Abstract

In all tests carried out showed a significant resistance of all tumorcells to radiation. Especially in the glioblastoma stem cell cultures, the radiation-induced apoptosis rate was very low. This supports the hypothesis that tumor stem cells are responsible for a new tumor regeneration after successful primary therapy (radiotherapy) in glioblastoma. Furthermore, the formation of multinucleated cells was observed in all cell lines by irradiation. Again, there was a significant difference between glioblastoma multiforme standard cells and stem cells showed. In stem cell cultures, a significantly higher rate polynuclear cells was observed than in the standard cell cultures. These were also in the stem cell cultures over the entire experimental period detectable, where in contrast to the standard cell cultures decreasing with increasing time number was seen to multinuclear cells. Consequently, this indicates a correlation between the formation of multinucleated cells and significantly increased the resistance of stem cells compared to standard cells. It appears that the tumor stem cells through the formation of multinucleated cells have the ability to replace or repair the damaged material, and thus to avoid the cell death. Another part of this work was dedicated with regard to their resistance behavior as a function of oxidative stress the study of glioblastoma standard cell cultures. Natriumselenit as prooxidant led in all three examined standard cell lines to a more rapid induction of apoptosis . The maximum number of apoptotic cells was reached earlier compared to radiotherapy alone by Natriumselenit . The maximum rate of apoptosis induced by 40 µM sodium, was consistent with the induced by irradiation with 7.5 Gy. N-acetylcystein affected, as also known from the literature, the cell lines U251 and U87 antioxidant that is, the apoptosis rate decreased after irradiation with 7.5 Gy. In contrast, the treatment of glioblastoma standard celllinien G112 with N-acetylcystein led to an increase in the apoptosis rate and clarified by a relevant influence of the particular genetic profile of the individual tumor of the connection between oxidative stress and apoptosis in glioblastoma cells.

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