation. This suggests that secondary radiation inhibits the repair of the cytogenetic damage.