Abstract

The objective of this study was to approach the basic mechanism(s) underlying reported ovarian apoptotic cell death and fecundity decrease induced by nonionizing radiation (NIR) in Drosophila melanogaster. ROS (Reactive Oxygen Species) levels were measured in the bodies and the ovaries of (sexually mature) 4-day-old flies, following exposure for 0.5, 1, 6, 24 and 96 h to a wireless DECT (Digital Enhanced Cordless Telephone) base radiation (1.88–1.90 GHz). Electrical field intensity was 2.7 V/m, measured within the fly vials and calculated SAR (Specific Absorption Rate) value = 0.009 W/Kg. Male and female bodies showed twofold increase in ROS levels (p < 0.001) after 6 h of exposure, slightly increasing with more irradiation (24 and 96 h). Ovaries of exposed females had a quick response in ROS increase after 0.5 h (1.5-fold, p < 0.001), reaching 2.5-fold after 1 h with no elevation thereafter at 6, 24 and 96 h. ROS levels returned to normal, in the male and the female bodies 24 h after 6 h of exposure of the flies (p < 0.05) and in the ovaries 4 h after 1 h exposure of the females (p < 0.05). It is postulated that the pulsed (at 100 Hz rate and 0.08 ms duration) idle state of the DECT base radiation is capable of inducing free radical formation albeit the very low SAR, leading rapidly to accumulation of ROS in a level-saturation manner under continuous exposure, or in a recovery manner after interruption of radiation, possibly due to activation of the antioxidant machinery of the organism.

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