[en] It has been generally accepted in the context of radiation protection that ionizing radiation has some adverse effect even at low doses. However, epidemiological studies of human populations cannot definitively show its existence or absence. Furthermore, recent studies of populations living in areas of different background radiation levels reported some decrease in adverse health effects at high background levels. Genetic studies of atomic bomb survivors failed to produce statistically significant findings on the mutagenic effects of ionizing radiation. A British study however, suggests that a father's exposure to low dose radiation on the job may increase his children's risk of leukemia. On the other hand, many experimental studies have raised the possibility that low doses of ionizing radiation may not be harmful or may even produce stimulating or adaptive responses. The term 'hormesis' has come to be used to describe these phenomena produced by low doses of ionizing radiation when they were beneficial for the organisms studied. At the end of the International Conference on Low Dose Irradiation one conclusion appeared to be justified: radiation produces an adaptive response, though it is not universally detected yet. The conference failed to obtain any consensus on risk assessment at low doses, but raised many problems to be dealt with by future studies. The editors therefore believe that the Proceedings will be useful for all scientists and people concerned with radiation protection and the biological effects of low-dose irradiation

[en] Cell culture techniques are widely used to evaluate radiation response in rapidly proliferating cells. Quantitative cell-survival curve analysis has been developed toward this end to study clonogen survival in selected transformed 'immortal' cell lines typically derived from mammalian malignant tissue. For example, the radiation-response of glioma-derived cell clones has been studied extensively. However, the metabolic properties of transformed cerebral cells growing in vitro cannot be extrapolated readily to normal cerebral cells. Transformed cells generally lack the distinguishing metabolic characteristics of normal differentiated cells and they typically manifest a markedly different response to irradiation. Moreover, mammalian brain tissue is highly structured with a complex cellular hierarchy, and it exhibits only limited proliferative potential. Therefore, a satisfactory in vitro model for evaluation of brain irradiation cannot rely solely on standard cell culture techniques. This report examines the early reaction of the oligodendrocyte population and the myelination process to radiation injury in mammalian brain in vitro. (author). 9 refs., 1 fig

[en] Ionizing radiation has been shown to induce specific-locus mutations resulting from two general types of genetic damage. Single gene mutations are attributed to intragenic alterations ranging from point mutations to intra-locus deletions. Multigene mutations result from extragenic alterations including chromosomal or multilocus deletions and chromosomal rearrangements such as non-disjunction and crossing-over. Although the involvement of these two general types of genetic alteration in radiation-induced mutations has been illustrated in mammalian cells including human cells, the precise mechanisms determining the proportion of the two types still remain to be fully characterized. (author). 11 refs., 1 fig., 1 tab

[en] It has been generally accepted that OH radicals produced by radiolysis of water in cells react with DNA and proteins, and thus OH radicals are the radical species primarily responsible for biological effects, while the other reactive species, such as H atoms, electrons and holes, are not significantly involved. These studies however, have been performed mainly by adding radical scavengers to cells, and such methods do not observe directly the free radicals produced by γ-irradiation. In order to examine the generally accepted mechanism that OH radicals are responsible for biological effects on irradiation cells, the trapping and reactivity of OH radicals in the frozen cells have been studied here by ESR. (author). 5 refs., 4 figs

[en] It is found that various pretreatments to induce hepatic metallo-thionein (MT) synthesis promoted radioresistance against lethal damage due to whole body high-dose irradiation in mice. Those pretreatments could activate host defense mechanism observed as significant increases in survival rates, percentages of peripheral PMNs and in the numbers of spleen colony formation (ESCF). (author). 7 refs., 1 fig., 3 tabs

[en] For many years, development of new concepts and elaborate experimental approaches to elucidate biological effects of low dose radiations, and their possible implications in risk-estimations for radiation workers and individuals of the general public in relation to their life-style were not even felt necessary. Recent reports of beneficial effects (hormesis) of low doses, however, suggest that molecular events induced by very low and high doses need not be the same. The need of the hour, therefore, is to make an appraisal of the currently known molecular events induced by low and high doses and assess their applicability to the rationale behind L and LQ models. (author). 32 refs

[en] In 1980 the hypothesis was put forward that activation of sensitivity of membrane receptors is the key mechanism of growth stimulation and biota development under influence of low-dose radiation. It was assumed that in the organism exposed to low-dose radiation, numerous membrane receptors become more sensitive to their natural effectors which arise during development according to a genetic program not affected by these low doses. This article studies the influence of serum growth factors on the growth rate of Raji cells in a presence and absence of low-level gamma-radiation. (author). 7 refs., 1 fig

[en] It is shown that prenatal exposure of rodents to chemical carcinogens may result in an increased risk of tumor development in subsequent generations. Thus, treatment of pregnant mice with 7,12-dimethyl-benza-anthracene (DMBA) increased the incidence of tumors in untreated F1 and F2 descendants of these mice and increased their susceptibility to postnatal application of skin tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA). These generations of at least part of the initiating effects of a chemical carcinogen, e.g. DMBA administered during pregnancy. In the experiment described, the effects were investigated of TPA promotion on skin tumor appearance in F1 and F2 descendants of male mice exposed to total-body X-ray irradiation before mating. (author). 9 refs., 1 tab

[en] The Atomic Bomb Casualty Commission and its successor, the Radiation Effects Research Foundation, have studied A-bomb survivors of Hiroshima and Nagasaki since 1950. Survivors were exposed to a broad range of whole-body radiation, and many received low doses. Indeed, among 86520 survivors assigned DS86 dose estimates, 90% received <0.5 Sv. Previous analysis of the dose response for cancer mortality and other indices of radiation damage within the low-dose range (<0.5 Gy under the T65DR system of dosimetry) among A-bomb survivors failed to suggest the existence of radiation hormesis. Availability of updated cancer and noncancer mortality data for 1950-1985 and cancer incidence data for 1958-1987 and of the revised dosimetry system (DS86) prompted an extensive analysis of dose response within the low-dose range among A-bomb survivors in the ABCC-RERF Life Span Study cohort. This study analyzes the dose-responses, within the low-dose range (defined here as <0.5 Sv) for cancer and noncancer mortality and incidence of breast and thyroid cancer, using DS86 doses and detailed dose groups within the range that was termed low dose. (author). 5 refs., 1 fig., 1 tab

[en] Determining cancer risks for humans exposed to ionizing radiation is of great concern. Although much is known, uncertainties remain about genotoxic actions of radiations, some of which may be resolved by studies with cultured mammalian cells. Although both intragenic and multilocus mutations cause cancer, specific, large mutations, including loss of whole chromosomes, underlie many prevalent tumors. Studies of large mutations are particularly important for ionizing radiations which are the classical generator of such damages. (author). 31 refs., 3 figs