Abstract
Exposure of mammals to ionizing radiation leads to the development of a complex dose-dependent series of physiological and pathological changes. The present study was undertaken to investigate the effect of whole body x-irradiation of male mice with a single w dose of 6 Gy on the levels of some cytokines and parameters of oxidative stress, after one and seven days, in the liver. The possible protective effect of the compatible solute ectoine, which is known to reduce cell stress effects on the molecular level, was evaluated. The x-irradiated mice showed elevated interleukins in the liver. The levels of both the pro-inflammatory (IL-1β and IL-6) and the anti-inflammatory (IL-10) interleukins reached several times the control value with quantitative differences. The disturbance by low-dose x-irradiation also affected PGE2. Malondialdehyde, used as indication of oxidative stress, was elevated in the livers of x-irradiated mice. Although, there were no statistically significant differences in the results of total glutathione among the irradiated mice as compared to control values, there were differences among the values of the reduced and oxidized forms. The calculated redox potentials, showed some variations in the different groups, but were all within the values indicating that the cells are in the proliferative phase and far from the apoptotic phase. Treatment with ectoine modulated all the tested biochemical effects induced by x-irradiation in the liver. All the tested parameters had a tendency to go back to near control values.
Highlights
X-rays represent a form of electromagnetic irradiation that may affect most exposed cells depending on the dose
Treatment of the irradiated mice with ectoine caused a significant decrease of 19.6% and 75.3% below the untreated group
One hypothesis proposes that there is no dose of radiation that can be considered completely safe and that the use of radiation must always be determined on the basis of risk and benefit
Summary
X-rays represent a form of electromagnetic irradiation that may affect most exposed cells depending on the dose. This type of radiation was proposed to cause increased oxidative stress and higher levels of reactive oxygen species (ROS), either directly or through radiolysis of water [1]. This leads to interference with signaling cascades through regulation of protein activities. Free radical signaling could be mediated by cytokines, the participation of which in cellular pathways is modulated by the redox status. The cytokine mediators of oxidative stress can alter redox equilibrium by affecting reduced/oxidized glutathione shuttling and recycling. This, by necessity, indicates alterations in the activity of the participating enzymes [1, 2]
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