The frequencies used by mobile phones range from 800 to 3500 MHz, while those described as 3G operate at a frequency of 2100 MHz. While the use of 4G is becoming more prevalent, the effects of the bandwidth of new generation technologies such as 5G and mobile phones on health are still unknown [1–3]. As technology develops, the use of mobile phones becomes more popular, resulting in further discussions on the possible detrimental effects on human health. It has been emphasized that long-term exposure to EMF leads to changes in biological systems through thermal and non-thermal effects resulting from the transfer of energy to tissue. From a biophysical perspective related to the potential thermal effects, it has been reported that the vibration of electrical charges on the cell membrane surface may lead to impaired electrochemical balance and cell dysfunction due to external oscillation, although studies of this subject to date are controversial [3, 4]. Previous studies have reported that the EMF emitted by mobile phones may have adverse effects on the cardiovascular system, immune system, thyroid and hormone secretion, the reproductive system and malignant tumors. Furthermore, studies have shown that at a cellular level, EMF can cause cell division and growth, oxidative stress, apoptosis and DNA replication [5–7].
Cyclins, which play an important role in cell cycle regulation, are a family of proteins that act by binding to cyclin-dependent kinases. D-cyclins (D1, D2, and D3) from the cyclin family bind and activate cyclin-dependent kinase-4 and 6 (CDK4/6) in the G1 phase of the cell cycle and form the cyclin D-CDK4 complex. This complex plays a critical role in the cell cycle by phosphorylating the retinoblastoma protein (RB). Phosphorylation of RB is a molecular switch for the cell cycle, in which the hypophosphorylated RB forms a tight complex with the transcription factor E2F, inhibiting the replication of cells. Phosphorylation of RB, in turn, dissociates the complex and eliminates the transcriptional activity barrier on E2F. It has been reported that the dysregulation of cell cycle control by D-cyclins plays a role in the pathogenesis of various diseases, and that the dysregulation of the activities of these proteins may lead to increased cell proliferation and/or cancer [8–10].
There are many hormones and growth factors that affect cell growth and modify the activity of cyclins through signal transduction. NF-κB is a transcription factor that is involved in such cellular processes as inflammatory and immune cell response, cell cycle regulation, differentiation and protection against apoptosis. Factors such as bacterial endotoxin, phorbol esters, ultraviolet radiation, oxidants, viral proteins and double-stranded RNA activate NF-κB, which has been reported to be effective in controlling cell cycle and cyclin D1 by increasing the activity of cyclin D1 and cyclin D1 kinase holoenzyme complex [9, 11, 12].
In the human metabolism, enzymatic and non-enzymatic antioxidant systems eliminate the harmful effects of free radicals. Among these antioxidants, Se protects cells against oxidative damage by optimizing the activity of glutathione peroxidase and thioredoxin reductase, as well as some other selenoproteins. Recent experimental studies have reported that Se plays an important role in the cell cycle and apoptosis as a micronutrient and chemopreventive agent, depending on the chemical form and dose; however, the mechanism of action has not been fully clarified [5, 13, 14].
The present study assesses cell viability, cyclin D1 levels, and nuclear factor-kappa b activity in an investigation of the effect of selenium on NIH/3T3 fibroblast cells exposed to a 2100 MHz mobile phone signal.