Effect of 2.45 GHz Microwave Radiation on the Inner Ear: A Histopathological Study on 2.45 GHz Microwave Radiation and Cochlea.

BACKGROUND: The present study aims to determine the possible low dose-dependent adverse effects of 2.45 GHz microwave exposure and Wi-Fi frequency on the cochlea. METHODS: Twelve pregnant female rats (n=12) and their male newborns were exposed to Wi-Fi frequencies with varying electric field values of 0.6, 1.9, 5, 10 V/m, and 15 V/m during the 21-day gestation period and 45 days after birth, except for the control group. Auditory brainstem response testing was performed before exposure and sacrification. After removal of the cochlea, histopathological examination was conducted by immunohistochemistry methods using caspase (cysteine-aspartic proteases, cysteine aspartates, or cysteine-dependent aspartate-directed proteases)-3, -9, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Kruskal-Wallis and Wilcoxon tests and multivariate analysis of variance were used. RESULTS: Auditory brainstem response thresholds in postexposure tests increased statistically significantly at 5 V/m and above doses. When the number of apoptotic cells was compared in immunohistochemistry examination, significant differences were found at 10 V/m and 15 V/m doses (F(5,15)=23.203, P=.001; Pillai's trace=1.912, η2=0.637). As the magnitude of the electric field increased, all histopathological indicators of apoptosis increased. The most significant effect was noted on caspase-9 staining (η2 c9=0.996), followed by caspase-3 (η2 c3=0.991), and TUNEL staining (η2 t=0.801). Caspase-3, caspase-9, and TUNEL-stained cell densities increased directly by increasing the electric field and power values. CONCLUSION: Apoptosis and immune activity in the cochlea depend on the electric field and power value. Even at low doses, the electromagnetic field in Wi-Fi frequency damages the inner ear and causes apoptosis.

Effect of transtympanic betamethasone delivery to the inner ear.

To investigate the effect of transtympanic betamethasone administration on hearing function with histologic correlation, rats were divided into three transtympanic treatment groups: isotonic saline (group I, n = 10), gentamicin (group II, n = 10) and betamethasone (group III, n = 10). Distortion product otoacoustic emission thresholds were compared on day 10. Also histological effects on cellular apoptosis in both the inner and outer hair cells in organ of Corti and spiral ganglion neurons were evaluated. Distortion product otoacoustic emission thresholds were comparable (p > 0.05) between group I and group III in all measurements. Distortion product otoacoustic emission thresholds of group II were significantly elevated in all measurements when compared with group I (p < 0.05) and group III (p < 0.05). In the Terminal deoxynucleotidyl transferase dUTP Nick End Labelling (TUNEL), Caspase-3, Caspase-8 and Caspase-9 staining method the amount of apoptotic cells in group II were significantly elevated in all measurements compared with group I (p < 0.05). In the TUNEL staining method the amount of apoptotic cells in Group III were significantly elevated compared with group I in both the organ of Corti and spiral ganglion neurons (p < 0.05). The overall histological results revealed that the severity of cellular apoptosis caused by betamethasone was somewhere between isotonic saline and gentamicin. Transtympanic betamethasone does not affect inner ear function as measured by distortion product otoacoustic emission responses, but some increase in cellular apoptosis in the organ of Corti and spiral ganglion neurons was observed. These findings suggest that transtympanic betamethasone may have mild ototoxic effects. Further studies are needed to obtain precise results for transtympanic application of betamethasone.