No abstract

Chemical and biological damage, caused by directly or indirectly ionizing radiations, is attributable to the action of the charged particle tracks in the absorbing medium. Attempts to elucidate the biophysical mechanisms involved, and to quantify the damage, are typically made in terms of one or more of the main physical parameters descriptive of the charged particle tracks. To meet a need for a ready reference source of such information, tables of the relevant parameters have been calculated for a liquid water medium. The full tables are obtainable elsewhere. Here, a description is given of the quantities calculated and an extended example is given of their application in elucidating the physical mechanisms of radiationinduced biological damage. A representative selection of data is displayed graphically to illustrate the extent of the information obtained and its value in, e.g., application to fundamental radiation dosimetry. Track structure data is tabulated for instantaneous energies of individual particles and for the fluence and dose-weighted spectra at charged particle equilibrium. Data are listed for incident electrons (50 eV to 30 MeV); characteristic K, X-rays from carbon to uranium; commonly used radioisotope sources of 241Am, I3'Cs, and 6oCo and for continuous X-ray spectra (5300 kV); Auger electron and beta-emitter radionuclides; heavy charged particles having specific energies of 0.5 keV/p to I GeV/p for 74 ion types ranging from protons to uranium ions, and for monoenergetic neutrons (0.5 keV to 100 MeV). Quantities listed are kerma factors; fluence of charged particles per unit source concentration; buildup factors; track and dose-average LET and restricted LET; W values; 2/@; pz; delta-ray yields, energies, and ranges; ion ranges; and the mean free path for primary ionization and the linear primary ionization. For indirectly ionizing radiations, the microdose quantities, frequency, and dose means of lineal energy are tabulated along with typical energy deposition distribution spectra for neutrons and gamma rays in micron and nanometer volumes.

Damaging effects to mammalian cells by heavy charged particles have been realized in terms of the mean free path for linear primary ionization (the spacing of ionizing events along the charged particle tracks) using in vitro radiobiological experimentation data. Damage is found to be optimum when the mean free path for linear primary ionization along the tracks in the cell nucleus matches the mean chord length of approximately 1.8 nm through a DNA segment. A simple semi-theoretical model is proposed to define absolute biological effectiveness based on effect inactivation cross section mwhich is interrelated to the mean free path for linear primary ionization . For heavy charged particles, the model shows a saturation region for the effect cross section, s m for ≤ nm. The model explains the mechanisms leading to cell death via DNA strand scissions. In the saturation region, double strand breaks of the DNA are predominant, unrepaired or mismatched repair processes lead to maximum damage. At higher mean free path; > nm, single strand breaks of the DNA is the main basic mechanism and thus repairable processes are possible.

The induction of oncogenic transformation to C3H10T1/2 cells by different types of ionizing radiation has been widely studied in various radiological laboratories. Based on the information available in literature, a database is structured to include radiological parameters, that manifest oncogenic effects as well as cellular inactivation of C3H10T1/2 cells, resulted from exposure to different types of heavy charged ions including neutrons. We find that oncogenic transformation effective cross-section is best correlated with mean free path for linear primary ionization. A simple radiobiological model is proposed merely to quantize cross-sections against mean free path. The model reveals saturations of; cellular inactivation cross-section of about 75 mm2, and oncogenic transformation cross-section of about 3.98 x 10-2 mm2, both started at mean free path of 1.8 nm (inflection points) and lower values. Since the interspacing distance between the DNA strands is about 1.8 nm, the model explains the crucial roles of DNA lesions (caused by heavy charged particles) to play as the starting point leading to cell death or oncogenic transformation. The effective cross -sections in the sloping regions are primarily due to repairable DNA single strand breaks while saturation regions are essentially due to unrepaired or incorrectly repaired DNA double strand breaks.