Electromagnetic radiation at 900 MHz induces sperm apoptosis through bcl-2, bax and caspase-3 signaling pathways in rats

Abstract

BackgroundThe decreased reproductive capacity of men is an important factor contributing to infertility. Accumulating evidence has shown that Electromagnetic radiation potentially has negative effects on human health. However, whether radio frequency electromagnetic radiation (RF-EMR) affects the human reproductive system still requires further investigation. Therefore, The present study investigates whether RF-EMR at a frequency of 900 MHz can trigger sperm cell apoptosis and affect semen morphology, concentration, and microstructure.MethodsTwenty four rats were exposed to 900 MHz electromagnetic radiation with a special absorption rate of 0.66 ± 0.01 W/kg for 2 h/d. After 50d, the sperm count, morphology, apoptosis, reactive oxygen species (ROS), and total antioxidant capacity (TAC), representing the sum of enzymatic and nonenzymatic antioxidants, were investigated. Western blotting and reverse transcriptase PCR were used to determine the expression levels of apoptosis-related proteins and genes, including bcl-2, bax, cytochrome c, and capase-3.ResultsIn the present study, the percentage of apoptotic sperm cells in the exposure group was significantly increased by 91.42 % compared with the control group. Moreover, the ROS concentration in exposure group was increased by 46.21 %, while the TAC was decreased by 28.01 %. Radiation also dramatically decreased the protein and mRNA expression of bcl-2 and increased that of bax, cytochrome c, and capase-3.ConclusionRF-EMR increases the ROS level and decreases TAC in rat sperm. Excessive oxidative stress alters the expression levels of apoptosis-related genes and triggers sperm apoptosis through bcl-2, bax, cytochrome c and caspase-3 signaling pathways.

Light and electron microscopic study on the effect of immobilization stress on adrenal cortex of adult rats and possible ameliorative role of vitamin E.

“…These results can be referred to degenerative changes in the cortical cells. The previous results were confirmed by Liu et al [21] who reported that excessive oxidative stress alters the expression levels of apoptosis-related genes and triggers cell apoptosis and degeneration through bcl-2, bax and caspase-3 signaling pathways. This occurs in response to increased secretion of ACTH due to stress as this hormone stimulates both ZF and ZR to produce cortisol.…”

Inhibition by Egb761 of the effect of cellphone radiation on the male reproductive system

“…Spermatozoa consist of a high rate of polyunsaturated fatty acids, and therefore they are easily affected by these factors (13). It has recently been reported that antioxidant capacity diminished in human semen depending on exposure to cellphone radiation, and as a result, fertilization potential could be diminished or destroyed (11,14,15). On the other hand, it is stated that the effect of antioxidant substances can improve sperm quality and increase fertility (16,17).…”

“…These pathologies cause oxidative damage, along with an increase in reactive oxygen radicals (ROS) and a decrease in antioxidant capacity (11). ROS target all structures of the cell, and especially the lipid membranes (12).…”

“…Although the effects of cellphone EMR were investigated by many studies, some current results are controversial (5,38). Cellphone EMR waves induce oxidative stress and affect testicular structure and functions; (9) spermatogenesis is impacted (11,39) and it may lead to future infertility. ROS formed as a result of oxidative stress in spermatozoa affect directly sperm motility and morphology as well (40)(41)(42).…”

The effects of radiofrequency electromagnetic radiation on sperm function

“…3). Considering that RF-EMR specifically promotes mitochondrial ROS production (De Iuliis et al 2009a, Burlaka et al 2013) associated with increased expression of mitochondrial apoptotic markers (Liu et al 2015) and decreased mitochondrial membrane potential (Lu et al 2012), we propose that this radiation potentiates the leakage of electrons within the electron transport chain. Such electron leakage may be achieved through interference with proton transmission through the transmembrane complexes of the inner mitochondrial membrane.…”