Ju Hwan Kim

The biological effects of radiofrequency electromagnetic fields (RF-EMFs) remain an unresolved scientific issue with important societal relevance, particularly in the context of the global deployment of fifth-generation (5G) wireless technologies. The skin is continuously exposed to both RF-EMFs and ultraviolet (UV) radiation, a well-established inducer of oxidative stress and DNA damage, making it a relevant model for assessing combined environmental exposures. In this study, we investigated whether post-exposure to 5G RF-EMFs (3.5 and 28 GHz) modulates ultraviolet A (UVA)-induced genotoxic stress in human keratinocytes (HaCaT) and murine melanoma (B16) cells. Post-UV RF-EMF exposure significantly reduced DNA damage markers, including phosphorylated histone H2AX (γH2AX) foci formation (by approximately 30–50%) and comet tail moments (by 60–80%), and suppressed intracellular reactive oxygen species (ROS) accumulation (by 56–93%). These effects were accompanied by selective attenuation of p38 mitogen-activated protein kinase (MAPK) phosphorylation (reduced by 55–85%). The magnitude of molecular protection was comparable to that observed with N-acetylcysteine treatment or pharmacological inhibition of p38 MAPK. In contrast, RF-EMF exposure did not reverse UV-induced reductions in cell viability or alterations in cell cycle distribution, indicating that its protective effects are confined to early molecular stress-response pathways rather than downstream survival outcomes. Together, these findings demonstrate that 5G RF-EMFs can facilitate recovery from UVA-induced molecular damage via redox-sensitive and p38-dependent mechanisms, providing mechanistic insight into the interaction between modern telecommunication frequencies and UV-induced skin stress.

The skin is the largest body organ that can be physiologically affected by exposure to radiofrequency electromagnetic fields (RF-EMFs). We investigated the effect of RF-EMFs on melanogenesis; Mel-Ab melanocytes were exposed to 1760 MHz radiation with a specific absorption rate of 4.0 W/kg for 4 h/day over 4 days. Exposure to the RF-EMF led to skin pigmentation, with a significant increase in melanin production in Mel-Ab melanocytes. The phosphorylation level of cAMP response element binding protein (CREB) and the expression of microphthalmia-associated transcription factor (MITF), which regulate the expression of tyrosinase, were significantly increased in Mel-Ab after RF-EMF exposure. Interestingly, the expression of tyrosinase was significantly increased, but tyrosinase activity was unchanged in the RF-EMF-exposed Mel-Ab cells. Additionally, the expression of p53 and melanocortin 1 receptor (MC1R), which regulate MITF expression, was significantly increased. These results suggest that the RF-EMF induces melanogenesis by increasing phospho-CREB and MITF activity. Importantly, when Mel-Ab cells were incubated at 38 °C, the melanin production and the levels of tyrosinase significantly decreased, indicating that the increase in melanin synthesis by RF-EMF exposure is not due to a thermal effect. In conclusion, RF-EMF exposure induces melanogenesis in Mel-Ab cells through the increased expression of tyrosinase via the activation of MITF or the phosphorylation of CREB, which are initiated by the activation of p53 and MC1R.

The widespread use of wireless communication devices has necessitated unavoidable exposure to radiofrequency electromagnetic fields (RF-EMF). In particular, increasing RF-EMF exposure among children is primarily driven by mobile phone use. Therefore, this study investigated the effects of 1850 MHz RF-EMF exposure at a specific absorption rate of 4.0 W/kg on cortical neurons in mice at postnatal day 28. The results indicated a significant reduction in the number of mushroom-shaped dendritic spines in the prefrontal cortex after daily exposure for 4 weeks. Additionally, prolonged RF-EMF exposure over 9 days led to a gradual decrease in postsynaptic density 95 puncta and inhibited neurite outgrowth in developing cortical neurons. Moreover, the expression levels of genes associated with synapse formation, such as synaptic cell adhesion molecules and cyclin-dependent kinase 5, were reduced in the cerebral cortexes of RF-EMF-exposed mice. Behavioral assessments using the Morris water maze revealed altered spatial learning and memory after the 4-week exposure period. These findings underscore the potential of RF-EMF exposure during childhood to disrupt synaptic function in the cerebral cortex, thereby affecting the developmental stages of the nervous system and potentially influencing later cognitive function.

Ju Hwan Kim and Rajnikant Patel. Korean J Physiol Pharmacol 2023;27:427-36. https://doi.org/10.4196/kjpp.2023.27.5.427

Ju Hwan Kim, Hak Rim Kim and Rajnikant Patel. Biomolecules & Therapeutics 2023;31:340-9. https://doi.org/10.4062/biomolther.2022.130

Exposure to radiofrequency electromagnetic fields (RF-EMFs) has increased rapidly in children, but information on the effects of RF-EMF exposure to the central nervous system in children is limited. In this study, pups and dams were exposed to whole-body RF-EMF at 4.0 W/kg specific absorption rate (SAR) for 5 h per day for 4 weeks (from postnatal day (P) 1 to P28). The effects of RF-EMF exposure on neurons were evaluated by using both pups’ hippocampus and primary cultured hippocampal neurons. The total number of dendritic spines showed statistically significant decreases in the dentate gyrus (DG) but was not altered in the cornu ammonis (CA1) in hippocampal neurons. In particular, the number of mushroom-type dendritic spines showed statistically significant decreases in the CA1 and DG. The expression of glutamate receptors was decreased in mushroom-type dendritic spines in the CA1 and DG of hippocampal neurons following RF-EMF exposure. The expression of brain-derived neurotrophic factor (BDNF) in the CA1 and DG was significantly lower statistically in RF-EMF-exposed mice. The number of post-synaptic density protein 95 (PSD95) puncta gradually increased over time but was significantly decreased statistically at days in vitro (DIV) 5, 7, and 9 following RF-EMF exposure. Decreased BDNF expression was restricted to the soma and was not observed in neurites of hippocampal neurons following RF-EMF exposure. The length of neurite outgrowth and number of branches showed statistically significant decreases, but no changes in the soma size of hippocampal neurons were observed. Further, the memory index showed statistically significant decreases in RF-EMF-exposed mice, suggesting that decreased synaptic density following RF-EMF exposure at early developmental stages may affect memory function. Collectively, these data suggest that hindered neuronal outgrowth following RF-EMF exposure may decrease overall synaptic density during early neurite development of hippocampal neurons.