Within our research, DNA strand breaks may have come from exposure of protein linked drug stabilised cleavable processes to the robust alkaline conditions of the comet assay. This model is supported by results obtained with DC3F and DC3F/C 10, a resistant cell line. DC3F/C 10 was clearly less sensitive and painful to DNA damages induced by topoisomerase I inhibitors, whereas topoisomerase II inhibitors induced Capecitabine price equivalent level of DNA damage in both cell lines. This specificity of response is well accounted by its DNA cleavage activity was reduced by qualitative alterations of DNA topoisomerase I in DC3F/C 10, which. The stabilisation of cleavable complexes by topoisomerase inhibitors is stopped after drug treatment or elimination. The comet assay was able to spot this reversible event since 24 h after treatment a in DNA fragmentation was observed in most of the circumstances without loss in cell counts. These results confirm our previous observations with etoposide in vitro in unstimulated human lymphocytes and in CHO cells, and in vivo after intraperitoneal injection to mice. Ellipticine and its structurally connected analogues 5,11 dimethyl Endosymbiotic theory 6H pyrido carbazoles led to similar results in the L1210 murine leukaemia cell line. After treatment by topoisomerase I inhibitors appears an exception persistence of DNA damage in CHO cells 24 h. Stabilisation of cleavable complexes by topoisomerase inhibitors can cause an of cell division and to cell killing. In as demonstrated by fragmentation and nuclear condensation revealed by DAPI staining and by the appearance of HDCs and SFs in the comet assay, our study, apoptosis seemed 48 h after treatment by the highest doses of topoisomerase inhibitors. The comet assay has the capacity to discriminate between early DNA damage and DNA fragmentation linked to apoptosis in dividing cells, as explained in a radiation induced apoptosis style of TK6 human B lymphoblast cells. The percentages of HDCs and SFs detected at 48 h were often more advanced than the percentage of apoptotic cells detected by DAPI. This confirms our previous assertion that the comet Carfilzomib solubility assay was more sensitive in detecting apoptotic cells as HDCs than old-fashioned practices. SFs reflect a higher degree of DNA fragmentation and their presence was generally speaking associated with that of cells with a brighter and irregular nuclear DAPI staining. Inside our study, DCs induced just after treatment by the cheapest amount of drug entirely disappeared after 24 h. Their presence was not linked with a cell death, even though a heightened frequency of chromosomal aberrations can not be ruled out. In comparison, the formation of HDCs just after treatment with the greatest dose, followed by their partial disappearance 24 h later, was associated with an essential cell death related DNA fragmentation after 48 h.