The effect of X-ray irradiation on cell survival, induction, and repair of DNA damage was studied by using 10 Chroococcidiopsis strains isolated from desert and hypersaline environments. After exposure to 2.5 kGy, the percentages of survival for the strains ranged from 80 to 35%. In the four most resistant strains, the levels of survival were reduced by 1 or 2 orders of magnitude after irradiation with 5 kGy; viable cells were recovered after exposure to 15 kGy but not after exposure to 20 kGy. The severe DNA damage evident after exposure to 2.5 kGy was repaired within 3 h, and the severe DNA damage evident after exposure to 5 kGy was repaired within 24 h. The increase in trichloroacetic acid-precipitable radioactivity in the culture supernatant after irradiation with 2.5 kGy might have been due to cell lysis and/or an excision process involved in DNA repair. The radiation resistance of Chroococcidiopsis strains may reflect the ability of these cyanobacteria to survive prolonged desiccation through efficient repair of the DNA damage that accumulates during dehydration.Members of the genus Chroococcidiopsis are characterized by a pronounced ability to withstand the lethal effects of desiccation (7). In nature these cyanobacteria dominate the most extreme arid habitats in hot and cold deserts, where they survive in a desiccated (or frozen) state most of the time (15).The cytology and ultrastructure of field-and laboratorydesiccated Chroococcidiopsis cells were investigated, and the development of thick multilayered envelopes, rich in polysaccharides, was found to be correlated with desiccation tolerance (8, 9). The molecular mechanisms that contribute to the dehydration resistance of Chroococcidiopsis cells are poorly understood, as are similar mechanisms in most prokaryotes (3,16,17), but it is widely accepted that the ability to survive desiccation is correlated with the ability to develop spores and/or the ability to produce extracellular polysaccharides (3,17).Because dehydration affects the membranous and proteinaceous components of a cell, as well as its nucleic acids, the ability to survive prolonged desiccation involves a complex array of factors at every level of cell structure and function (3,16,17). For example, it appears that at the onset of rehydration, the capacity to repair DNA damage that accumulates during desiccation is critical for desiccation tolerance (5). Desiccation tolerance and radiation resistance in Deinococcus radiodurans have a common basis, as DNA repair-deficient mutants lack both properties (11). On the other hand, in Escherichia coli, dehydration-induced mortality is not correlated with induction of DNA breaks, suggesting that differences between radiation-resistant and radiation-susceptible microorganisms extend beyond the ability of the organisms to repair DNA damage (11).In order to elucidate the mechanisms of desiccation tolerance in Chroococcidiopsis cells, nine strains isolated from different extreme arid environments and one strain isolated from a hypersaline environment we...

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In this review I begin with a brief history of Auger processes, and then present a more detailed review of recent literature reports on physical, molecular, and cellular aspects of Auger emitters, and potential therapeutic applications.

Chinese hamster ovary cells were pulse-labels with 125I-iodo-deoxyuridine during early S phase, and cell samples were harvested 30 min or 5 h after labeling. The samples were frozen (with or without 25 mM cysteamine) and stored at-196˚C for accumulation of 125I decays. X-ray control experiments were performed at 37˚C and-196˚C. Aliquots of cells were plated for evaluating micronucleus formation and cell survival. The results demonstrated a striking shift in micronucleus formation an sell death with time after labeling. Cells frozen 30 min after labeling exhibited effects typical of low-Let radiation, but cells frozen 5 h after labeling showed a response characteristic of high-LET radiation. Cysteamine provided protection against the effects of 125I during the initial phase of effects characteristic of low-LET radiation, but no protection was seen during the phase characteristic of high-LET radiation. When cell survival was evaluated as a function of micronucleus frequency rather than dose in decays/cell, the survival curves for all treatment groups became superimposed. Previous work using the same experimental system had failed to show a direct link between 125I-induced DNA double-strand breaks and cell death. These findings are consistent with the hypothesis that DNA damage may not be the sole mechanism for cell killing and that damage to higher-order structures in the cell nucleus may contribute to (or modify) radiation-induced cell death.