## 1 Introduction  
Fluoride toxicity is linked with, among others, the induction of oxidative stress. A redox imbalance disrupts the cell cycle, the proliferation process and contributes to the induction of programmed cell death [1, 2]. Moreover, changes at the cellular as well as molecular levels lead to the development of many diseases such as cancer, neurodegenerative diseases or cardiovascular diseases [3, 4, 5].  
Static magnetic fields (SMF) are ubiquitous in everyday life. Magnetic fields are widespread in the natural environment, and their effect on living organisms has been the subject of many investigations. The presence of magnetic fields in everyday life leads to the hazard of functional disturbances in cells, tissues and biological systems [6]. The results of research to date have not given an unequivocal answer about the beneficial and/or adverse impact of a SMF on the human body. However, it is known that, by affecting the cell membranes, it can alter the intracellular signaling, which can then stimulate the transcription and translation processes, which has implications for numerous cellular processes [7, 8].  
Despite the fact that the mechanisms of SMF are not fully understood and although research is still ongoing, there have been reports of the possibility of reducing oxidative stress due to the effects of SMF [PERSON] et al. [9] detected a decrease in the levels of malondialdehydedehyde (MDA), nitric oxide (NO) and the glycation end products (AGEs) after exposure to SMF for five days in an animal model. In addition, in a study of men, [PERSON] et al. [10] found a decrease in the oxidative stress index (OSI) and total oxidant status (TOS) after exposure to a SMF. A similar SMF effect was also observed at the cellular level [11; 12].  
One of the pathways that are important for redox homeostasis is the Nrf2-ARE signaling pathway (NRF2/NFE2L2--nuclear factor, erythroid 2 like 2; ARE--antioxidant responsive element) [13], which is activated by oxidation reactions. A further mechanism of action is the induction of target genes (Nrf2 binds to an ARE). The expression of these genes creates resistance to oxidative stress [14; 15]. This is related to the protection of cellular homeostasis and detoxifying genes. This is especially important in the course of inflammation, stress or carcinogenic processes [16]. Due to its mechanism of action, the Nrf2 transcription factor has been used as a modulator in diseases related to oxidative stress. In their study, [PERSON] et al. [17] observed an induction of the NRF2 pathway as a result of exposure to perfluorooctanesulfonate (PFOS) along with an improvement as a result of treatment with the reactive oxygen species (ROS) scavenger N-acetyl-1 cysteine (NAC). However, in the study of [PERSON] et al. [18], a significant decrease in the level of the antioxidant enzymes and an increase in ROS as a result of the down-regulation of si-NRF2 in pregnant women was observed relative to the control group. In addition, the Nrf2 transcription factor has been used as a marker of the effectiveness of the insoluble-bound polyphenols of the adlay seed in inhibiting oxidative stress in Hep G2 cells [14].  
In summary, both fluoride and SMF are associated with oxidative stress, and thus programmed cell death. In addition, there is an environmental and occupational exposure to both factors. Therefore, it is important to learn about the possible effects of exposure to them in order to protect workers. Therefore, the aim of our study was to assess the relationship between oxidative stress and apoptosis in cells that had been simultaneously exposed to fluoride and a SMF with a different magnetic induction and to determine whether the Nrf2-signaling pathway is involved in these effects.