Abstract
Uranium tailings (UT) are formed as a byproduct of uranium mining and are of potential risk to living organisms. In the present study, we sought to identify potential biomarkers associated with chronic exposure to low dose rate γ radiation originating from UT. We exposed C57BL/6J mice to 30, 100, or 250 μGy/h of gamma radiation originating from UT samples. Nine animals were included in each treatment group. We observed that the liver central vein was significantly enlarged in mice exposed to dose rates of 100 and 250 μGy/h, when compared with nonirradiated controls. Using proteomic techniques, we identified 18 proteins that were differentially expressed (by a factor of at least 2.5-fold) in exposed animals, when compared with controls. We chose glycine N-methyltransferase (GNMT), glutathione S-transferase A3 (GSTA3), and nucleophosmin (NPM) for further investigations. Our data showed that GNMT (at 100 and 250 μGy/h) and NPM (at 250 μGy/h) were up-regulated, and GSTA3 was down-regulated in all of the irradiated groups, indicating that their expression is modulated by chronic gamma radiation exposure. GNMT, GSTA3, and NPM may therefore prove useful as biomarkers of gamma radiation exposure associated with UT. The mechanisms underlying those changes need to be further studied.
Highlights
The biological effects of chronic low dose rate on normal tissues have attracted much attention in recent years [1]
Histological analysis of mouse liver tissue obtained from animals that received different dose rates of Uranium tailings (UT) irradiation over a 500 day period was performed to determine whether any gross change in tissue morphology had occurred
Increased attention has been given to biological effects of low dose rate or low dose radiation (LDR) on normal tissues
Summary
The biological effects of chronic low dose rate on normal tissues have attracted much attention in recent years [1]. Many studies have shown that sustained low dose radiation (LDR) can cause harm to organisms, such as chromosome aberrations [2], genomic instability [3], cell inactivation [4], and tumorigenicity [5]. There is evidence to suggest that ionizing radiation, in addition to other factors, may have an impact on the pathology of neurodegenerative diseases such as Alzheimer’s [7]. There is a large body of literature describing the beneficial effects of LDR exposure, such as the prevention of doxorubicin-induced cardiotoxicity by suppressing mitochondrial-dependent oxidative stress and apoptosis signaling [8]. Research has shown that LDR can activate the adaptive immune response, promoting immune-dependent tumor inhibition [9]
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