Ece MİSER SALİHOĞLU, Mualla Pınar ELÇİ, Tuğba FATSA, Sema ÖREN, Meriç EŞMEKAYA, Sevgi YARDIM
Turkish Journal of Pharmaceutical Sciences - 2026;23(3):130-139
Objectives: Radiofrequency (RF) fields have been classified as probable human carcinogens and nonthermal. RF radiation can increase oxidative stress and inflammation in tissues. Vitamin D has been studied for many years for its anti-cancer properties and its ability to suppress cancer cell growth. In this study, we aimed to examine the effects of RF exposure on cell viability, free radical formation, and inflammation, as well as the therapeutic effect of vitamin D against such effects. MCF-7 and MDA-MB-231 cells were exposed to 2.1-GHz W-CDMA-modulated RF radiation. Materials and Methods: The MTT was used for cell viability, and the FITC-conjugated annexin-V/PI was applied for apoptosis. The vitamin D receptor (VDR), NF-kappaB, cyclooxygenase-2 (COX-2), and p53 gene expression levels were studied using real-time PCR. Reactive oxygen species (ROS) analysis was performed using flow cytometry. Results: A statistically significant decrease in MCF-7 cell viability (p < 0.001) was observed with increasing doses of calcitriol compared to the control group; no significant difference in MDA-MB-231 cell viability was observed (p > 0.05). ROS analysis revealed that calcitriol caused significant decreases in cell viability in both cell types. Both cell lines showed a statistically significant increase in p53 expression with increasing calcitriol doses. An increase in the expression of VDR, NF-kappaB B, and COX-2 was also observed in MCF-7 cells. Conclusion: We observed that while calcitriol administered after RF exposure did not cause statistically significant changes in ROS levels, we observed that it caused an increase in messenger RNA expression of apoptosis and inflammation markers, which could be evaluated in cancer treatment or prevention.
