Whole Body Radiation Effects

2014 ◽  
pp. 179-190
Keyword(s):  
Radiation Effects ◽  
Whole Body

scholarly journals Simulated nuclear contamination scenario, solid cancer risk assessment, and support to decision

Nukleonika ◽  
2019 ◽  
Vol 64 (2) ◽  
pp. 41-48 ◽  
Author(s):  
Sergio X. Lima ◽  
Karolina P. S. Costa ◽  
Zelmo R. Lima ◽  
Fagner C. Rother ◽  
Olga M. O. Araujo ◽  
...  
Keyword(s):  
Radiation Effects ◽  
Radioactive Material ◽  
Cancer Risk Assessment ◽  
Whole Body ◽  
Decision Making Process ◽  
Solid Cancer ◽  
Health Physics ◽  
Output Data ◽  
Mathematical Relationships ◽  
Atmospheric Release

Abstract The detonation of an (hypothetical) improvised nuclear device (IND) can generate atmospheric release of radioactive material in the form of particles and dust that ultimately contaminate the soil. In this study, the detonation of an IND in an urban area was simulated, and its effects on humans were determined. The risk of solid cancer development due to radiation was calculated by taking into account prompt radiation and whole-body exposure of individuals near the detonation site up to 10 km. The excess relative risk (ERR) of developing solid cancer was evaluated by using the mathematical relationships from the Radiation Effects Research Foundation (RERF) studies and those from the HotSpot code. The methodology consists of using output data obtained from simulations performed with the HotSpot health physics code plugging in such numbers into a specific given equation used by RERF to evaluate the resulting impact. Such a preliminary procedure is expected to facilitate the decision-making process significantly.

Effect of Two Graded Doses of Whole-Body X-Irradiation and Radioprotection by the Use of S-Phenethyl Formamidino 4 (N-Ethyl Isothioamide) Morpholine Dihydrochloride

1983 ◽  
Vol 22 (05) ◽  
pp. 237-245 ◽  
Author(s):  
P. K. Chaturvedi ◽  
S. N. Pandeya ◽  
S. S. Hasan
Keyword(s):  
Radiation Effects ◽  
Whole Body ◽  
X Irradiation ◽  
Radiation Induced ◽  
Induced Changes ◽  
The Brain

The protection offered by a newly synthesized compound (S-phenethyl-formamidino-4(N-ethyl isothioamide) morpholine dihydrochloride) against radiation effects on DNA, RNA and protein biosynthetic processes in the brain, and on metabolites of 5-HT and nor-adrenalin, i.e., 5-HIAA and VMA, in the urine, including the radiobiological damage to thyroid and testes, was evaluated. The use of the compound prior to irradiation prevented radiation-induced changes in the thyroid and testes. The radiation-induced alterations in the pattern of DNA, RNA, protein in the brain, and in 5-HIAA and VMA in urine could be averted by treatment with this compound prior to each dose of X-irradiation.

scholarly journals Metabolomic Studies of Tissue Injury in Nonhuman Primates Exposed to Gamma-Radiation

2019 ◽  
Vol 20 (13) ◽  
pp. 3360 ◽  
Author(s):  
Amrita K. Cheema ◽  
Khyati Y. Mehta ◽  
Meena U. Rajagopal ◽  
Stephen Y. Wise ◽  
Oluseyi O. Fatanmi ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Radiation Effects ◽  
Nonhuman Primates ◽  
Clinical Symptoms ◽  
Tissue Injury ◽  
Predictive Biomarkers ◽  
Whole Body ◽  
Biomarkers Of Exposure ◽  
Radiation Induced ◽  
Over Time

Exposure to ionizing radiation induces a complex cascade of systemic and tissue-specific responses that lead to functional impairment over time in the surviving population. However, due to the lack of predictive biomarkers of tissue injury, current methods for the management of survivors of radiation exposure episodes involve monitoring of individuals over time for the development of adverse clinical symptoms and death. Herein, we report on changes in metabolomic and lipidomic profiles in multiple tissues of nonhuman primates (NHPs) that were exposed to a single dose of 7.2 Gy whole-body 60Co γ-radiation that either survived or succumbed to radiation toxicities over a 60-day period. This study involved the delineation of the radiation effects in the liver, kidney, jejunum, heart, lung, and spleen. We found robust metabolic changes in the kidney and liver and modest changes in other tissue types at the 60-day time point in a cohort of NHPs. Remarkably, we found significant elevation of long-chain acylcarnitines in animals that were exposed to radiation across multiple tissue types underscoring the role of this class of metabolites as a generic indicator of radiation-induced normal tissue injury. These studies underscore the utility of a metabolomics approach for delineating anticipatory biomarkers of exposure to ionizing radiation.

Actions of a novel therapeutic formulation: Zn, Se and Mn plus Lachesis Muta venom (O-LM) on radiation deleterious immune effects

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14116-14116
Author(s):  
E. Rivera ◽  
G. Cremaschi ◽  
A. M. Genaro ◽  
M. Croci ◽  
L. Sambuco ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Radiation Effects ◽  
Protective Action ◽  
Malignant Cell ◽  
Whole Body ◽  
Normal Tissues ◽  
T Lymphocyte Proliferation ◽  
Lymphocyte Activity ◽  
High Doses ◽  
Lachesis Muta

14116 Background: We have previously reported that O-LM inhibits malignant cell proliferation and increases survival in rodent tumor models (Int J Cancer S13:183, 2002). Molecular and immunological basis of O-LM action were reported (J Clin Oncol 24:18S, 2006). As O- LM selectively protects normal tissues from high doses of ionizing radiation (Proc Int Cancer Congress,1495–9, 1998), we here investigated O- LM protective action upon radiation effects on immune cells. Methods: Balb/c mice (n=15 each group) were employed: control (C); 2Gy whole body irradiated (IR); treated with O-LM (Zn, Se, Mn 4μg/ml each; L. Muta 4 ng/ml; 0.1 ml/day, sc) for 15 days and 2Gy irradiated (O-LM+IR). Mice were sacrificed at day 3, 7 or 15 post-irradiation (PI). Proliferation was evaluated in lymphocytes by [3H]- Thymidine incorporation after T- or B selective mitogen stimulation. In cell-free supernatants (SN) from mitogen-stimulated cultures cytokines involved in lymphocyte regulation and/or inflammation were determined by ELISA. Results: Irradiation induced a decrease in T lymphocyte proliferation at 3 and 7 days PI (% of decrease in IR: 47.6±9.0, p<0.05; 42.0±7.2, p<0.02 respectively). Pretreatment with O-LM recovered proliferation to basal values (day 3 PI 93.4±10.2%; day 7 PI 130.9±15.3%, O-LM+IR vs. C; p=NS). No modifications were observed in B cells. At day 3 PI, a marked decrease in IFN? levels was obtained in SN of IR mice that was reverted by O-LM treatment (pg/ml: IR 1653±419; C 10884±2783, p<0.02; O-LM+IR 16924±4284, p<0.05 vs C). Also, at day 7 PI, an important increase in TNFa was observed in IR mice, that were reverted by O-LM (pg/ml: IR: 300.7±62.3 vs O-LM+IR: 28.7±2.3, p<0.02). No differences were found in IL-2 levels. Conclusions: The therapeutic action of O-LM is based on its ability of targeting simultaneously multiple pathways involved in cancer development. Present data demonstrate that O-LM protects animals from irradiation by recovering the immune function, improving T lymphocyte activity and modulating the production of key cytokines as IFN? and TNFa. The reported effect may represent a potential benefit for cancer patients undergoing radiotherapy. No significant financial relationships to disclose.

scholarly journals The Double Threshold: Consequences for Identifying Low-Dose Radiation Effects

Dose-Response ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. 155932582094972
Author(s):  
Alan Waltar ◽  
Ludwig Feinendegen
Keyword(s):  
Dose Response ◽  
Radiation Effects ◽  
Low Dose ◽  
Development Program ◽  
Absorbed Dose ◽  
Current Data ◽  
Whole Body ◽  
Radiation Quality ◽  
Adaptive Protection ◽  
New Research

Prior to observing low-dose-induced cell signaling and adaptive protection, radiogenic stochastic effects were assumed to be linearly related to absorbed dose. Now, abundant data prove the occurrence of radiogenic adaptive protection specifically at doses below ∼ 200 mGy (with some data suggesting such protection at a dose even higher than 200 mGy). Moreover, cells do not thrive properly when deprived of radiation below background dose. Two threshold doses need be considered in constructing a valid dose-response relationship. With doses beginning to rise from zero, cells increasingly escape radiation deprivation. The dose at which radiation-deprived cells begin to function homeostatically provides dose Threshold A. With further dose increase, adaptive protection becomes prominent and then largely disappears at acute doses above ∼ 200 mGy. The dose at which damage begins to override protection defines Threshold B. Thresholds A and B should be terms in modeling dose-response functions. Regarding whole-body responses, current data suggest for low-LET acute, non-chronic, irradiation a Threshold B of about 100 mGy prevails, except for leukemia and probably some other malignancies, and for chronic, low dose-rate irradiation where the Threshold B may well reach 1 Gy per year. A new Research and Development Program should determine individual Thresholds A and B for various radiogenic cell responses depending on radiation quality and target.

scholarly journals Quantitative Analysis of Effects of a Single 60Co Gamma Ray Point Exposure on Time-Dependent Change in Locomotor Activity in Rats

2019 ◽  
Author(s):  
Keiko Otani ◽  
Megu Ohtaki ◽  
Nariaki Fujimoto ◽  
Aisulu Saimova ◽  
Ynkar Kairkhanova ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Radiation Exposure ◽  
Radiation Effects ◽  
Gamma Ray ◽  
Single Point ◽  
Whole Body ◽  
Dependent Manner ◽  
Cumulative Number ◽  
Daily Fluctuation ◽  
60Co Gamma

AbstractFatigue is one of the earliest nonspecific symptoms of radiation exposure in humans, but its etiology, mechanism, and dose dependency remain unexplained. Investigating initial behavioral changes caused by irradiation of animals might provide important information to aid understanding of early health effects of radiation exposure and clinical features of radiation injury. Although previous studies in rodents suggested that radiation exposure leads to reduced activity, detailed properties of the effects were unrevealed due to a lack of proper statistical analysis, which is needed to better elucidate details of changes in locomotor activity. Ten-week-old male Wistar rats were subjected to single point external whole-body irradiation with 60Co gamma rays at 0, 2.0, 3.5, and 5.0 Gy (4 rats per group). Infrared sensors were used to continuously record locomotor activity of each rat. Cumulative number of movements during the night was defined as “activity” for each day. A non-linear mixed effects model accounting for individual differences and daily fluctuation of activity was applied to analyze the rats’ longitudinal locomotor data. Despite a small number of animals per group, our statistical method successfully revealed characteristics of the changes in locomotor activity after radiation exposure, showing that 1) reduction in activity occurred immediately—and in a dose-dependent manner—after irradiation and 2) recovery to pre-irradiation levels required almost one week, with the same recovery rate in each dose group. In addition to improving our understanding of radiation effects on locomotor activity, this statistical framework should be useful to analyze other data with similar structure.

scholarly journals Out-of-Field Hippocampus from Partial-Body Irradiated Mice Displays Changes in Multi-Omics Profile and Defects in Neurogenesis

2021 ◽  
Vol 22 (8) ◽  
pp. 4290
Author(s):  
Simonetta Pazzaglia ◽  
Barbara Tanno ◽  
Francesca Antonelli ◽  
Paola Giardullo ◽  
Gabriele Babini ◽  
...  
Keyword(s):  
Radiation Effects ◽  
Critical Role ◽  
Hippocampal Neurogenesis ◽  
Whole Body ◽  
Potential Contribution ◽  
X Rays ◽  
Neurocognitive Dysfunction ◽  
Post Irradiation ◽  
Radiation Induced ◽  
Partial Body

The brain undergoes ionizing radiation exposure in many clinical situations, particularly during radiotherapy for brain tumors. The critical role of the hippocampus in the pathogenesis of radiation-induced neurocognitive dysfunction is well recognized. The goal of this study is to test the potential contribution of non-targeted effects in the detrimental response of the hippocampus to irradiation and to elucidate the mechanisms involved. C57Bl/6 mice were whole body (WBI) or partial body (PBI) irradiated with 0.1 or 2.0 Gy of X-rays or sham irradiated. PBI consisted of the exposure of the lower third of the mouse body, whilst the upper two thirds were shielded. Hippocampi were collected 15 days or 6 months post-irradiation and a multi-omics approach was adopted to assess the molecular changes in non-coding RNAs, proteins and metabolic levels, as well as histological changes in the rate of hippocampal neurogenesis. Notably, at 2.0 Gy the pattern of early molecular and histopathological changes induced in the hippocampus at 15 days following PBI were similar in quality and quantity to the effects induced by WBI, thus providing a proof of principle of the existence of out-of-target radiation response in the hippocampus of conventional mice. We detected major alterations in DAG/IP3 and TGF-β signaling pathways as well as in the expression of proteins involved in the regulation of long-term neuronal synaptic plasticity and synapse organization, coupled with defects in neural stem cells self-renewal in the hippocampal dentate gyrus. However, compared to the persistence of the WBI effects, most of the PBI effects were only transient and tended to decrease at 6 months post-irradiation, indicating important mechanistic difference. On the contrary, at low dose we identified a progressive accumulation of molecular defects that tended to manifest at later post-irradiation times. These data, indicating that both targeted and non-targeted radiation effects might contribute to the pathogenesis of hippocampal radiation-damage, have general implications for human health.

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