## 3 Results
Treatment of glioblastoma cells with two types of nanoselenium composites contributed to changes in mRNA expression of a number ER resident selenoproteins, as well as selenium-containing glutathione peroxididases (GPX1 and GPX4) and thioredoxin reductases (TXNRD1 and TXNRD3). So, as shown in Figure 8A, it can be noted that at SeNPs concentrations of 5 and 10 \(\upmu\)g/mL the expression of mRNA of the selenoproteins SELENOM, SELENOM, SELENOM, and SELENOF was significantly increased, while SeNrs at the same concentrations cause the increase in selenoproteins SELENOM and SELENOK (Figure 8A, orange columns). Interestingly, the main effect of enhancing selenoprotein mRNA expression was observed after the exposure of A-172 cells to SeNrs at concentration of 5 \(\upmu\)g/mL rather than 10 \(\upmu\)g/mL. This is typical for such selenoproteins as SELENOS, SELENOT, SELENOF and SELENON, and two thioredoxin reductases (TXNRD1 and TXNRD3), whose mRNA expression increased two or more times. At the same time, a more than two-time decrease in the expression of SELENOT and TXNRD3 mRNA was recorded after these cells were influenced by SeNrs at a concentration of 10 \(\upmu\)g/mL. Significant changes in mRNA expression of most of the studied selenoprotein genes do not occur when SeNrs are applied to L-929 mouse fibroblasts (Figure 8B, orange columns). Incubation of cells of this line with different concentrations of SeNPs resulted in an mRNA expression increase in the SELENOK, SELENOS, SELENOT and GPX1 genes (Figure 8B, gray columns). Thus, both selenium nanocomposites are characterized by a pronounced increase in the mRNA expression of ER stress genes, selenoproteins and proapoptotic genes in glioblastoma cancer cells, excluding fibroblast cells. At the same time, there is a trend of a more pronounced pro-apoptotic effect of SeNrs, since they had an effect at lower concentrations compared to SeNPs. Figure 8: The expression patterns of genes encoding selenoproteins and selenium-containing proteins in A-172 (**A**) and L-929 (**B**) cells after 24-h incubation with different concentrations (1, 5, 10 \(\upmu\)g/mL) of selenium nanofibers (SeNrs) or selenium nanoparticles (SeNPs). The gene expression level was taken as 1 in control cells. \(n=3\). The Effect of Various SeNrs and SeNPs Concentrations on the Ca\({}^{2+}\) Capacity of the Endoplasmic Reticulum of Human Glioblastoma Cells and Mouse Fibroblasts  
We have previously shown that SeNPs selectively act on cancer cells and deplete the Ca\({}^{2+}\) stores of the endoplasmic reticulum without affecting the Ca\({}^{2+}\) depot of astrocytes [29]. A-172 cell pre-incubation with SeNPs with concentrations ranging from 1 to 10 \(\mu\)g/mL during 24 h caused a dose-dependent depletion of ER Ca\({}^{2+}\) stores. Application of thapsigargin (TG) to A-172 cells in medium nominally free of calcium led to high [Ca\({}^{2+}\)] growth (Figure 9A, black curve). However, there was a significant decrease in the amplitude of Ca\({}^{2+}\) cell signals in response to the use of TG after 24-h incubation of cells with SeNPs (Figure 9A, blue, pink and purple curves). Pre-incubation of glioblastoma cells with the same SeNrs concentrations for 24 h led to a similar or more pronounced suppression of the signal amplitudes of calcium ions to the application of TG (Figure 9A, red, green and light pink curves). Pre-incubation of A-172 cells with SeNPs or SeNrs during a 48-h period resulted in the complete absence of cellular Ca\({}^{2+}\) signals to the application of TG (Figure 9C), which indicates a complete depletion of the ER Ca\({}^{2+}\) pool. Figure 9: Effect of A-172 human glioblastoma cells incubation (**A,C**) and L-929 mouse fibroblast cells (**B,D**) with different (1, 5, 10 \(\mu\)g/mL) selenium nanorod (SeNrs) or selenium nanoparticle (SeNPs) concentrations on Ca\({}^{2+}\) capacity of endoplasmic reticulum.