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The authors, after a short review of the literature, report four cases of acute accidental irradiation from Co60 exposure, however of slight degree. A cytogenetic study showed chromosome changes of unstable type only, which were also found in the case with 1,5 rem absorption.
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The review presents possible causes of endemic goiter since only iodine deficiency fails to explain such a great spread of this disease. Etiological factors of endemic goiter, such as the imbalance of trace elements, the use of contaminated drinking water, the toxic action of chemicals, exposure to ionizing radiation, genetic factors, are discussed. Prevalence rates of endemic goiter in Russia and other countries of the world are presented. The causes of a significant increase in the incidence of this disease are discussed.
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We have shown that natural drosophila populations from the settlement Vetka of Gomel region with increased radiation background are more adapted to mutagenic effect of radiation than drosophila populations from Berezinsky reserve (the control). After the populations were placed into laboratory thermostat adaptation of Vetka population remained within 6-8 generations without irradiation. However the control population became more resistant too. So, the keeping of natural drosophila populations under laboratory conditions was a stress and led to unspecific adaptation the same as a low level of radiocontamination did. These facts should be considered in studying dynamics of the mutation level during radionuclide removal in animals caught in radiocontaminated regions and placed in vivaria conditions.
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Radiosensitization by misonidazole of biologically active phi X174 DNA, mediated by cytochrome c, is most probably at least partly due to formation of an adduct between sensitizer and DNA, which can be removed from the DNA by a mild alkaline treatment thereby restoring the activity of the DNA.
Microtubule organizing centers (MTOC) in control, irradiated and heated C3H 10T1/2 mouse embryo cells and two radiation-transformed sublines, R1 and R25, were made visible by indirect immunofluorescence using antibody against tubulin. The MTOC were reformed by 5-min incubation in fresh medium after the microtubules were depolymerized with nocodazole. The R1 line had a different distribution of MTOC/cell than the parent 10T1/2 line or R25, which had similar distributions. After irradiation, multiple MTOC appeared in the normal and radiation-transformed cells irradiated to 10 Gy and incubated for 24 or 48 h. The multiple foci of microtubule reformation in the irradiated cells indicate that radiation damage is expressed in structural elements in the cytoplasm. After heat treatment of the three cell lines (43 degrees C for 93 min and 45 degrees C for 25 min), the MTOC were disrupted and many cells did not have visible organizing centers at 24 or 48 h, while others had a large number of small centers of microtubule reformation. The distribution of MTOC/cell seen in R25 cells after the treatment had similar patterns to those of the 10T1/2 line rather than to those of the other radiation-transformed line, R1. Thus, the radiation or heat response seen in the MTOC is not dependent upon cell transformation.
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The computer analysis of cell radioresistance (D0) in 79 organisms distributed by Sparrow among 8 radiotaxons, and in those randomly chosen among 183 organisms has demonstrated the existence of the hierarchic system of clusters as 2, 3 and 4 taxons that are completely consistent with the external and internal criteria of the classification quality. The results obtained indicate a general biological importance of radiotaxonomy that directly reflects the basic steps of structural rearrangements of the genome in the course of evolution.
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Chinese hamster V79 cells (subline MI2G) were exposed repeatedly to fractionated doses of germicidal 254 nm light (far-uv) at 6 J.m-2/fraction/day or sunlight-simulating 290-330 nm (mid-uv) at 150 J.m-2/fraction/day and sensitivities to cell killing action and mutation of far-uv and mid-uv were examined. As the number of exposure fractions increased, the cell cultures became resistant to cell killing induced by both far-uv and mid-uv. Increases in both Do and Dq were observed. Treatment with exposures of 6 J.m-2 far-uv is more efficient in yielding cell cultures that are resistant than exposures of 150 J.m-2 mid-uv. In contrast to the cells exposed to repeated far-uv, the cells exposed to repeated mid-uv were relatively more resistant to cell killing effects of mid-uv than far-uv, suggesting a possible role of photolesions other than pyrimidine dimers. When mutants resistant to 6-thioguanine were assayed during repeated exposure to far- or mid-uv light, the yield was initially linear with accumulating dose. At high total accumulated doses, the frequency decreased gradually (6 J.m-2 mid-uv) or reached a plateau (150 J.m-2 mid-uv). The sensitivity of N80 cells (exposed to 80 fractions of mid-uv) to mutation induction by uv light is higher than that of the original MI2G cells, whereas U81 cells (exposed to 81 fractions of far-uv) have a sensitivity similar to that of the original cells. Although an initial decrease in resistance to cell killing was observed, resistant cells retained their characteristics after 100 days in culture without further exposure. Cross-resistance to X rays was not shown. The data in this paper suggest that the capacity for repair of photolesions in DNA by repair processes was enhanced in cell cultures by repeated exposure to far-uv or mid-uv and that this altered the cells' ability to cope with lethal and mutagenic lesions. It remains to be seen if these changes in cell sensitivity were brought about by selective or inductive processes or a combination of both.
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Human tumor cells and cells from cancer-prone individuals, compared with those from normal individuals, show a significantly higher incidence of chromatid breaks and gaps seen in metaphase cells immediately after G2 X irradiation. Previous studies with DNA repair-deficient mutants and DNA repair inhibitors strongly indicate that the enhancement results from a G2 deficiency(ies) in DNA repair. We report here biochemical evidence for a DNA repair deficiency that correlates with the cytogenetic studies. In the alkaline elution technique, after a pulse label with radioactive thymidine in the presence of 3-acetylaminobenzamide (a G2-phase blocker) and X irradiation, DNA from tumor or cancer-prone cells elutes more rapidly during the postirradiation period than that from normal cells. These results indicate that the DNA of tumor and cancer-prone cells either repairs more slowly or acquires more breaks than that of normal cells; breaks can accumulate during incomplete or deficient repair processes. The kinetic difference between normal and tumor or cancer-prone cells in DNA strand-break repair reaches a maximum within 2 h, and this maximum corresponds to the kinetic difference in chromatid aberration incidence following X irradiation reported previously. These findings support the concept that cells showing enhanced G2 chromatid radiosensitivity are deficient in DNA repair. The findings could also lead to a biochemical assay for cancer susceptibility.
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