Pustaka Ilmiah Universitas Padjadjaran

Abstrak

Protective Effects Of Sodium Selenite Supplementation Against Irradiation-induced Damage In Non-cancerous Human Esophageal Cells

The administration of radioprotective compounds is one approach to preventing radiation damage in non-cancerous tissues. Therefore, radioprotective compounds are crucial in clinical radiotherapy. Selenium is a radioprotective compound that has been used in previous clinical studies of radiotherapy. However, evidence regarding the effectiveness of selenium in radiotherapy and the mechanisms underlying theselenium-induced reduction of the side effects of radiotherapy remains insufficient. To further investigate the effectiveness of selenium in radiotherapy, the present study examined the protective effects of sodium selenite supplementation administered prior to X-ray radiation treatment in CHEK-1 non-cancerous human esophageal cells. Sodiumselenite supplementation increased glutathione peroxidase 1 (GPx-1) activity in a dose-and time-dependent manner. The sodium selenite dose that induced the highest GPx-1 activity was determined to be 50 nM for 72 h prior to radiotherapy. The half-maximal inhibitory concentration of sodium selenite in CHEK-1 cells was 3.6 µM. Sodium selenite supplementation increased the survival rate of the cells in a dose-dependent manner and enhaced the egree of cell viability at 72 h post-irradiation (P<0.05). Combined treatment with 50 nM sodium selenite and 2 gray (Gy) X-ray irradiation decreased the number of sub-G cells from 5.9 to 4.2% (P<0.05) and increased the proportion of G1 cells from 58.8 to 62.1%, compared with 2 Gy X-ray irradiation alone; however, this difference was not statistically significant (P=1.00). Western blot analysis revealed that treatment with 2 Gy X-ray irradiation significantly increased the expressionlevels of cleaved poly (ADP-ribose) polymerase (PARP;P<0.05). In addition, combined treatment with 50 nMsodium selenite and 2 Gy X-ray irradiation reduced theexpression levels of cleaved PARP protein, compared with2 Gy X-ray irradiation alone; however, this reduction wasnot statistically significant (P=0.423). These results suggestthat 50 nM sodium selenite supplementation administeredfor 72 h prior to irradiation may protect CHEK-1 cells fromirradiation-induced damage by inhibiting irradiation-inducedapoptosis. Therefore, sodium selenite is a potential radioprotective compound for non-cancerous cells in clinicalradiotherapy.