Written by Angeline A. De Leon, Staff Writer. Twenty-four hours of continuous exposure at 1950 MHz 3 W/kg radiation led to adverse effects on proliferation of TM3 cells and dysfunction of testosterone secretion in a male mouse model.
Over the last several decades, reproductive studies have found a significant decline in male fertility 1, likely attributable to several environmental factors, such as exposure to toxic chemicals and radiofrequency (RF) radiation 2. Cell phone use, for example, shows a correlation with negative effects on the male reproductive system 3, including lower sperm count and motility, changes in testicular morphology, and even alterations in sperm DNA integrity 4. Researchers theorize that the negative impact of RF electromagnetic radiation (EMR) is fundamentally linked to elevated levels of oxidative stress in the reproductive organs 5-7. Leydig (TM3) cells are interstitial cells responsible for the production and secretion of testosterone 8, and in mouse models, exposure of Leydig cells to RF-EMR has been associated with disrupted interstitial cell function 9. In a study 10 published by the International Journal of Environmental Research and Public Health (2018), investigators sought to explore the in vitro effects of 1950 MHz RF-EMR on the viability and function of Leydig cells in mice.
TM3 cells were harvested, cultured, and placed into an exposure chamber with an RF generator. One set of cells received sham irradiation, while the other was exposed to 1950 MHz GSM-Talk signal continuously for 24 hours at a specific absorption rate (SAR) of 3 W/kg. Prior to treatment and at Day 1, 2, 3, 4, and 5 post-treatment, a cell proliferation assay was conducted using a cell-counting kit. Flow cytometry was used to analyze different phases of the cell cycle as well as the number of apoptotic cells, and testosterone content was measured using an enzyme-linked immunosorbent assay (ELISA) kit. P450scc (enzyme involved in production of steroid hormones) mRNA expression in TM3 cells was also measured by real-time polymerase chain reaction (PCR).
Compared to the sham group, at Day 3 to Day 5, the exposure group demonstrated significant inhibition of cell proliferation (p < 0.01). At Day 3 and Day 5, the exposure group also showed a significant decrease in the proportion of TM3 cells in the G1 (growth) phase of the cycle and an increase in the proportion of cells in the S (DNA synthesis) phase at all time points (p < 0.05 for all). At Days 1, 2, and 4, testosterone content in the supernatant was found to be diminished in the treated group, relative to sham (p < 0.05 for all), and at Day 1 and Day 2, intracellular testosterone content was also relatively lower (p < 0.05 for both). Finally, P450scc mRNA expression was found to be significantly downregulated, compared to the sham group, at Day 2 to Day 5 post-treatment (p < 0.05 for all).
Current findings confirm the adverse effects of RF-EMR exposure on the reproductive health of males, namely the alteration of cell proliferation, normal cell cycle distribution, and testosterone secretion in the interstitial cells of the testis. RF-EMR, at the frequency of 1950 MHz, was shown to not only directly affect cellular processes involved in spermatogenesis, but to also impact mRNA expression of enzymes associated with testosterone production. Although the literature suggests that reactive oxygen species (ROS) production plays a key role in inducing reproductive dysfunction (5, 6, 7), no significant between-group differences were found following radiation treatment in the current study. Given that RF-EMR also showed no significant impact on apoptosis in the present study, further research is warranted to explore the potential mechanisms responsible for the observed effects of RF-EMR on reproductive cells. Future studies should also examine how different cell lines might be affected as a function of specific EMR frequencies.
Source: Lin Y, Wu T, Liu J, et al. 1950 MHz Radio Frequency Electromagnetic Radiation Inhibits Testosterone Secretion of Mouse Leydig Cells. International Journal of Environmental Research and Public Health. 2018; 15: 17. DOI: 10.3390/ijerph15010017.
© 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
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Posted October 28, 2019.
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