Radiation Induced Cancer from Low Doses of Ionizing Radiation : Risk Analysis Using the Cell Dose Concept

High doses of ionizing radiations are known to bear the risk of cancer to the exposed individual. In order to appreciate potential carcinogenesis from low doses also, the action of ionizing radiation in the human body has to be considered in holistic approach: energy depositions to individual cells trigger effects within a hierarchical structure of interacting levels of biological systems, consisting consecutively of atoms, molecules, cells and organ tissue. The present paper describes the cell dose concept which is an essential factor in assessing the risk due to the ionizing radiation to the cells and tissues. Low dose of ionizing radiation induces adaptive response in individual cells which could be linked to the action of molecular radicals. Enzyme activities in bone marrow cells and bilayer lipid membranes and radicals are directly related to radiation effects. Temporary improvements of the detoxification of molecular radicals also improve the cellular defence. The risk analysis calls for more attention as it is important for radiation protection and other beneficial effects due to low doses of irradiation

Alpha-emitters for medical therapy workshop

A workshop on ``Alpha-Emitters for Medical Therapy`` was held May 30-31, 1996 in Denver Colorado to identify research goals and potential clinical needs for applying alpha-particle emitters and to provide DOE with sufficient information for future planning. The workshop was attended by 36 participants representing radiooncology, nuclear medicine, immunotherapy, radiobiology, molecular biology, biochemistry, radiopharmaceutical chemistry, dosimetry, and physics. This report provides a summary of the key points and recommendations arrived at during the conference

A different approach to evaluating health effects from radiation exposure

Absorbed dose D is shown to be a composite variable, the product of the fraction of cells hit (I/sub H/) and the mean /open quotes/dose/close quotes/ (hit size) /ovr z/ to those cells. D is suitable for use with high level (HLE) to radiation and its resulting acute organ effects because, since I/sub H/ = 1.0, D approximates closely enough the mean energy density in the cell as well as in the organ. However, with low-level exposure (LLE) to radiation and its consequent probability of cancer induction from a single cell, stochastic delivery of energy to cells results in a wide distribution of hit sizes z, and the expected mean value, /ovr z/, is constant with exposure. Thus, with LLE, only I/sub H/ varies with D so that the apparent proportionality between /open quotes/dose/close quotes/ and the fraction of cells transformed is misleading. This proportionality therefore does not mean that any (cell) dose, no matter how small, can be lethal. Rather, it means that, in the exposure of a population of individual organisms consisting of the constituent relevant cells, there is a small probabililty of particle-cell interactions which transfer energy. The probability of a cell transforming and initiating a cancer can only be greater than zero if the hit size (/open quotes/dose of energy/close quotes/) to the cell is large enough. Otherwise stated, if the /open quotes/dose/close quotes/ is defined at the proper level of biological organization, namely, the cell and not the organ, only a large dose z to that cell is effective. The above precepts are utilized to develop a drastically different approach to evaluation oif risk from LLE, that holds promise of obviating any requirement for the components of the present system: absorbed organ dose, LET, a standard radiation, REB(Q), dose equivalent and rem. 12 refs., 11 figs

A Stochastic Markov Model of Cellular Response to Radiation

A stochastic model based on the Markov Chain Monte Carlo process is used to describe responses to ionizing radiation in a group of cells. The results show that where multiple relationships linearly depending on the dose are introduced, the overall reaction shows a threshold, and, generally, a non-linear response. Such phenomena have been observed and reported in a number of papers. The present model permits the inclusion of adaptive responses and bystander effects that can lead to hormetic effects. In addition, the model allows for incorporating various time-dependent phenomena. Essentially, all known biological effects can be reproduced using the proposed model

Non-invasive investigations of the growth kinetics of a solid experimental tumor (sarcoma-180).

The investigations reported were performed to test the applicability of non-invasive methods for the measurement of the parameters determining the growth of a solid experimental tumor and to measure these data for the tumor system sarcoma-180/NMRI-mice. It could be shown that non-invasive methods can be used for the measurement of tumor growth, especially the fraction of proliferating cells (growth fraction) which is of special importance for tumor therapy. For the tumor system under investigation, the growth is completely determined by an exponential decrease of the growth fraction