Biophysik

Ausgehend von den ersten Arbeiten von Fricke u. Dale über die Strahleninaktivierung von Enzymen wird die Entwicklung dieses Forschungsgebietes der Strahlenbiologie aufgezeigt. Durch die Anwendung biochemischer Analysentechnik war es möglich geworden, strahleninduzierte Veränderungen der Struktur und der Sequenz sichtbar zu machen. Neue Ergebnisse der Strahlenchemie ermöglichen es, diese Veränderungen auf chemische Reaktionen mit den Primärradikalen der Wasserradiolyse zurückzuführen. Die Geschwindigkeitskonstanten der Wasserradikale mit den Aminosäureresten und mit Proteinen konnten mit Hilfe der Pulsradiolyse gemessen werden. Experimente, bei denen Wasserradikale abgefangen wurden, ergaben, daß die OH -Radikale die Inaktivierung von Enzymen bewirken, während solvatisierte Elektronen, die einen starken Abbau vom Cystin bewirken, kaum zur Inaktivierung beitragen.

This paper analyzes data for the osteosarcoma incidence in life-time experiments of 224Ra injected mice with respect to the importance of initiating and promoting action of ionizing high LET-radiation. This was done with the biologically motivated two step clonal expansion (TSCE) model of tumor induction. Experimentally derived osteosarcoma incidence in 1,194 mice following exposure to 224Ra with different total radiation doses and different fractionation patterns were analyzed together with incidence data from 1,710 unirradiated control animals. Effects of radiation on the initiating event and on the clonal expansion rate, i.e. on promotion were found to be necessary to explain the observed patterns with this model. The data show a distinct inverse protraction effect at high doses, whereas at lower doses this effect becomes insignificant. Such a behavior is well reproduced in the proposed model: At dose rates above 6 mGy/day a longer exposure produces higher ERR per dose, while for lower rates the reverse is the case. The TSCE model permits the deduction of several kinetic parameters of a postulated two-step bone tumorigenesis process. Mean exposure rates of 0.13 mGy/day are found to double the baseline initiation rate. At rates above 100 mGy/day, the initiation rate decreases. The clonal expansion rate is doubled at 8 mGy/day, and it levels out at rates beyond 100 mGy/day.

A general equation for mammalian cell survival has been derived in the previous paper. This paper presents the results of comparison of theoretical evaluations with survival data available from the literature, including different cell lines, variations in linear energy transfer, dose rate and dose fractionation effects and the effects of ultrasoft X-rays and superheavy ions. Merits and demerits of the model are considered in comparison with other models of radiation-induced killing of mammalian cells published in the literature.

Recently there has been a renewed interest in biological scaling relationships between parameters, such as those between, for example, body mass, dry matter intake and biological half-times of radionuclides that are useful in predicting the transfer of radiocaesium to different animal species, particularly to wild animals. However, there is still a considerable unexplained variability in transfer coefficient estimates between individuals of the same species. This paper discusses the physiological parameters that affect the transfer of radiocaesium to ruminants, and it shows how a better understanding of these parameters may help to reduce the within-species variability in radiocaesium transfer coefficients. In light of the improved understanding during the past 10–15 years of the importance of source-dependent bioavailability on absorption of radiocaesium from the gastrointestinal tract, it is concluded that further studies are required on the effects of feed digestibility and physiological factors on absorption and endogenous faecal excretion of radiocaesium to better understand the variability in transfer coefficients.

The peculiarities of radiation response in animals at low environmental temperatures are analyzed in the context of radiation safety of the Arctic/Northern wildlife. The paper includes a data review on radiation effects in cold environments based on international and Russian publications since 1948, which forms a supplement to the EPIC and FREDERICA data collections. In homoiothermic and heterothermic animals, imbalances in thermoregulation caused by ionizing radiation are discussed, which increase energy loss of animals, and decrease their fitness to the Arctic/Northern climate. In poikilothermic animals, both radiation damage and recovery are temperature dependant, their rates being slow in the cold environment. At low temperatures, radiation damage of biological tissues is conserved in hidden form; when the temperature of poikilothermic animal rises to a normal level, radiation injury is developed rapidly similar to acute dose response. Additionally, a mathematical model is described, demonstrating the combined effects of chronic radiation exposures and seasonal temperature variations on a fish population. Computer simulations show that at the same level of irradiation, the overall radiation damage to Arctic/Northern poikilothermic fish is higher than that to the fish from warm climate. Considering the peculiarities of radiation effects in the cold climate, the Arctic/Northern fauna might be expected to be more vulnerable to chronic radiation stress compared to temperate fauna. In the case of acute radiation exposure during winter periods, hibernation of heterothermic and cooling of poikilothermic animals may provide temporary protection from acute radiation effects.

The Semipalatinsk region (Kazakhstan Republic) has been affected by extensive radioactive contamination due to more than 450 nuclear tests of which almost 100 were exploded in the atmosphere. The present results refer to cytogenetic assessments in a study cohort of the population of Dolon, a settlement located on the NE boundary of the nuclear weapon test site, which was exposed to elevated doses of ionising radiation primarily due to the first Soviet nuclear test in 1949. Conventional cytogenetic analyses were carried out on 21 blood samples from individuals (more than 50 years old) living in Dolon since the very beginning of nuclear testing. A matched control group included 20 individuals living in non-contaminated areas. Higher frequencies of chromosome aberrations were found in the Dolon cohort compared to the control group, even though they remain within the range of the background levels reported for large normal human population studies on elderly individuals.

A two-mutation carcinogenesis model was used to calculate the expected lung cancer incidence caused by both smoking and exposure to radon in two populations, i.e. those of the Netherlands and Sweden. The model parameters were taken from a previous analysis of lung cancer in smokers and uranium miners and the model was applied to the two populations taking into account the smoking habits and exposure to radon. For both countries, the smoking histories and indoor radon exposure data for the period 1910–1995 were reconstructed and used in the calculations. Compared with the number of lung cancer cases observed in 1995 among both males and females in the two countries, the calculations show that between 72% and 94% of the registered lung cancer cases may be attributable to the combined effects of radon and smoking. In the Netherlands, a portion of about 4% and in Sweden, a portion of about 20% of the lung cancer cases (at ages 0–80 years) may be attributable to radon exposure, the numbers for males being slightly lower than for females. In the Netherlands, the proportions of lung cancers attributable to smoking are 91% for males and 71% for females; in Sweden, the figures are 70% and 56%, respectively. The risk from radon exposure is dependent on gender and cigarette smoking: the excess absolute risk for continuous exposure to 100 Bq m–3 ranges between 0.003 and 0.006 and compares well with current estimates, e.g. 0.0043 of the International Commission on Radiological Protection (ICRP). The excess relative risk for continuous exposure to 100 Bq m–3 shows a larger variation, ranging generally between 0.1 for smokers and 1.0 for non-smokers. The results support the assumption that exposure to (indoor) radon, even at a level as low as background radiation, causes lung cancer proportional to the dose and is consistent with risk factors derived from the miners data.