Soon after the discovery of X-ray by Rontgen in 1895, it became evident that radiation can cause some somatic damage to tissues. The hazards of X-ray exposure were clearly known when many large hospitals had radiology departments. The greatest increased in knowledge about X-ray risks had accrued from the dropping of the two atomic bombs in Japan in 1945 and some other atomic accident. For example, among the Japanese bomb survivors from Hiroshima and Nagasaki, there have been about 400 extra cancer deaths. These were the origin of radiology personnel and people fear from radiation exposure and resistant in against simple X-ray exam (radio phobia). However, new scientific data on the effects radiation on survivors, especially about biologic effect of ionizing rays, background radiation exposure, amount of endogenous radiation, osmosis phenomenon and comparison radiation risk with other risk over lifetime are still being continuously revised and risk estimates updated. Fundamentally, this risk is much lower than whatever already estimated and it is insignificant in diagnostic domain. Better perception of physician from these instances help to prevent of false radio phobia and to make proper use of diagnostic and therapeutic advantages of ionizing beam.

Background: The use of the ionizing radiation in the medical practice has evolved since its beginnings. Their benefit for the patient is considerable in term of comfort, diagnostic and therapeutic effectiveness. It is estimated that 30% to 50% of critical decisions in medical approaches is based on x-ray examination. Using the X-ray as a diagnostic means by clinicians requires appropriate and accurate knowledge about its advantages and negative biologic effects. Purpose: to evaluate the knowledge of medical students in clinical courses in Birjand University of Medical Sciences on ionizing radiation hazards. Methods: In this cross-sectional study, knowledge of medical students (in clinical courses) on 3 categories ( of basic principles of radiobiology, radiation protection and practical issues in radiation protection) assessed by a 20-item questionnaire which its reliability and validity had been well established. chi-square and independent-t tests were employed to analyze data gathered via these questionnaires. Results: Total number of medical students involved in this study was 100. Mean knowledge score was 9.07+/-2.1 (for clerkship students, p <0.05) and 10.13+/-2.73 (for interns p <0.05). Of clerkship students 51.4% and of interns 25.4% obtained good scores (p<0.03) in the radiobiology. But in the other categories (radiation protection and practical aspects of radiation protection) no group achieved good scores. Conclusion: The results indicate that despite the importance of radiation and its consequent hazards, knowledge of medical students is not adequate. It is suggested that the content relevant to radiation and radioactive hazards in medical curricula should be revised, including quantitative and qualitative aspects of the subject. A reasonable step to more effective education regarding radiation and relevant issues is to integrate safety practices in clinical courses.

Backgrounds: It remains unclear whether radiation-induced haemorrhage in the spleen causes iron accumulation, and subsequently, ferroptosis in splenic lymphocytes. In this study, we investigated the occurrence of ferroptosis in splenic lymphocytes of gamma-irradiated mice. Materials and Methods: Mice were subjected to gamma radiation from a 137Cs source. Iron, Ferroportin 1, and iron regulatory protein (IRP) levels in the spleen, and serum iron and hepcidin levels in the blood were measured to study the change in iron metabolism of the irradiated spleen. After Ferrostatin 1/LDN193189 was intraperitoneally injected into mice post-irradiation, the viability of splenic lymphocytes and the splenic index were evaluated to investigate the mechanism of damage induction in splenic lymphocytes. The survival rate of mice was evaluated to identify the radiation mitigator based on the inhibition of ferroptosis. Results: Iron accumulation (up to 0. 62 g/g) observed in the spleen of irradiated mice was due to haemorrhage-based haemosiderin. The iron accumulation triggered the IRP-ferroportin 1 axis to increase the level of serum iron to 121. 65 mmol/l. LDN193189 was used to demonstrate that the iron accumulation decreased the viability of splenic lymphocytes in irradiated mice, which was subsequently demonstrated to attribute to ferroptosis with the use of Ferrostatin 1 and through detection of ferroptosis-related parameters. The survival rate of irradiated mice was improved upon Ferrostatin-1 (60% with a duration of 120 days) or LDN193189 (40% for the same duration) treatment. Conclusion: radiation-induced haemorrhage causes ferroptosis in splenic lymphocytes, and anti-ferroptosis is a potential strategy to alleviate immune damage in hematopoietic acute radiation sickness.

Background: Avoiding exposure to ionizing radiation due to environmental factors is almost inevitable in daily life. Here, we aimed to investigate the possible immunomodulatory effects of ionizing radiation on NK and T cell activation using Peripheral Blood Mononuclear Cells (PBMC). We measured the pro-inflammatory cytokines INFγ, , IL-2 and TNFα, , as well as Granzyme B. In addition, we determined the expression levels of CD28, NKG2D (CD314) receptors, which play a key role in the activation of T and NK cells, respectively. Materials and Methods: 20 ml peripheral blood samples were taken from healthy volunteer donors and exposed to radiation doses of 0, 1, 3 and 5 Gy. ELISA analysis was used to measure Granzyme B, INFy, TNFα,and IL2. Expression of CD28, NKG2D (CD314) receptors was measured by qRT-PCR analysis. Apoptosis and necrosis were measured by AnnexinV/7AAD analysis. Catalase activity was measured using hemolysates from irradiated blood samples. Results: Here we show that IR exposure induces necrotic cell death in PBMCs as the main response. IR exposure significantly induced secretions of Granzyme B, TNFα, , IL2, and INFγ,in a dose-dependent manner. In addition, mRNA levels of CD28 and NKG2D expressions were increased by 3 Gy IR exposure, but decreased by 5 Gy, while catalase activity increases with 1 Gy IR treatment, 3 and 5 Gy decreases. Conclusions: Our results suggest that not only high doses but even low doses of radiation can modulate the immune response through cytokine secretion and activation of T and NK cell receptors.