Tolerance of rats to a cold environment during multiple exposures to a low dose of x rays

1961 ◽  
Vol 200 (5) ◽  
pp. 1039-1042 ◽  
Author(s):  
Bernard D. Newsom ◽  
Donald J. Kimeldorf

A lethal dose of X irradiation can be made sublethal by the fractionation of a dose into a series of smaller doses separated by adequate time intervals. The results reported here demonstrate how an environmental stress, such as cold, may affect this mitigating action of dose fractionation. Rats were maintained at 6 C while receiving a total dose of 600 r in one or eight exposures with various intervals between exposures. A greater interval was required between radiation exposures at 6 C than at 23 C to reduce the lethal response following irradiation. From the results of the food consumption measurements, it appears that cold exposure emphasizes the consequence of the reduced food intake which follows daily doses of 75 r in the rat. The irradiated rat was able to increase the amount of food consumed during cold exposure; however, the increase was not sufficient for adaptation. The lowered consumption which followed eight daily 75-r exposures was sufficient to cause death in pair-fed rats maintained at 6 C, but not at 23 C.

1996 ◽  
Vol 06 (01n02) ◽  
pp. 291-298 ◽  
Author(s):  
Y. MATSUDA ◽  
M. YONEZAWA ◽  
F. NISHIYAMA

It is not only important for maintenance and improvement of health, but also indispensable for diagnosis and remedy of diseases to make inquiries into the biological defence mechanisms. Yonezawa et al. came across an induction of yet unknown defence mechanism(s) in mice which acquired radioresistance two weeks after low dose X-irradiation with 0.5 Gy. The 30-day survival rate after midlethal X-irradiation of the mice significantly increased by the pre-irradiation, but contrary to the common knowledge on radiation protection, recovery of the blood cell counts of thrombocytes, leukocytes and erythrocytes were not stimulated by the pre-irradiation. This study was planned to find some keys to elucidate the mechanism for the acquired radioresistance. Metal ions are well known to be important for enzyme activities as well as for metabolisms. Eleven elements, Cl, K, Ca, Cr, Mn, Fe, Ni, Cu, Zn, Se and Br were analysed in mice sera by PIXE.


1957 ◽  
Vol 106 (4) ◽  
pp. 485-500 ◽  
Author(s):  
Theodore T. Puck ◽  
Dimitry Morkovin ◽  
Philip I. Marcus ◽  
Steven J. Cieciura

Survival curves of normal human cells from a variety of tissues exposed to varying doses of x-irradiation have been constructed, which permit definition of the intrinsic radiation sensitivity of the reproductive power of each cell type. The mean lethal dose of x-irradiation for all the cells employed, including those from normal and cancerous organs, those exhibiting diploid and polyploid chromosome number; those from embryonic and adult tissues, including recently isolated cells and cultures which had been maintained in vitro for many years, and cells exhibiting either epithelioid or fibroblastic morphology, was found to be contained between the limits of 50 to 150 r. Other similarities in the pattern of radiation effects, such as giant formation and abortive colonial growth, in these cells and that of the HeLa S3, previously studied, confirm the hypothesis that the pattern of reaction to x-irradiation previously elucidated, is representatative, at least in over-all outline, for a large variety of human cells. While the radiation survival curves of various human cells are similar in the gross, small but important characterizing differences have been found. All epithelioid cells so far studied are approximately 2-hit, and more radioresistant than the fibroblast-like cells whose survival data correspond to a mean lethal dose of around 60 r, and which so far can be fitted by either 1-hit or 2-hit curves. The earlier prediction that the major radiobiologic damage to mammalian cells is lodged in the genetic apparatus was confirmed by the demonstration of high frequency of mutants among the survivors of doses of 500 to 900 r. All the data on the x-radiosensitivity of these cells can be explained on the basis of a defect resulting from primary damage localized in one or more chromosomes. These considerations afford a convincing explanation of several aspects of the mammalian radiation syndrome.


2002 ◽  
Vol 80 (8) ◽  
pp. 828-832 ◽  
Author(s):  
Yukihisa Miyachi ◽  
Takahisa Koike ◽  
Kenzo Muroi ◽  
Tomoko Kanao ◽  
Taro Kawamoto ◽  
...  

Acute emesis response to harmful doses of X-rays on frogs (Rana porosa porosa) was examined. Results showed that the number of radioemesis events following exposure to 0.85 Gy was slightly higher than in the sham control animals. The increase in emesis action became more pronounced when the total dose of radiation was raised to 2.5 Gy. Only 1 frog out of a total of 12 did not show vomiting following radiation, while no response was observed in sham control animals. Note that animals in which the low dose rate of radiation was applied to whole body did not display any changes in the emesis response relative to control animals. The present studies, and those by others, showed that a brief dose of X-rays prior to a second exposure to a sub-lethal dose might induce a tolerance to radiation. An additional experiment was conducted to examine whether a small conditioning dose could induce a depression of radioemesis (tolerance) following an exposure to high dose X-ray. With prior exposure to 0.3 Gy, only 1 frog out of a total of 5 frogs vomited as a result of radiation exposure. Suppression of the emetic response became significant when the pre-radiation dose was decreased to 0.1 Gy. On the contrary, increasing the small conditioning dose to 0.5 Gy resulted in a remarkable rise of radiation-induced emesis. This results indicate that exposure to the smaller dose of X-rays elicits a tolerance effect to toxic dose level of radiation.Key words: emesis, hormesis, low-dose X-rays, resistance, frog.


1958 ◽  
Vol 195 (2) ◽  
pp. 271-275 ◽  
Author(s):  
Bernard D. Newsom ◽  
Donald J. Kimeldorf

Prolonged exposure to a low ambient temperature increases the 30-day mortality rate of irradiated rats. To determine if the increased mortality is due to a failure of the irradiated rat to adapt to the higher metabolic demands of a cold environment, the food consumption of irradiated (500r, 600r, 250 kv x-rays) animals was measured during 30 days of exposure at normal (23°C) or lowered (6°C) environmental temperature. The food consumption of irradiated animals was increased by exposure to cold; however, this increase was not sufficient to maintain body weight at a level comparable to nonirradiated animals. When the food consumption of nonirradiated animals was limited to that of irradiated animals during exposure to a 6°C environment, the mortality observed among nonirradiated animals was comparable to the increase in mortality induced by cold exposure of irradiated animals. These results suggest that the increased mortality rate of irradiated animals in a cold environment is related to an inadequate food intake.


Author(s):  
D. E. Philpott ◽  
W. Sapp ◽  
C. Williams ◽  
Joann Stevenson ◽  
S. Black

The response of spermatogonial cells to X-irradiation is well documented. It has been shown that there is a radiation resistent stem cell (As) which, after irradiation, replenishes the seminiferous epithelium. Most investigations in this area have dealt with radiation dosages of 100R or more. This study was undertaken to observe cellular responses at doses less than 100R of X-irradiation utilizing a system in which the tissue can be used for light and electron microscopy.Brown B6D2F1 mice aged 16 weeks were exposed to X-irradiation (225KeV; 15mA; filter 0.35 Cu; 50-60 R/min). Four mice were irradiated at each dose level between 1 and 100 rads. Testes were removed 3 days post-irradiation, fixed, and embedded. Sections were cut at 2 microns for light microscopy. After staining, surviving spermatogonia were identified and counted in tubule cross sections. The surviving fraction of spermatogonia compared to control, S/S0, was plotted against dose to give the curve shown in Fig. 1.


Author(s):  
Gregory L. Finch ◽  
Richard G. Cuddihy

The elemental composition of individual particles is commonly measured by using energydispersive spectroscopic microanalysis (EDS) of samples excited with electron beam irradiation. Similarly, several investigators have characterized particles by using external monochromatic X-irradiation rather than electrons. However, there is little available information describing measurements of particulate characteristic X rays produced not from external sources of radiation, but rather from internal radiation contained within the particle itself. Here, we describe the low-energy (< 20 KeV) characteristic X-ray spectra produced by internal radiation self-excitation of two general types of particulate samples; individual radioactive particles produced during the Chernobyl nuclear reactor accident and radioactive fused aluminosilicate particles (FAP). In addition, we compare these spectra with those generated by conventional EDS.Approximately thirty radioactive particle samples from the Chernobyl accident were on a sample of wood that was near the reactor when the accident occurred. Individual particles still on the wood were microdissected from the bulk matrix after bulk autoradiography.


Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut

ABSTRACT When females of Drosophila melanogaster are treated with chemical or physical mutagens, not only in one but also in both of the two homologous X chromosomes of a given oocyte, a recessive sex-linked lethal mutation may be induced. A method is described that discriminates between such "single" and "double mutations." A theory is developed to show how a comparison between the expected and the observed frequency of double mutations yields an indication of the intercellular distribution (random or nonrandom) of recessive lethal mutations induced by mutagenic agents in oocytes and, consequently, of the distribution (homogeneous or nonhomogeneous) of those agents.—Three agents were tested: FUdR (12.5, 50.0 and 81.0,μg/ml), mitomycin C (130.0 μg/ml) and X rays (2000 R, 150 kV). After FUdR feeding, no increase in the mutation frequency usually observed in D. melanogaster without mutagenic treatment was obtained (u=0.13%, namely three single mutations among 2332 chromosomes tested). After mitomycin C feeding, 104. single and three double mutations were obtained. All of the 50 mutations observed after X irradiation were single mutations. The results obtained in the mitomycin C and radiation experiments favor the assumption of a random intercellular distribution of recessive lethal mutations induced by these two agents in oocytes of D. melanogaster. Reasons are discussed why for other types of mutagenic agents nonrandom distributions may be observed with our technique.


2002 ◽  
Vol 21 (2) ◽  
pp. 85-90 ◽  
Author(s):  
L E Feinendegen

This review first summarizes experimental data on biological effects of different concentrations of ROS in mammalian cells and on their potential role in modifying cell responses to toxic agents. It then attempts to link the role of steadily produced metabolic ROS at various concentrations in mammalian cells to that of environmentally derived ROS bursts from exposure to ionizing radiation. The ROS from both sources are known to both cause biological damage and change cellular signaling, depending on their concentration at a given time. At low concentrations signaling effects of ROS appear to protect cellular survival and dominate over damage, and the reverse occurs at high ROS concentrations. Background radiation generates suprabasal ROS bursts along charged particle tracks several times a year in each nanogram of tissue, i.e., average mass of a mammalian cell. For instance, a burst of about 200 ROS occurs within less than a microsecond from low-LET irradiation such as X-rays along the track of a Compton electron (about 6 keV, ranging about 1 μm). One such track per nanogram tissue gives about 1 mGy to this mass. The number of instantaneous ROS per burst along the track of a 4-meV ¬-particle in 1 ng tissue reaches some 70000. The sizes, types and sites of these bursts, and the time intervals between them directly in and around cells appear essential for understanding low-dose and low dose-rate effects on top of effects from endogenous ROS. At background and low-dose radiation exposure, a major role of ROS bursts along particle tracks focuses on ROS-induced apoptosis of damage-carrying cells, and also on prevention and removal of DNA damage from endogenous sources by way of temporarily protective, i.e., adaptive, cellular responses. A conclusion is to consider low-dose radiation exposure as a provider of physiological mechanisms for tissue homoeostasis.


Sign in / Sign up

Export Citation Format

Share Document