An Evaluation of Neuronal PARP-1 and Caspase-3 Levels in the Brain Tissue of Female Rats Exposed to Electromagnetic Fields at Different Gestational Stages

Abstract

Foetal exposure to electromagnetic fields (EMFs) may cause marked neurocognitive impairment, although the mechanisms involved are still unclear. EMF induces region-specific neuronal and astroglial death in the rat hippocampus. Poly (ADP-ribose) polymerase-1 (PARP-1) regulates necrosis, apoptosis and other cellular processes occurring following injury. This study, therefore, investigated whether PARP-1 also regulates neuronal responses in the hippocampus of rats subjected to EMF radiation during different developmental periods. Male and female rats were first allowed to mate in separate cages. Rats identified as pregnant were then divided into four groups. A 900-MHz EMF was applied for 2 h daily on gestational days (GD) 1–7, GD 8–14 and GD 15–21. The female offspring were sacrificed at the end of the 28th postnatal day, and PARP-1 and Caspase-3 expressions in the hippocampus were then evaluated. No special treatment was applied to the control group. In the EMF-exposed group, pyramidal neurons in the cornu ammonis (CA) region appeared normal after exposure on GD 1–7 but were darkly stained and shrunken after exposure on GD 15–21, while the majority of granular cells exhibited a normal appearance during all GDs. The group exposed to EMF on GD 15–21 exhibited strong PARP-1 and Caspase-3 immune reactivity in CA and dentate gyrus (DG) cells. Higher H-scores were also observed in the EMF-exposed group following GD 15–21 irradiation. As a result, a 900-MHz EMF application at GD 15–21, which coincides with hippocampal neurogenesis, triggered hippocampal neuron cell death by activating PARP-1 and Caspase-3.