## 4 Discussion  
This work complements our previous works on the effects of fluoride on cell systems [11; 12; 23]. The toxicity of fluorine compounds has been proven and the results of the research have been widely described [24; 25; 26]. Among studies of a SMF as a neutralizer for the toxic effects of fluoride, in this study we focused on the process of apoptosis in correlation with oxidative stress and the NRF2 pathway. The process of apoptosis and the oxidative stress process are often discussed in the literature due to the number of diseases they cause [27; 28; 29; 30]. It is known that free radicals induce apoptosis [27]. Although high levels of reactive oxygen species/reactive nitrogen species (ROS/RNS) are associated with apoptosis, the modulation of the activity of the transcription factors is triggered by low levels of free radicals [31]. There are extensive studies that show the influence of fluorine compounds on the apoptosis process and the oxidative system. In a study by [PERSON] et al. [32], an increase in the production of ROS in microglia cells that had been treated with fluoride was proven. Additionally, [PERSON] et al. [33] proved the toxic effect of NaF on the vital functions of Wistar rats based on an analysis of the oxidative system. Moreover, in a study by [PERSON] et al. [34], the effect of NaF on the process of apoptosis and oxidative stress in the livers of mice was demonstrated. Despite numerous studies that confirm the toxic effect of fluoride, there are few studies that show the impact of SMFs in relation to fluorine compounds. Therefore, in our study we analysed the transcriptional activity of the genes that are related to the cellular oxidative system and the genes that are related to apoptosis in a fluoride-treated cell culture and SMF. The analyses showed an increase in the expression of the \(SOD1\), \(SOD2\) and \(GSR\) genes in the culture that had been treated with a high-intensity SMF. Moreover, the analysis of the transcriptional activity of the selected genes that are related to apoptosis indicated a decrease in the expression of the genes that are involved in the induction of apoptosis under the influence of a SMF. This gives rise to the assumption that exposure to a SMF causes the normalization of apoptosis and redox homeostasis in cells that have been disturbed by fluoride. A SMF is another factor that may be involved in neutralizing the toxic effects of fluorine compounds [35]. Figure 2: The protein interaction network created in a STRING database. The thickness of the line between the proteins indicates the degree of confidence prediction of the interaction. The toxicity of fluorine compounds [36; 37] was confirmed once again in the next stage of our own study on cell viability, which was assessed using the flow cytometer method. It was reaffirmed that exposure to a SMF reduced programmed cell death. Fluoride is also known to inhibit Nrf2, which results in a reduction in the ability of cells to defend themselves against free radicals and oxidative stress [13]. In turn, a SMF activates the pathway that is associated with Nrf2 by increasing the expression of this gene, which strengthens the antioxidant defense of cells and increases the activity of the antioxidant enzymes. In our study, we showed the relationship between the apoptotic process and the antioxidant system by linking them to Nrf2, which was confirmed by previous studies. [PERSON] el al. [38] demonstrated that the inhibition of the activation of IL-1\(\beta\) induced external and internal apoptotic pathways as a result of the activation of Nrf2 in the OA chondrocytes. Other studies have also indicated a decrease in the rate of apoptosis after an increase in the expression of Nrf2 followed by a decrease in the activity of the caspases and an increase in the expression of Bcl-2/Bax, HO-1 [39]. However, [PERSON] et al.