Search

Purpose: To analyse the cell inactivation frequencies induced by low energy protons in human cells with different sensitivity to photon radiation. Materials and methods: Four human cell lines with various sensitivities to photon irradiation were used: the SCC25 and SQ20B derived from human epithelium tumours of the tongue and larynx, respectively, and the normal lines M/10, derived from human mammary epithelium, and HF19 derived from a lung fibroblast. The cells were irradiated with γ-rays and proton beams with linear energy transfer (LET) from 7 to 33keV/μm. Clonogenic survival was assessed. Results: Survival curves are reported for each cell line following irradiation with γ-rays and with various proton LETs. The surviving fraction after 2 Gy of γ-rays was 0.72 for SQ20B cells, and 0.28–0.35 for the other cell lines. The maximum LET proton effectiveness was generally greater than that of γ-rays. In particular there was a marked increase in beam effectiveness with increasing LET for the most resistant cells (SQ20B) whose 2 Gy-survival varied from 0.72 with γ-radiation down to 0.37 with 30keV/μm protons. The relative biological effectiveness (RBE(2Gy γ)) with the 30 keV/μm beam, evaluated as the ratio of 2Gy to the proton dose producing the same inactivation level as that given by 2 Gy of γ-rays, was 3.2, 1.8, 1.3 and 0.8 for SQ20B, M/10, SCC25, and HF19, respectively. Conclusions: RBE for inactivation with high-LET protons increased with the cellular radioresistance to γ-rays. The cell line with the greatest resistance to γ-rays was the most responsive to the highest LET proton beam. A similar trend has also been found in studies reported in the literature with He, C, N ions with LET in the range 20–125keV/μm on human tumour cell lines. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the mechanisms underlying the induction of chromosome aberrations by ionizing radiation, focusing attention on DNA damage severity, interphase chromosome geometry and the distribution of DNA strand breaks. Methods: An ab initio biophysical model of aberration induction in human lymphocytes specific for light ions was developed, based on the assumption that 'complex lesions' (clustered DNA breaks) produce aberrations, whereas less severe breaks are repaired. It was assumed that interphase chromosomes are spatially localized and that chromosome break free-ends rejoin pairwise randomly; the unrejoining of a certain fraction of freeends was assumed to be possible, and small fragments were neglected in order to reproduce experimental conditions. The yield of di erent aberrations was calculated and compared with some data obtained using Giemsa or FISH techniques. Results: Dose-response curves for dicentrics and centric rings (Giemsa) and for reciprocal, complex and incomplete exchanges (FISH) were simulated; the ratio between complex and reciprocal exchanges was also calculated as a function of particle type and LET. The results showed agreement with data from lymphocyte irradiation with light ions. Conclusions: The results suggest that clustered DNA breaks are a critical damage type for aberration induction and that interphase chromosome localization plays an important role. Moreover, the e ect of a given particle type is related both to the number of induced complex lesions and to their spatial distribution. [ABSTRACT FROM AUTHOR]

Purpose : To measure clonogenic death of Chinese hamster V79 cells following exposure to a defined number of 4.3 MeV alpha particles (track-averaged LET 105 keV/ mu m). Materials and methods : Cells were irradiated at the radiobiological facility installed at the TTT-3 Tandem accelerator in Naples by using a 'Biostack' approach, which allows the positions of incident tracks relative to cells to be carefully determined. Subcellular structure was identified by fluorescence microscopy, while tracks were visualized by LR-115 solid state nuclear track detectors. Results : Particle hits in the cytoplasm did not significantly affect cell survival, yet survival probability decreased exponentially as a function of the number of nuclear traversals. Measured probability of surviving to exactly one 4.3 MeV alpha -particle traversal in the cell nucleus was 0.67 0.10. Inactivation cross-section was substantially higher than expected from conventional survival curves. However, folding of the data with Poisson statistics showed that survival level expected if a mean of one alpha -particle goes through a nucleus is higher than the measured value after exactly one particle traversal. Conclusions : V79 cells have about 67% probability to survive a single alpha -particle traversal in the cell nucleus. Single-particle survival curves are consistent with conventional dose-survival relationships, once Poisson distribution of traversals is taken into account. [ABSTRACT FROM AUTHOR]