Abstract
Previous studies have shown that UV radiation and oxidative stress inducers (included also in the ageing process) provoked apoptosis in FRTL-5 cells. In order to examine how UV-C radiation and oxidative stressors affect human primary thyroid cells, the cultured cells kept in the proliferation medium were exposed to increasing doses of UV radiation (254 nm wavelength) and buthionine sulfoxymine (BSO). The cell cycle analysis 18h and 24h after irradiation showed a G0/G1 block. However, 48h after UV exposition, S-phase significantly increased compared to the control, non irradiated cells, indicating possible DNA repair during S-phase of the cell cycle. Additionally, the results pointed out that the younger cells more actively proliferating, were more sensitive to UV radiation or BSO treatment as compared to older and less proliferative cells. The number of apoptotic cells, estimated by annexin V test, increased gradually over time after the UV radiation. The significant difference was seen after 40-48h of UV radiation in comparison with the control, non irradiated cells (p< 0.05). However, the number of apoptotic cells after treatment with BSO was significantly higher as compared to control cells (p<0,05). The difference was even more pronounced after exposing BSO treated cells to UV radiation when about 74% of cells entered apoptosis 96h after treatment. The results show that human primary thyroid cells were more resistant to UV radiation than to oxidative stressors. A difference from FRTL-5 cells that almost all entered apoptosis 48h after irradiation, human cells reather inhibited cell proliferation trying to repair damaged DNA. However, exposing cells to additional oxidative stress induced earlier appearance and higher percentage of apoptosis. In conclusion, the human primary thyroid cells could be a good model to study the influence of different factors that are involved in the ageing process on human tissues.