Evaluating the radioprotective effect of green barley juice on male rats.

PURPOSE: DNA damage accounts for most biological effects of ionizing radiation. Antioxidants are known for their protective effect by preventing DNA damage. This pilot study aimed to evaluate the potential radioprotective effect of Natural SOD®, a green barley juice rich in antioxidants, on DNA damage in the testes and lymphocytes of Wistar rats exposed to ionizing radiation. MATERIALS AND METHODS: Male Wistar rats (n = 15) were selected and equally divided into three groups. Rats in one of the groups were pretreated orally with Natural SOD® for 14 days, while rats in another group were sham-pretreated with saline solution. Rats in both these groups were afterwards subjected to a single dose of 6 Gy X-ray whole-body irradiation. The control group did not receive any treatment and was not irradiated. Shortly after X-ray exposure, all rats were sacrificed and testes and blood were collected. Gamma-H2AX and histopathological assessment in the testes, along with comet assay of lymphocytes were performed. RESULTS: Histopathological examination of the testes showed no significant architectural alterations. Immunofluorescent staining of γ-H2AX revealed more DNA double-strand break sites in testicular cells from sham animals compared to Natural SOD® pretreated rats. Alkaline comet assay results showed increased DNA damage in lymphocytes of irradiated rats compared to the control group with little differences between the pretreated groups. Animals pretreated with Natural SOD showed slightly reduced DNA damage compared to sham-pretreated rats. These findings suggest a potential protective effect of Natural SOD® against radiation-induced DNA damage. CONCLUSIONS: Natural SOD® exhibited a potential prophylactic radioprotective effect in rats, particularly in testes. Further investigations to determine medium and long-term effects of X-ray in animals administered Natural SOD® are needed to better estimate the radioprotective effect.

Pilot Study of the Long-Term Effects of Radiofrequency Electromagnetic Radiation Exposure on the Mouse Brain.

The increasing radiofrequency (RF) electromagnetic radiation pollution resulting from the development and use of technologies utilizing RF has sparked debate about the possible biological effects of said radiation. Of particular concern is the potential impact on the brain, due to the close proximity of communication devices to the head. The main aim of this study was to examine the effects of long-term exposure to RF on the brains of mice in a real-life scenario simulation compared to a laboratory setting. The animals were exposed continuously for 16 weeks to RF using a household Wi-Fi router and a laboratory device with a frequency of 2.45 GHz, and were compared to a sham-exposed group. Before and after exposure, the mice underwent behavioral tests (open-field test and Y-maze); at the end of the exposure period, the brain was harvested for histopathological analysis and assessment of DNA methylation levels. Long-term exposure of mice to 2.45 GHz RF radiation increased their locomotor activity, yet did not cause significant structural or morphological changes in their brains. Global DNA methylation was lower in exposed mice compared to sham mice. Further research is needed to understand the mechanisms behind these effects and to understand the potential effects of RF radiation on brain function.

Inflammatory status of the pancreas in NOD mice that do not develop overt diabetes.

Type 1 diabetes (T1D) is an autoimmune disease in which immune cells target the pancreatic islets and destroy the ß-cells, resulting in hyperglycemia and decreased plasmatic insulin levels. The non-obese diabetic (NOD) mouse is the most used animal model for studying diabetes because it spontaneously develops T1D and shares similarities with the human disease. A hallmark feature of this model is the appearance of insulitis, defined as an inflammatory cell infiltration of the pancreatic islets. However, a small percentage of NOD mice do not develop overt diabetes even after 28-35 weeks of age. Thus, we questioned the status of the pancreatic islets in these non-diabetic NOD mice, with particular focus on islet inflammation and plasmatic insulin levels, in comparison to pre-diabetic (11 weeks old) and new-onset diabetic mice. Diabetes progression was evaluated by assessing blood glucose and pancreas histology. The inflammatory score was determined on Hematoxylin-Eosin (HE)-stained sections of pancreas. Plasma insulin was detected by enzyme-linked immunosorbent assay (ELISA). The results showed that inflammation increased in an age-dependent manner in all mice, irrespective of their diabetic status. Mostly affected within the analyzed groups were the 28 weeks old non-diabetic NOD mice, in which insulin production was reduced and inversely correlated with the inflammatory status. We conclude that in NOD mice, pancreatic inflammation progresses independently of diabetes onset and clinical signs of disease. Most likely, the NOD females that do not develop overt diabetes preserve a small mass of functional ß-cells, which is able to provide the physiological insulin levels and avoid diabetes onset.

Hypoxic preconditioning - A nonpharmacological approach in COVID-19 prevention.

Hypoxia is defined by low oxygen concentration in organs, tissues, and cells. Maintaining oxygen homeostasis represents the essential cellular metabolic process for the structural integrity of tissues in different pathological conditions, including severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. Considering the role of hypoxia-inducible factor-1 as the regulator of cellular response to hypoxia and its involvement in angiogenesis, erythropoiesis, glucose metabolism, inflammation, we propose hypoxic preconditioning (HPC) as a novel prevention therapeutic approach on healthy contacts of patients with coronavirus disease-2019 (COVID-19). To date, several studies revealed the beneficial effects of HPC in ischemia, kidney failure, and in pulmonary function recovery of patients who underwent lung surgery. HPC increases the expression of factors that promote cell survival and angiogenesis, induces an anti-inflammatory outcome, triggers coordinated hypoxia responses that promote erythropoiesis, and mobilizes the circulating progenitor cells. Furthermore, the mesenchymal stem cells (MSC) exposed to HPC show improvement of their regenerative capacities and increases the effectiveness of stem cell therapy in different pathologies, including COVID-19. In conclusion, HPC should be considered as an approach with beneficial outcomes and without significant side effects when the organism is severely exposed to the same stressor. HPC appears as a trigger to mechanisms that improve and maintain tissue oxygenation and repair, a main goal in different pathologies, including COVID-19 or other respiratory conditions.