## 4 Discussion
The cytotoxic effect of resveratrol may induce the formation of large amounts of ROS, which may lead to the failure of a cell's defense mechanisms and its death. In addition, resveratrol can induce oxidative stress in the endoplasmic reticulum and reticulum stress can then lead to cell apoptosis. In the study by [PERSON] et al. [25], resveratrol inhibited the viability of melanoma (A375 SM) cells by increasing the expression of p21 and p27, which inhibited the expression of cyclin B and promoted cell cycle death. In addition, resveratrol increased the production of cellular ROS and simultaneously induced the ER stress pathway in the melanoma cells. Moreover, in this study, resveratrol induced the mitochondrial apoptotic pathway in the melanoma cells through the ROS-p38-p53 pathway by upregulating the p-p38 MAPK protein and also via the p53 and ER stress pathway by upregulating the p-elF2\(\alpha\) and CHOP protein expression. Enhanced ROS-p38-p53 and ER stress pathways promoted apoptosis by downregulating Bcl-2 and upregulating Bax. In the studies of [PERSON] et al. [26], it was found that resveratrol caused a significant decrease in the proliferation rate of melanoma cells (HT-144 line). It was observed that the decrease was dependent on the dose of resveratrol that had been used. Another MEK \(\frac{1}{2}\) factor, which is a member of the MAPK signaling pathway, is responsible for ERK \(\frac{1}{2}\) inhibition. In turn, [PERSON] et al. [27] investigated whether the anticancer effect of resveratrol is related to the change in the cell cycle of melanoma. Their studies showed a strong accumulation in the S phase and a very strong decrease in the G1 phase, and immunoblotting analyses showed that resveratrol caused an increase in the expression of cyclin A. In a study by [PERSON] et al. [28], it was confirmed that, at a concentration of 80 \(\upmu\)M, resveratrol had a cytotoxic effect on the cells of murine macrophages (RAW264.7) by producing large amounts of free radicals. Moreover, in the studies by [PERSON] et al. [29], it was found that resveratrol and its synthetic derivatives can act against cancer by initiating the lipid peroxidation process in colon cancer cells, thus leading to the phenomenon of ferroptosis. Ferroptosis is a non-autophagous programmed cell death that results from the accumulation of lipid peroxidation products and is dependent on iron ions and free radicals. Many researchers believe that the induction of ferroptosis in cancer cells may be the one of the most effective methods of fighting cancer [30; 31]. The free radical process of lipid peroxidation occurs during the course of physiological metabolism. However, when the concentration of free radicals that can initiate it increases, this process is stimulated. Increased lipid peroxidation damages the cell and subcellular membranes, thereby disrupting the transport of ions and metabolites. In our study, the concentration of malondialdehydedehyde (MDA), one of the markers that are used to assess the advancement of the lipid peroxidation process, was also determined. The accumulation of MDA probably leads to ferroptosis and contributes to the oxidation-reduction damage in melanoma cells. [PERSON] et al. [32] also reported that the use of immunotherapy caused an increased lipid peroxidation, MDA accumulation and ferroptosis, which led to the death of ovarian and melanoma cancer cells. The main purpose of our study was to investigate the effect of the co-exposure of C32 and Colo829 cells to a static magnetic field and resveratrol on the oxidation-reduction parameters of cells. To date, there have been no studies on the interaction of an SMF and resveratrol; therefore, it is not known whether a magnetic field will enhance the anticancer properties of resveratrol or will have a protective effect on melanoma cells. In a study by [PERSON] et al. [33], it was found that the induction of a 1 T SMF increased the anticancer efficacy of an mTOR inhibitor in nasopharyngeal cancer cells. Moreover, in their studies,Sabo et al.