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• W2933467724 abstract "The aim of this study was to investigate the molecular mechanisms underlying thermal radiosensisation in dependence of cell cycle position. The experiments were performed with the human tumor cell line HeLa. Cells synchronised in G1 and S-phase were exposed to X-rays alone or in combination with prior heating at 44°C for 20 min. Cell kill was determined by means of colony forming assay, double-strand breaks using constant-field gel electrophoreses (CFGE) and apoptotic cell death was scored using the fraction of detached cells. For the experiments the cells were synchronised either in G1- or S-phase. The synchronisation in the G1-phase was achieved by confluent growth of cell cultures leading to an accumulation of up to 70% of cells in the G1-phase. The synchronisation in the S-phase was obtained in a stepwise procedure. Cells grown to confluence were restimulated and arrested at the G1/S border by the addition of Aphidicolin. Release from block resulted into a synchronous proliferation with an accumulation of up to 80% in the S-phase. After irradiation alone G1-phase-cells showed a slightly higher cellular radiosensitivity than S-phase-cells. Prior heating at 44°C for 20 minutes resulted into an increased radiosensitivity which was moderate for G1-cells (thermal enhancement factor, TER=1.2) but pronounced for S-phase-cells (TER=2.0). Detection of DNA-double-strand breaks in G1- and S-phase-cells using CFGE showed substantial differences. For the same dose the fraction of DNA migrating into the gel was clearly lower in S-phase-cells when compared to G1-phase-cells. This reduction was attributed to a hindrance of the DNA migration in S-phase cells due to the complex structure of DNA replication forks. Prior heating at 44°C was found to have no effect on the induction but substantially to alter the repair of DNA double-strand breaks. For both cell cycle phases kinetics of dsb repair was found to be described by biphasic kinetics. The kinetics of the fast phase was almost identical for the two phases, whereas the kinetics of the second, slow phase During the first fast phase showed no difference, the second slow phase demonstrated that S-phase-cells were smaller in repair than G1-.phase-cells.The double-strand break was only slightly obstructed by a heating up with 44°C in to the G1.phase-cells, while for S-phase-cells a clear impairment was observed. For the number of slowly repairing double-strand breaks, as it was measured 360 minutes after irradiation, an increase resulted around the factor TER=1,7 for G1-phase-cells, on the other hand for S-phase-cells by TER= 3,4. This clear increase the S-phase-cells was attributed to the fact that additionaly double-strand breaks developed after a combined treatment. Altogether the results showed that the dependence of the thermo-ray-sensitivity on the cell-cycle and above all the pronounced sensitivity of the S-phase-cells with the effect of warmth on the DNA-double-strand breaks repair and in particular the clear increase in the number of the slowly repairing double-strand breaks are to be explained there." @default.
• W2933467724 created "2019-04-11" @default.
• W2933467724 creator A5035806513 @default.
• W2933467724 date "2003-01-01" @default.
• W2933467724 modified "2023-09-26" @default.
• W2933467724 title "Der Einfluss von Wärme auf die Strahlenempfindlichkeit und die Reparatur strahleninduzierter Doppelstrangbrüche in HeLa-Zellen in Abhängigkeit vom Zellzyklus" @default.
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