ionizing radiation
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2022 ◽  
Vol 31 ◽  
pp. 100799
Hong Zhang ◽  
Yini Wang ◽  
Jingjie Wu ◽  
Lei Zhu ◽  
Yining Xia

2022 ◽  
Vol 10 (1) ◽  
pp. 190
Ida Romano ◽  
Carlo Camerlingo ◽  
Lisa Vaccari ◽  
Giovanni Birarda ◽  
Annarita Poli ◽  

A main factor hampering life in space is represented by high atomic number nuclei and energy (HZE) ions that constitute about 1% of the galactic cosmic rays. In the frame of the “STARLIFE” project, we accessed the Heavy Ion Medical Accelerator (HIMAC) facility of the National Institute of Radiological Sciences (NIRS) in Chiba, Japan. By means of this facility, the extremophilic species Haloterrigena hispanica and Parageobacillus thermantarcticus were irradiated with high LET ions (i.e., Fe, Ar, and He ions) at doses corresponding to long permanence in the space environment. The survivability of HZE-treated cells depended upon either the storage time and the hydration state during irradiation; indeed, dry samples were shown to be more resistant than hydrated ones. With particular regard to spores of the species P. thermantarcticus, they were the most resistant to irradiation in a water medium: an analysis of the changes in their biochemical fingerprinting during irradiation showed that, below the survivability threshold, the spores undergo to a germination-like process, while for higher doses, inactivation takes place as a consequence of the concomitant release of the core’s content and a loss of integrity of the main cellular components. Overall, the results reported here suggest that the selected extremophilic microorganisms could serve as biological model for space simulation and/or real space condition exposure, since they showed good resistance to ionizing radiation exposure and were able to resume cellular growth after long-term storage.

Kevin Goodman ◽  
Sam McHenry ◽  
Jeff Titus ◽  
Robert Cooper ◽  
Hemant Ghadi ◽  

Plants ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 222
Gian Marco Ludovici ◽  
Andrea Chierici ◽  
Susana Oliveira de Souza ◽  
Francesco d’Errico ◽  
Alba Iannotti ◽  

The aim of this work is to analyze the effects of ionizing radiation and radionuclides (like 137Cs) in several higher plants located around the Fukushima Dai-ichi Nuclear Power Plant (FNPP), evaluating both their adaptive processes and evolution. After the FNPP accident in March 2011 much attention was focused to the biological consequences of ionizing radiation and radionuclides released in the area surrounding the nuclear plant. This unexpected mishap led to the emission of radionuclides in aerosol and gaseous forms from the power plant, which contaminated a large area, including wild forest, cities, farmlands, mountains, and the sea, causing serious problems. Large quantities of 131I, 137Cs, and 134Cs were detected in the fallout. People were evacuated but the flora continued to be affected by the radiation exposure and by the radioactive dusts’ fallout. The response of biota to FNPP irradiation was a complex interaction among radiation dose, dose rate, temporal and spatial variation, varying radiation sensitivities of the different plants’ species, and indirect effects from other events. The repeated ionizing radiations, acute or chronic, guarantee an adaptation of the plant species, demonstrating a radio-resistance. Consequently, ionizing radiation affects the genetic structure, especially during chronic irradiation, reducing genetic variability. This reduction is associated with the different susceptibility of plant species to chronic stress. This would confirm the adaptive theory associated with this phenomenon. The effects that ionizing radiation has on different life forms are examined in this review using the FNPP disaster as a case study focusing the attention ten years after the accident.

2022 ◽  
Vol 8 (1) ◽  
pp. 107-113
R. Aldashukurov ◽  
A. Abdykarova ◽  
D. Israilova ◽  
G. Askarbekova ◽  
Zh. Abdullaeva

Research relevance: article presents the incidence of children and grandchildren for 2018–2019 of liquidator workers who took part in cleaning up the contaminated area around the Chernobyl nuclear power plant, as well as residents evacuated from the city of Pripyat and other settlements within a radius of 70 km from the station. The consequences of radiation exposure of Chernobyl accident remain a topical issue. Research objectives: in order to study health status of children and grandchildren of liquidators, outpatient cards and reporting forms no. 15-zdrav “On medical care for people affected by radiation and included in the Kyrgyz State Medical and Dosimetric Register” examined. Research materials and methods: diseases of the endocrine and nervous systems, nutritional disorders, metabolic disorders, mental disorders, diseases of the eye and its adnexa, ear diseases of and mastoid process were studied. Circulatory and respiratory system diseases were analyzed. Research results: animal and cell culture studies show that high doses of ionizing radiation can lead to mutations in offspring. However, there have not been sufficiently large-scale studies on humans that would allow assessing the effect of radiation on the health of offspring. The exposure provokes mutations and incurable diseases, but it is still unclear how it might affect the children affected. It is known that exposure to ionizing radiation increases DNA mutagenesis compared to background values. Conclusions: obtained data substantiate the need for further monitoring of their health, organization of differentiated dispensary observation of this contingent and timely implementation of medical, rehabilitation and preventive measures in order to preserve health of “children and grandchildren of Chernobyl” at all subsequent stages of their life.

2022 ◽  
Vol 8 (1) ◽  
Ni An ◽  
Zhenjie Li ◽  
Xiaodi Yan ◽  
Hainan Zhao ◽  
Yajie Yang ◽  

AbstractThe lung is one of the most sensitive tissues to ionizing radiation, thus, radiation-induced lung injury (RILI) stays a key dose-limiting factor of thoracic radiotherapy. However, there is still little progress in the effective treatment of RILI. Ras-related C3 botulinum toxin substrate1, Rac1, is a small guanosine triphosphatases involved in oxidative stress and apoptosis. Thus, Rac1 may be an important molecule that mediates radiation damage, inhibition of which may produce a protective effect on RILI. By establishing a mouse model of radiation-induced lung injury and orthotopic lung tumor-bearing mouse model, we detected the role of Rac1 inhibition in the protection of RILI and suppression of lung tumor. The results showed that ionizing radiation induces the nuclear translocation of Rac1, the latter then promotes nuclear translocation of P53 and prolongs the residence time of p53 in the nucleus, thereby promoting the transcription of Trp53inp1 which mediates p53-dependent apoptosis. Inhibition of Rac1 significantly reduce the apoptosis of normal lung epithelial cells, thereby effectively alleviating RILI. On the other hand, inhibition of Rac1 could also significantly inhibit the growth of lung tumor, increase the radiation sensitivity of tumor cells. These differential effects of Rac1 inhibition were related to the mutation and overexpression of Rac1 in tumor cells.

2022 ◽  
Giovanni Visci ◽  
Emanuele Rizzello ◽  
Carlotta Zunarelli ◽  
Francesco Saverio Violante ◽  
Paolo Boffetta

Brenna Norton-Baker ◽  
Megan A. Rocha ◽  
Jessica Granger-Jones ◽  
Dmitry A. Fishman ◽  
Rachel W. Martin

2022 ◽  
Kate M MacDonald ◽  
Shirony Nicholson-Puthenveedu ◽  
Maha M Tageldein ◽  
Cheryl Arrowsmith ◽  
Shane M Harding

Micronuclei (MN) are aberrant cytosolic compartments containing broken genomic fragments or whole lagging chromosomes. MN envelopes irreversibly rupture, allowing the viral receptor cGAS to localize to MN and initiate an inflammatory signalling cascade. Here, we demonstrate that MN envelope rupture is not sufficient for cGAS localization. Unlike MN that arise following ionizing radiation (IR), ruptured MN generated from acute transcription stressors DRB or siSRSF1 are refractory to cGAS localization. Recruitment of cGAS to MN is blocked by inhibiting the histone methyltransferase DOT1L prior to IR exposure, demonstrating that cGAS recruitment to MN is dictated by nuclear chromatin organization at the time of DNA damage. Loss of cGAS+ MN, caused either by acute transcription stressors or by preventing DOT1L-deposited histone methylation, corresponded to significantly decreased cGAS-dependent inflammatory signalling. These results implicate nuclear chromatin organization in micronuclear composition and activity, influencing the ability of damage-induced MN to retain cytosolic proteins upon rupture.

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