60. Radiobiological Effectiveness of Different HZE Beams on Cells
Yoshiya Furusawa, Mizuho Aoki, Hideki Matsumoto1, Akihisa Takahashi2, Tetsuya Kawata3, Kerry George3 and Marco Durante4 (1Fukui Med Univ, 2Nara Med Univ, 3Johnson Space Center, 4Univ Fedellico II.)
Keywords: HZE beam, LET, RBE, cell killing, chromosome aberration
A method to estimate cell killing induced by accelerated heavy ions as a function of ion species and LETs was considered from LET-RBE spectra for V79 cells. The cells were exposed to 3He-, 12C-, 20Ne-, 28Si-, 40Ar- and 56Fe-ion beams at HIMAC and the Medical Cyclotron at NIRS, RRC at RIKEN, and AGS at BNL with an LET ranging over approximately 10-4000 keV/m under aerobic conditions. Cell-survival curves were fitted by equations from the linear-quadratic model to obtain survival parameters, and the RBE values were analyzed as a function of LET. The RBE increased with LET, reaching a maximum at around 200 keV/m, then decreased with a further increase in LET. Clear splits of the LET-RBE spectrum were found among ion species. The LET-RBE spectra were fitted by a newly contrived equation that included three parameters. The parameters indicate the LET that gives the maximum RBE, a related value for the maximum RBE, and the width of the RBE peak. The parameters can also be defined as functions of atomic mass numbers of the accelerated ions. At a given LET, the RBE value for lighter ions was higher than that for heavier ions at lower LET. The position of the maximum RBE shifted to higher LET values for heavier ions, and the width of the peak of RBE increased with the atomic mass number of the irradiated ions.
High-LET radiation-induced aberrations in prematurely condensed G2 chromosomes of human fibroblasts were studied. To determine the number of initial chromatid breaks induced by low- or high-LET irradiations, and to compare the kinetics of chromatid break rejoining for radiations of different quality, exponentially growing human fibroblast cells AG1522 were irradiated with gamma-rays, and carbon-, silicon- and iron-ions. Chromosomes were prematurely condensed using calyculin A. Chromatid breaks and exchanges in G2 cells were scored. PCC were collected after several post-irradiation incubation times, ranging from 5 to 600 min. The kinetics of the chromatid break rejoining following low- or high-LET irradiation consisted of two exponential components representing a rapid and a slow time constant. Chromatid breaks decreased rapidly during the first 10min after exposure, then continued to decrease at a slower rate. The rejoining kinetics were similar for exposure to each type of radiation. Chromatid exchanges were also formed quickly. Compared to low-LET radiation, isochromatid breaks were produced more frequently and the proportion of unrejoined breaks was higher for high-LET radiation. Compared with gamma-rays, isochromatid breaks were observed more frequently in high-LET irradiated samples, suggesting that an increase in isochromatid breaks is a signature of high-LET radiation exposure.
The new method for chemical-induced premature chromosome condensation combined with fluorescence in situ hybridization (FISH) was used to analyze chromosomal damage in peripheral blood mononuclear lymphocytes of patients undergoing radiation treatment for esophageal cancer with high-energy X-rays or accelerated carbon ions at NIRS. The total number of aberrant cells correlated with radiation field size, but no correlation was found for acute toxicity. A high frequency of complex-type exchanges was also recorded. This aberration type presented a high individual variability, and correlated well with the acute morbidity. Cytogenetic analysis by interphase chromosome painting is proposed as a useful tool for monitoring normal tissue effects during radiotherapy.
1) Furusawa, Y., et al.: Radiat Res 154: 485-96, 2000.
2) Furusawa, Y.: In; Exploring Future Research Strate- gies in Space Radiation Sciences. Iryoukagakusha, pp.104-109, Tokyo. 2000.
3) Aoki, M. et al.: J. Radiat. Res. 41: 163-75, 2000.
4) Durante, M., et al.: Int. J. Radiat. Oncol. Biol. Phys. 47: 793-8, 2000.
5) Kawata, T., et al.: Int. J. Radiat. Biol. 76: 929-37, 2000.
6) Matsumoto, H., et al.: Int. J. Radiat. Biol. 76: 1649-57 2000.
7) Takahashi, A., et al.: Int. J. Radiat. Oncol. Biol. Phys. 47: 489-94, 2000.
8) Takahashi, A., et al.: Int. J. Radiat. Biol.76: 335-41, 2000.
9) Yamada, S., et al.: Cancer Lett. 150: 215-21, 2000.
10) George, K., et al.: Int. J. Radiat. Biol. 77: 175-83, 2001.
11) Kawata, T., et al.: Int. J. Radiat. Biol. 77: 165-74, 2001.
12) Shigematsu, N., et al.: Int. J. Mol. Med. 7: 509-513, 2001.
[Back to index]