A better understanding of the effects of energy deposited in cells by incorporated isotopes can be expected from an analysis of differential cell doses. With this thought in mind, the distributions of specific energies in tissue were calculated for 239Pu and 131I. A program written in Fortran IV makes use of a matrix of spherical cells and cell nuclei of 10 and 8 mum diameter, respectively. The cells are arranged in close-packed structure. The radioactivity is considered as being compiled to point sources of 1 dps activity. The sources are located in the common centers of cells and nuclei. The calculations yield discrete values of specific energy using the mass of the nuclei for mass of reference. The numbers of cell nuclei receiving given amounts of specific energy are functions of the specific activity of the isotopes in the tissue. The specific activity is varied by changing the number of sources per g of tissue. The program also allows to calculate the numbers of cell nuclei with zero energy deposition. From the 1 dps point sources an average specific energy of 831 rads/h results for plutonium for cell nuclei within the range of the 5.14 MeV alpha-particles. For iodine, the value is 35 mrads/h within the range of the beta-particles of 188 KeV mean energy. If the volumes irradiated by the sources begin to overlap these values begin to increase accordingly.
BNL Swiss Albino mice were exposed (five in tandem) in a 2.5-cm I.D. Lucite tube to a parallel beam of 2.2-BeV protons. The LD5o was 1.81+/-0.03 X 10(10) p/cm(2), or 641 rads. The corresponding LD50 for 250-kVp x-rays was 557 rads, yielding an RBE of 0.87. No difference in time pattern of death was observed between the x-irradiated and proton-irradiated animals. It is concluded that, with the exposure geometry used in these experiments, ionization by primary and high-energy secondary protons was the major dose constituent. A comparison is made with other experiments on the lethal effects of protons in which different geometries were employed. There is evidence that, with exposure in material of larger diameter in which there is a larger contribution to dose from lateral scatter, high-LET components of the beam may play a more dominant role. It was also observed in these experiments that the presence of Pseudomonas aeruginosa may result in a lower LD50 and "early death," following either x-irradiation or proton radiation. This may have accounted for some of the "early deaths" following proton irradiation reported earlier.
The effect of oxygen, expressed as the oxygen enhancement ratio (OER), on the number of single-strand breaks (SSB) and double-strand breaks (DSB) induced in DNA by the radioactive decay of tritium was measured in human T1 cells whose DNA had been labeled with tritium at carbon atom number 6 of thymidine. Decays were accumulated in vivo under aerobic conditions at 0-1 degrees C and at -196 degrees C and in a nitrogen atmosphere at 0-1 degrees C. The number of SSB and DSB produced was analyzed by sucrose gradient centrifugation. For each tritium decay there were 0.25 DSB in cells exposed to air at 0-1 degrees C and 0.07 in cells kept under nitrogen, indicating an OER of 3.6, a value expected for such low-LET radiation. However, for each tritium decay there were 1.25 SSB in cells exposed to air at 0-1 degrees C and 0.76 in cells kept under nitrogen indicating an OER of only 1.7. The corresponding values for 60Co gamma radiation, expressed as SSB per 100 eV absorbed energy, were 4.5 and 1.0, giving an OER of 4.5. The low OER value found for SSB induced by tritium decay can be explained if 31% of the total SSB produced in air result from transmutation by a mechanism which does not produce DSB and is unaffected by oxygen.
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