Abstract
Introduction: Post-Chernobyl epidemiological studies appointed ionizing radiation (IR) exposure as high-risk factor for thyroid cancer development. Currently, the general population is increasingly exposed to IR deriving from natural and human-made sources. In particular, low-dose IR is of major concern. On the other hand, epidemiological studies demonstrated that iodine deficiency (ID), affecting more than 2 billion individuals worldwide, is also a determinant in thyroid cancer development. However, there are still uncertainties about the combined effects of ID and low-dose IR exposure on thyroid cells. We hypothesize that low-dose IR and ID both stress thyroid cells by an enhanced production of reactive oxygen species (ROS), affecting proliferation and survival.Material & methods: Rat thyroid PCCL3 cells were cultured in iodine-deficient or iodine-sufficient conditions for 6h, 24h or 48h and were irradiated with low (0 Gy, 0.05 Gy, 0.1 Gy), intermediate (0.5 Gy) or high (3 Gy) X-ray doses. Protein expressions of Catalase, (p)AKT1, (p)STAT3, NFkB p52 were determined by Western blot. ROS production and gH2AX/53BP1 foci were dtected by respectively CM-H2DCFDA fluorescent imaging and immunocytochemistry visualized using fluorescence microscopy. Finally, cell cycle distribution was examined by a BrdU/7-AAD assay using flow cytometry. Statistical significance (p
Details
Original language | English |
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Supervisors/Advisors | - Derradji, Hanane, SCK CEN Mentor
- Vandormael, Patrick, Supervisor, External person
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Publisher | - UHasselt - Universiteit Hasselt
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Publication status | Published - 13 Jun 2016 |
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