[en] In August 1985, a conference has been held in Oakland, California, U.S.A., on the subject of radiation hormesis. There were many conference papers that only presented the theoretical aspects, or built up a hypothesis on the basis of data that are insufficient from the scientific point of view; but there were also papers showing quite reasonably that under certain conditions, low-dose radiation may initiate a protective mechanism in various cell systems against recurrent radiation exposure. Also, direct, stimulating effects have been reported. The contribution in hand summarizes some essential findings reported at this conference and presents some further considerations and data of the authors. (orig./MG)

[en] By the use of labelled iododeoxyuridine as DNA-precursor, the effect of radiation and cis-platinum-dichloro-diammine on rate of precursor incorporation on the one hand, and on rate of cell loss from the tumor on the other hand, was examined. The combination of 4 μg PDD/g and different γ-doses produces long-lasting effects on the relative incorporation of the precursor. The cell loss rate of the average tumor cells was increased after treatment with PDD alone; combined treatment was only slightly more efficient than PDD alone. (orig.)

[en] In sarcoma-180 of NMRI mice, euoxic tumour cells were labeled with ¹³¹I-iododeoxyuridine, and the average tumour cells were labeled with ¹²⁵I-iododexyuridine. An external counting technique permitted in vivo measurements of radiation effects on rates of loss of incorporated activity from the different labeled tumour areas. The technique was employed to study the effect of tumour exposure to gamma irradiation with and without chemical radiosensitization by misonidazole (La Roche 07-0582). Injecting 500 mg/kg of Ro-07-0582 15 minutes before irradiation reduced the measurable oxygen effect by a factor of 1.54. The dose modifying factor evaluated from the 50% tumour regression at 100 days was 1.57. (orig.)

[en] Published in summary form only

[en] Whereas in general the property of biologic systems to react to harming stimuli by changing in a way to immunize against later stimuli (hormesis), is well-known, the corresponding mechanism for low-dose ionizing radiation is doubtful. First, a short report is given of a conference on hormesis by ionizing radiation August 1985 in Oakland, Cal.. Second, own experiments on the immediate and delayed reaction of the cellular enzyme thymidine kinase in the marrow of mice after irradiation are presented. This enzyme is important for DNA synthesis. For several hours after a low dose irradiation the enzyme is inhibited and therefore the effect of a later second dose on the enzyme reduced. 10 refs., 9 figs. (qui)

[en] Whole-body irradiation of mice causes the dose-dependent appearance of a humoral factor in blood serum which inhibits incorporation of 125-IUdR into tissue culture cells. This factor appears even at doses below 0.01 Gy gamma irradiation and thus is probably not related to cell death. Data are presented relating this humoral factor to thymidine. Since at low doses the target size for this effect was calculated to be the entire cell, a cellular effect is postulated linking the site of few primary absorption events, anywhere in the cell, with the cellular membrane, thus causing changes in membrane charge, structure and/or fluidity. This may lead to blocking thymidine acceptance by the cell, and thus would cause a pile-up of thymidine in the reutilization pathway in peripheral blood and would give rise to the observed effect. The effect appears as a temporary disturbance of the physiological equilibrium and should not be related at present to any cellular damage. The acute low-dose effect described has implications for the measurement of low-dose exposure by biological dosimeters and on basic research on membrane function. (author)

No abstract available

[en] The present work was designed to study in vivo the mode of action of the antitumor agent cis-diammine dichloride platinum (II) (DDP) either alone or in combination with ionizing radiation on a solid experimental murine tumor. C57 BL/6J mice bearing the solid syngeneic adenocarcinoma EO 771 in one hind leg received an injection of 4 μg DDP per gram of body weight alone or 15 minutes prior to ₆₀Co gamma or cyclotron neutron irradiation (mean energy 6 MeV). The effects were assayed in vivo by volumetric measurements. In addition, 125-iodo-deoxyuridine (₁₂₅I-UdR) was used for tracing DNA precursor incorporation; activity loss from euoxic and average tumor cells was evaluated with a double tracer technique. Tumor growth delay was enhanced by a factor 3 to 5 after gamma or neutron irradiation. Dose modifying factors were identical for I-UdR incorporation 24 hours after treatment and tumor growth delay. DDP affected recovery of euoxic cells but had no lethal effect, whereas an enhanced rate of activity loss from the average tumor cell population was observed

[en] Thymidine kinase (TdR-K) and the incorporation of iododeoxyuridine (IUdR) into DNA of murine bone marrow cells are acutely and temporarily inhibited by low doses (0.01 Gy) of whole-body γ-radiation with a maximal effect at 4 h after exposure and full recovery at 10 h. The inhibitory effect was totally abolished by whole-body exposure to a strong static magnetic field of 1.4 T. The present investigation was designed to gain insight into the mechanism(s) underlying the inhibition of TdK-K activity and the incorporation of ¹²⁵I-UdR by challenging the system with various pharmacological and biochemical means. The data point to the involvement of the cellular radical-detoxification system in changing the activity of TdR-K, especially on the basis of the concurrent increase of glutathione concentration and decrease in TdR-K activity. (author)

[en] The influence of a strong homogeneous, stationary magnetic field (SMF) on thymidine kinase (TdR-K) in bone marrow cells, and thus on the incorporation of ¹²⁵I-labelled 5-iodo-2-deoxyuridine (¹²⁵IUdR) into DNA of mice and isolated bone marrow cells in vitro was assayed after exposure of immobilized mice. Moving mice showed no effect, nor cell suspensions nor enzyme in solution. Response depended on body temperature during exposure: at 27⁰C and 29⁰C there was an increase, and at 37⁰C and 39.5⁰C a depression of activity. TdR-K activity at low temperature increased with field strength ranging from 0.2 to 1.4 T. Maximum effect at 1.4 T was at 30 min; return to base-line took 5-10 min. Total-body irradiated mice (0.1 Gy ¹³⁷Cs γ-rays) exposed immediately to a magnetic field at 1.4 T for 30 min (27⁰C body temperature) showed no enzyme inhibition. Exposure to the magnetic field further removed from the irradiation time did not negate the inhibitory effect. The results support the hypothesis that magnetic field affects TdR-K activity by way of a mediating structure such as a membrane. (U.K.)