Human lymphocytes pretreated with low (0.01 Gy) but not high (0.5 Gy) doses of X-rays become somewhat refractory to the induction of chromatid deletions by subsequent exposure to high (1.5 Gy) doses of X-rays (i.e. the yield of chromatid deletions is less than the sum of the yields induced by the pre-exposure and the subsequent challenge doses). This adaptive response can also be induced by pretreating the cells with very low, or even high, concentrations of tritiated thymidine. Because high concentrations of tritiated thymidine result in high doses of radiation that are delivered at very low dose-rates (i.e. less than 0.01 Gy/min), the lack of adaptation following high pre-treatment doses of X-rays could be attributed to their higher dose-rates. To test the effect of X-ray intensity on the induction of the adaptive response, lymphocytes were irradiated with 0.5 Gy of X-rays at 0.005-0.5 Gy/min at 28-30 h of culture, and then irradiated with 1.5 Gy at 48 h. Chromatid deletions were measured 6 h later. The results show that 0.5 Gy of X-rays given at low dose-rates (0.005 or 0.01 Gy/min), but not at high dose-rates (0.1, 0.2, or 0.5 Gy/min), are capable of inducing the adaptive response. Furthermore, experiments in which a male subject's cells exposed to 0.5 Gy given at 0.005 Gy/min were cocultivated with a female subject's cells irradiated with 0.5 Gy at 0.5 Gy/min showed that cells exposed to radiation at low and high intensity progress to metaphase equally and, therefore, that the lack of an adaptive response at high dose-rates cannot be attributed to selection of radioresistant cells. Although the induction of the adaptive response at higher X-ray doses occurs at low radiation intensity, there seems to be a minimum dose required for this effect; e.g., 0.01-Gy pretreatments induced the adaptive response when given at 0.2 Gy/min, but not at 0.005 Gy/min. Thus, the adaptive response is dependent both on the total dose of the pretreatment and on the rate at which the dose is given.

In previous studies we have shown that low doses of radiation from incorporated tritiated thymidine can make human lymphocytes less susceptible to the genetic damage manifested as chromatid breakage induced by a subsequent high dose of X rays. We have also shown that this adaptive response to ionizing radiation can be induced by very low doses of X rays (0.01 Gy; i.e., 1 rad) delivered during S phase of the cell cycle. To see if a low dose of X rays could induce this response in cells at other phases of the cell cycle, human lymphocytes were irradiated with 0.01 or 0.05 Gy before stimulation by phytohemagglutinin (G0) or with 0.01 Gy at various times after stimulation (G1), followed by 1.5 Gy (150 rad) at G2 phase. Although G0 lymphocytes failed to exhibit an adaptive response, G1 cells irradiated as early as 4 h after stimulation did show the response. Experiments were also carried out to determine how long the adaptive response induced by 0.01 Gy could persist. A 0.01-Gy dose was delivered to lymphocytes in the first S phase, followed by 1.5 Gy in the same or subsequent cell cycles. Lymphocytes receiving a 1.5-Gy dose at 40, 48, or 66 h after stimulation exhibited an adaptive response, whereas those receiving a 1.5-Gy dose at 90 or 114 h did not. Duplicate cultures containing bromodeoxyuridine showed that at 40 h all the lymphocytes were in their first cell cycle after stimulation, at 48 h half of the lymphocytes were in their first cell cycle and half in their second, and at 66 h 80% of the lymphocytes were in their third cell cycle. Thus the adaptive response persists for at least three cell cycles after it is induced by 0.01 Gy of X rays. In other experiments, the time necessary for maximal expression of the adaptive response was determined by delivering 0.01 Gy at hourly intervals 1-6 h before the 1.5-Gy dose. While a 4-h interval was enough for expression of the adaptive response, shorter intervals were not.

Cultured human lymphocytes exposed to very low doses of X-rays become less susceptible to subsequent higher doses of X-rays. Cells exposed to doses as low as 0.5 rad (cGy) or 1 rad of X-rays at 32-34 h of culture become adapted so that less cytogenetic damage in the form of chromosome breakage is induced by 150 rad administered at 48 h. This response, which does not occur after high initial doses of X-rays, can be eliminated by 3-aminobenzamide, an inhibitor of poly(ADP-ribose) polymerase.

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The r-X1 deficiency in maize produces high frequencies of aneuploid progeny by inducing nondisjunction during embryo sac development. The purpose of this investigation was to determine the embryo sac division at which the nondisjunctive event takes place. Monosomic-6 individuals were generated by crossing r-X1 containing plants by those carrying the y-pastel-8549 allele of the Y locus on chromosome 6. A strict dosage relationship exists between the number of dominant alleles of the Y locus and the level of β-carotene in the endosperm. We found that the level of β-carotene in the endosperm of kernels containing monosomic-6 embryos was comparable with that found in endosperms with one Y allele. This indicated that they contained only one maternally contributed chromosome 6. Only nondisjunction at the second postmeiotic division could have produced such an endosperm; thus, the nondisjunctive event occurs at this division. Another endosperm type expected from nondisjunction at this same division, with three dominant Y alleles, was not found. The absence of this endosperm type suggests that the egg nucleus and the polar nucleus originating at the micropylar pole are sister nuclei that arose from the same cell at the third embryo sac mitotic division. Key words: aneuploidy, embryo sac, nondisjunction, r-X1 deficiency, Zea.