A total of 690 adult female flies, wild type or mutants, were exposed at two different specific absorption rates: at 1.6 W/kg representing the exposure limit proposed by the American National Standards Institute (ANSI) and at 4 W/kg. At least three independent experiments were performed in each electromagnetic field exposure condition. To prove whether decreased viability after exposure is related to changed anti-oxidant status two transgenic mutant flies exhibiting defective superoxide dismutase were crossed (Actin5C-Gal4 and UAS-SOD1IR or UAS-SOD2IR).
|Exposure duration||continuous for 6, 12, 18, 24, 30, and 36 h|
|Chamber||The exposure device was placed in a chamber maintained at 25 ± 0.1 °C to avoid thermal effects.|
|Setup||Flies were exposed in the device in a 100-mm Petri dish with a wet filter paper to maintain humidity.|
|Additional info||At least three independent experiments were performed in each exposure condition.|
At the specific absorption rate 1.6 W/kg, more than 90% of the flies were viable even after the 30 hours exposure. However, at the specific absorption rate 4 W/kg, viability was decreasing from the 12 hours exposure. Only 10% of the flies survived after the 30 hours exposure.
The exposure significantly increased intercellular ROS levels by time and intensity. Superoxide dismutase defect mutants showed lower viability compared to the wild type.
The electromagnetic field exposures activated ERK and JNK signal transduction pathway, but not p38 kinase signal transduction pathway. Interestingly, the specific absorption rate 1.6 W/kg activated mainly ERK signal transduction pathway and expression of an anti-apoptotic gene, whereas the specific absorption rate 4 W/kg strongly activated JNK signal transduction pathway and expression of apoptotic genes.
In addition, the specific absorption rate 4 W/kg amplified the number of apoptotic cells in the fly brain.