Stellenbosch University - Scopus Tygerberg Hospital Publications

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Browsing Stellenbosch University - Scopus Tygerberg Hospital Publications by Subject "3T3 Cells"

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    In vitro influence of sublethal hypoxia on differentiation of the 3T3-L1 preadipose cell line and its physiological implications
    (1997) Macfarlane C.M.
    Exposure of cultures of 3T3-L1 preadipose cells to nitrogen for 16 hours kills almost all of the cells, but after exposure to 5% oxygen for 16 hours most of the cells survive, and recover when culture is continued in 20% oxygen. The extent of recovery depends on the insulin concentration of the medium. Isotope incorporation and flow cytometry experiments show that exposure to 5% oxygen for 16 hours growth arrests the cells and leads to an elongation of the G1-phase of the cell cycle. When 3T3-L1 cells are growth arrested in the presence of 5% oxygen and allowed to recover in the presence of 5μg/ml insulin under 20% oxygen, they can be induced to differentiate by treatment with carbacyclin during the period of growth arrest. Activity of the marker enzyme glycerol-3-phosphate dehydrogenase increases from 46.5±17 mU/mg protein to 1506±271 mU/mg protein. The extent of differentiation is exponentially related to the concentration of carbacyclin in the medium.
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    Radiosensitization and DNA repair inhibition by pentoxifylline in NIH3T3 p53 transfectants
    (2002) Binder A.; Theron T.; Donninger H.; Parker M.; Bohm L.
    Purpose: To examine the role of p53 mutations in the modulation of DNA repair and radiotoxicity by pentoxifylline. Materials and methods: NIH3T3 murine cells transfected with mutant p53 constructs were examined for the influence of pentoxifylline on radiotoxicity to Co60 γ-irradiation by colony assay. DNA repair (0-100Gy) was measured by constant-field gel electrophoresis. Apoptosis was assessed by flow cytometry with the annexin-V-binding assay. Results: In the two p53 hot-spot mutant cell lines p53-S269R and p53- + 15, the SF10 radiotoxicity enhancement factors induced by the pentoxifylline were 8.0 and 9.7, respectively. In the p53 deletion mutant p53-ΔA cell line, the radiotoxicity enhancement factor was 2.6. No radiosensitization was obtained in the untransfected p53 wild-type cell line U-Wt and in the transfected p53 double-wild-type p53-Wt cell line. When pentoxifylline was added after irradiation at the time of maximum G2 block expression, no radiosensitization was observed in any of the five cell lines. Constant-field gel electrophoresis analyses after 20 h of repair showed that pentoxifylline suppresses DNA double-strand break repair in all p53 mutant cell lines, as indicated by repair inhibition factors of 2.0-2.3. No repair suppression was found in the p53 wild-type cell lines. Conclusions: p53 mutations are a general requirement for radiosensitization by pentoxifylline and the level of radiosensitization depends upon the location of the p53 mutation.