Chapter 8: Perspectives for the use of biological indicators for the assessment of radiation induced responses and impairments: Are there ‘common denominators’ in different radiation exposure scenarios as a target for predictive assessment? reflections on a panel discussion under the chairmanship ofT. M. Fliedner

Stem Cells ◽  
1995 ◽  
Vol 13 (S1) ◽  
pp. 307-317 ◽  
Author(s):  
Dirk Densow
2021 ◽  
Author(s):  
Halida Thanveer Asana Marican ◽  
Hongyuan Shen

Metaphase-based cytogenetic methods based on scoring of chromosome aberrations for the estimation of the radiation dose received provide a powerful approach for evaluating the associated risk upon radiation exposure and form the bulk of our current knowledge of radiation-induced chromosome damages. They mainly rely on inducing quiescent peripheral lymphocytes into proliferation and blocking them at metaphases to quantify the damages at the chromosome level. However, human organs and tissues demonstrate various sensitivity towards radiation and within them, self-proliferating progenitor/stem cells are believed to be the most sensitive populations. The radiation-induced chromosome aberrations in these cells remain largely unknown, especially in the context of an intact living organism. Zebrafish is an ideal animal model for research into this aspect due to their small size and the large quantities of progenitor cells present during the embryonic stages. In this study, we employ a novel metaphase-based cytogenetic approach on zebrafish embryos and demonstrate that chromosome-type and chromatid-type aberrations could be identified in progenitor cells at different cell-cycle stages at the point of radiation exposure. Our work positions zebrafish at the forefront as a useful animal model for studying radiation-induced chromosome structural changes in vivo.


2021 ◽  
Vol 66 (4) ◽  
pp. 18-24
Author(s):  
I. Ushakov ◽  
Vladimir Fyodorov

Purpose: Comparative assessment of radiation-induced changes in neurons of the cerebral cortex after a single and fractionated exposure to ionizing radiation in doses of 0.1 – 1.0 Gy. Material and methods. The study was carried out in compliance with the rules of bioethics on 180 white outbred male rats at the age of 4 months. by the beginning of the experiment, exposed to a single or fractionated exposure to γ-quanta of 60Co in total doses of 0.1; 0.2; 0.5 and 1.0 Gy. Neuromorphological and histochemical methods were used to assess morphometric and tinctorial parameters of nerve cells, as well as changes in the content of protein and nucleic acids in neurons in the early and late periods of the post-radiation period. Using one-way analysis of variance, a comparative assessment of neuromorphological indicators under various modes of radiation exposure is given. Results: In the control and irradiated animals throughout their life, undulating changes in the indicators of the state of the neurons of the brain occur with a gradual decrease by the end of the experiment. Despite a number of features of the dynamics of neuromorphological parameters, these irradiation regimes do not cause functionally significant changes in the neurons of the cortex. However, in some periods of the post-radiation period, the changes under the studied irradiation regimes were multidirectional and did not always correspond to age control. Significant differences in the response of neurons to these modes of radiation exposure in the sensory and motor areas of the cerebral cortex have not been established. Conclusion: No functionally significant radiation-induced changes in neurons were found either with single or fractionated irradiation. At the same time, different modes of irradiation in general caused the same type of changes in neurons. However, in some periods of observation, changes in neuromorphological parameters under the studied irradiation regimes were not unidirectional and differed from age control, which indicates a possible risk of disturbances in the functioning of the nervous system against the background of other harmful and dangerous factors.


2018 ◽  
Vol 32 (10) ◽  
pp. 905-906
Author(s):  
Florian Distler ◽  
Josefin Hartmann ◽  
Sascha Pahernik ◽  
Michael Wucherer

2015 ◽  
Vol 5 (1) ◽  
pp. 19-32 ◽  
Author(s):  
Andrea L. DiCarlo ◽  
Joseph M. Kaminski ◽  
Richard J. Hatchett ◽  
Bert W. Maidment

2008 ◽  
Vol 43 (5) ◽  
Author(s):  
J.-M. Bertho ◽  
L. Roy ◽  
M. Souidi ◽  
Y. Gueguen ◽  
J.-J. Lataillade ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xianghong Li ◽  
Wanchang Cui ◽  
Lisa Hull ◽  
Li Wang ◽  
Tianzheng Yu ◽  
...  

Abstract Recent studies suggested that radiation exposure causes local and systemic inflammatory responses and induces cell and tissue damage. We have reported that IL-18 plays an important role in radiation-induced injury. Here, we demonstrate that IL-18 binding protein (IL-18BP), a natural antagonist of IL-18, was significantly increased (1.7–63 fold) in mouse serum on day 1 after 0.5–10 Gy TBI. However, this high level of IL-18BP was not sufficient to neutralize the active IL-18 in irradiated mice, resulting in a radiation dose-dependent free IL-18 increase in these mice’s serum which led to pathological alterations to the irradiated cells and tissues and finally caused animal death. Administration of recombinant human (rh) IL-18BP (1.5 mg/kg) with single (24, 48 or 72 h post-TBI) or double doses (48 h and 5 days post-TBI) subcutaneous (SC) injection increased 30-day survival of CD2F1 mice after 9 Gy TBI 12.5–25% compared with the vehicle control treated group, respectively. Furthermore, the mitigative effects of rhIL-18BP included balancing the ratio of IL-18/IL-18BP and decreasing the free IL-18 levels in irradiated mouse serum and significantly increasing blood cell counts, BM hematopoietic cellularity and stem and progenitor cell clonogenicity in mouse BM. Furthermore, IL-18BP treatment inhibited the IL-18 downstream target interferon (IFN)-γ expression in mouse BM, decreased reactive oxygen species (ROS) level in the irradiated mouse heart tissues, attenuated the stress responsive factor GDF-15 (growth differentiation factor-15) and increased the intestine protector citrulline level in total body irradiated mouse serum, implicating that IL-18BP may protect multiple organs from radiation-induced inflammation and oxidative stress. Our data suggest that IL-18 plays a key role in radiation-induced cell and tissue damage and dysfunction; and for the first time demonstrated that IL-18BP counters IL-18 activation and therefore may mitigate/treat radiation-induced multiple organ injuries and increase animal survival with a wider therapeutic window from 24 h and beyond after lethal doses of radiation exposure.


2019 ◽  
Vol 90 (11) ◽  
pp. 966-977
Author(s):  
Rebecca S. Blue ◽  
Jeffery C. Chancellor ◽  
Rahul Suresh ◽  
Lisa S. Carnell ◽  
David P. Reyes ◽  
...  

INTRODUCTION: Analysis of historical solar particle events (SPEs) provides context for some understanding of acute radiation exposure risk to astronauts who will travel outside of low-Earth orbit. Predicted levels of radiation exposures to exploration crewmembers could produce some health impacts, including nausea, emesis, and fatigue, though more severe clinical manifestations are unlikely. Using current models of anticipated physiological sequelae, we evaluated the clinical challenges of managing radiation-related clinical concerns during exploration spaceflight.METHODS: A literature review was conducted to identify terrestrial management standards for radiation-induced illnesses, focusing on prodromal symptom treatment. Terrestrial management was compared to current spaceflight medical capabilities to identify gaps and highlight challenges involved in expanding capabilities for future exploration spaceflight.RESULTS: Current spaceflight medical resources, such as those found on the International Space Station, may be sufficient to manage some aspects of radiation-induced illness, although effective treatment of all potential manifestations would require substantial expansion of capabilities. Terrestrial adjunctive therapies or more experimental treatments are unavailable in current spaceflight medical capabilities but may have a role in future management of acute radiation exposure.DISCUSSION: Expanded medical capabilities for managing radiation-induced illnesses could be included onboard future exploration vehicles. However, this would require substantial research, time, and funding to reach flight readiness, and vehicle limitations may restrict such capabilities for exploration missions. The benefits of including expanded capabilities should be weighed against the likelihood of significant radiation exposure and extensive mission design constraints.Blue RS, Chancellor JC, Suresh R, Carnell LS, Reyes DP, Nowadly CD, Antonsen EL. Challenges in clinical management of radiation-induced illnesses during exploration spaceflight. Aerosp Med Hum Perform. 2019; 90(11):966–977.


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