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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Radiation and environmental biophysics 24 (1985), S. 161-174 
    ISSN: 1432-2099
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Physics
    Notes: Summary It has been suggested that nascent DNA located at the DNA replication fork may exhibit enhanced sensitivity to radiation damage. To evaluate this hypothesis, Chinese hamster ovary cells (CHO) were labeled with125I-iododeoxyuridine (125IUdR) either in the presence or absence of aphidicolin. Aphidicolin (5 µg/ml) reduced cellular125IUdR incorporation to 3–5% of the control value. The residual125I incorporation appeared to be restricted to low molecular weight (sub-replicon sized) fragments of DNA which were more sensitive to micrococcal nuclease attack and less sensitive to high salt DNase I digestion than randomly labeled DNA. These findings suggest that DNA replicated in the presence of aphidicolin remains localized at the replication fork adjacent to the nuclear matrix. Based on these observations an attempt was made to compare the lethal consequences of125I decays at the replication fork to that of125I decays randomly distributed over the entire genome. Regardless of the distribution of decay events, all treatment groups exhibited identical dose-response curves (D0: 101125I decays/cell). Since differential irradiation of the replication complex did not result in enhanced cell lethality, it can be concluded that neither the nascent DNA nor the protein components (replicative enzymes, nuclear protein matrix) associated with the DNA replication site constitute key radiosensitive targets within the cellular genome.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1615-6102
    Keywords: Cancer ; Cell death ; Cytoskeleton ; Hyperthermia ; Membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Mammalian cells subjected to hyperthermia in the presence of glycerol exhibit greatly enhanced resistance to thermal death. The mechanisms responsible for this effect remain unknown, but it has been suggested that glycerol may act by stabilizing cell membranes or by preventing heat induced disruption of cytoskeletal networks. To test these hypotheses, BP-8 murine sarcoma cells were treated with various combinations of glycerol, procaine, colcemid, and cytochalasin B, followed by 1 hour in vitro heating at temperatures ranging from 37°C to 45.5°C. After heating, the tumor cells were inoculated intraperitoneally into mice and cell survival was evaluated in vivo with the125I-iododeoxyuridine prelabeling assay. Addition of 5% glycerol to the incubation medium caused a pronounced increase in the heat resistance of BP-8 cells. Exposure to colcemid (microtubule disrupting agent) or cytochalasin B (micro-filament disrupting agent) did not influence the thermal response of control cells, nor did it counteract the protective effects of glycerol. This suggests that the ability of heat to dissociate cytoskeletal networks may not be an important factor in cellular heat death. In contrast, treatment with the membrane modulator procaine induced significant thermal sensitization in control cells, and caused a complete reversal of the protective action of glycerol. These findings are consistent with the hypothesis that membranes play an important role in the genesis of cellular heat death.
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2011-08-24
    Description: 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.
    Keywords: Life Sciences (General)
    Type: Applied and environmental microbiology (ISSN 0099-2240); Volume 66; 4; 1489-92
    Format: text
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