OBJECTIVES/HYPOTHESIS: The aim of this study was to investigate the effects of a 1.8 GHz continuous electromagnetic fields (EMF) on human nasal mucociliary transport, and to determine the pathophysiology of ciliary beat frequency (CBF) during an EMF-induced change. METHODS: Human nasal mucosa cells were exposed to a 1.8 GHz EMF (SAR=1.0 W/kg), and CBF was analyzed using an optical flow technique with the peak detection method. RESULTS: The 1.8 GHz-exposed group showed a decreased CBF when compared to the control group. In the cytotoxicity assay, difference in survival rates was not found between the two groups. In the EMF-exposed group, protein kinase C (PKC) activity was increased during a PKC activity assay. The broad PKC inhibitor, Calphostin C abolished the EMF-induced decrease of CBF. The EMF-induced decrease of CBF was abolished by GF 109203X, a novel PKC (nPKC) isoform inhibitor, whereas the decrease was not attenuated by Gö-6976, a specific inhibitor of conventional PKC (cPKC) isoform. CONCLUSIONS: EMF may inhibit CBF via an nPKC-dependent mechanism. Therefore, we have confirmed that EMF could decrease CBF by increasing PKC activity.
OBJECTIVES/HYPOTHESIS: The aim of this study was to investigate the effects of a 1.8 GHz continuous electromagnetic fields (EMF) on human nasal mucociliary transport, and to determine the pathophysiology of ciliary beat frequency (CBF) during an EMF-induced change. METHODS:Human nasal mucosa cells were exposed to a 1.8 GHz EMF (SAR=1.0 W/kg), and CBF was analyzed using an optical flow technique with the peak detection method. RESULTS: The 1.8 GHz-exposed group showed a decreased CBF when compared to the control group. In the cytotoxicity assay, difference in survival rates was not found between the two groups. In the EMF-exposed group, protein kinase C (PKC) activity was increased during a PKC activity assay. The broad PKC inhibitor, Calphostin C abolished the EMF-induced decrease of CBF. The EMF-induced decrease of CBF was abolished by GF 109203X, a novel PKC (nPKC) isoform inhibitor, whereas the decrease was not attenuated by Gö-6976, a specific inhibitor of conventional PKC (cPKC) isoform. CONCLUSIONS: EMF may inhibit CBF via an nPKC-dependent mechanism. Therefore, we have confirmed that EMF could decrease CBF by increasing PKC activity.