## 3 Results
Application of SeNrs to L-929 mouse fibroblasts caused the generation of Ca\({}^{2+}\) signals even at a concentration of 0.5 \(\upmu\)g/mL, and Ca\({}^{2+}\) signals had a combined form of kinetics, a quick rise in [Ca\({}^{2+}\)]\({}_{\mathrm{i}}\) followed by a slow increase in the baseline level of [Ca\({}^{2+}\)]\({}_{\mathrm{i}}\) (Figure 3C). However, the application of SeNPs to L-929 cells did not cause Ca\({}^{2+}\) signals comparable with the application of SeNrs. In L-929 cells, a slow increase in [Ca\({}^{2+}\)]\({}_{\mathrm{i}}\) was recorded upon 2.5 and 5 \(\upmu\)g/mL SeNPs, while 10 \(\upmu\)g/mL resulted in a transient increase in [Ca\({}^{2+}\)]\({}_{\mathrm{i}}\) (Figure 3D). The cellular Ca\({}^{2+}\) signals were a low amplitude. For L-929 cells, the EC\({}_{50}\) value upon application of SeNrs was 2.5 \(\pm\) 0.005 \(\upmu\)g/mL, and for SeNPs, it was 2.9 \(\pm\) 0.011 \(\upmu\)g/mL (Figure 3F). Thus, two different sources of nanoselenium have different effects on the Ca\({}^{2+}\) signaling system of cells. In A-172 cells, SeNrs induce a slow increase in [Ca\({}^{2+}\)]\({}_{\mathrm{i}}\) to the new stationary level of [Ca\({}^{2+}\)]\({}_{\mathrm{i}}\), while SeNPs induce a temporary growth in [Ca\({}^{2+}\)]\({}_{\mathrm{i}}\). In L-929 mouse fibroblast cells, the Ca\({}^{2+}\) signaling system was activated only when SeNrs was used, and the application of SeNPs caused Ca\({}^{2+}\) signals only in a high concentration range. Comparative Analysis of the Praopoptotic Effect of Selenium Nanofibers and Selenium Nanoparticles on Human Glioblastoma Cells A-172 and Mouse Fibroblast Cells L-929  
An increase in cellular [Ca\({}^{2+}\)]\({}_{\mathrm{i}}\) can regulate both cell survival pathways and activate pro-apoptotic signaling cascades [27; 28]. Preincubation of A-172 cells with different SeNrs concentrations during 24 h resulted in 5-15% of cells on the early stage of apoptosis. Late stages of apoptosis were observed in 52-67% of cells (Figure 4A and Table 3). The pro-apoptotic effect of SeNrs was dose-dependent and increased with an increase in the SeNrs concentration. An increase in the pro-apoptotic effect occurred with an increase in the time of incubation of A-172 cells with SeNrs up to 48 h. Approximately 19-26% of the cells were registered in the early stages of apoptosis and 69-73% of the cells were detected in the late stages of apoptosis. At the same time, necrosis was detected only in single cells and when using high (5-10 \(\upmu\)g/mL) concentrations of SeNrs (Figure 4C, Table 3). Early stages of apoptosis were activated in 2-8% of cells and late stages of apoptosis in 18-59% of cells after 24 h pre-incubation of glioblastoma A-172 cells with various concentrations of SeNPs (Figure 4B, Table 4). After 24 h exposure of A-172 cells with SeNPs, we did not register necrotic cells. Early stages of apoptosis were recorded in 4-17% of cells and late stages in 44-57% of cells after 48 h of pre-incubation (Figure 4D, Table 4). At the same time, necrotic death was recorded in 14-52% of cells after pre-incubation with 5 \(\upmu\)g/mL and 10 \(\upmu\)g/mL SeNPs, respectively (Figure 4D, Table 4). Early stages of apoptosis were observed in 4-11% of cells after 24-h pre-incubation of mouse fibroblasts (L-929) with SeNrs, with the highest percentage of such cells observed when using 1 \(\upmu\)g/mL (Figure 5A and Table 5). Under the action of SeNrs for 24 h, there was no mass death of fibroblasts. Increasing the preincubation time with SeNrs up to 48 h resulted in a increase in the percentage of cells at the early stage of apoptosis (9-14% of cells). The late stages of apoptosis and necrosis were not induced (Figure 5C and Table 5).