ID Number		2651
Study Type		In Vivo
Model		900 MHz RFR exposure-induced oxidative stress causes DNA damage in germ cells, which alters cell cycle progression leading to low sperm count in mice.
Details		AUTHORS' ABSTRACT: Pandey et al. 2016 (IEEE #6547): Even though there are contradictory reports regarding the cellular and molecular changes induced by mobile phone emitted radiofrequency radiation (RFR), the possibility of any biological effect cannot be ruled out. In view of a widespread and extensive use of mobile phones, this study evaluates alterations in male germ cell transformation kinetics following RFR exposure and after recovery. Swiss albino mice were exposed to RFR (900 MHz) for 4 h and 8 h duration per day for 35 days. One group of animals was terminated after the exposure period, while others were kept for an additional 35 days post-exposure. RFR exposure caused depolarization of mitochondrial membranes resulting in destabilized cellular redox homeostasis. Statistically significant increases in the damage index in germ cells and sperm head defects were noted in RFR-exposed animals. Flow cytometric estimation of germ cell subtypes in mice testis revealed 2.5-fold increases in spermatogonial populations with significant decreases in spermatids. Almost fourfold reduction in spermatogonia to spermatid turnover (1C:2C) and three times reduction in primary spermatocyte to spermatid turnover (1C:4C) was found indicating arrest in the premeiotic stage of spermatogenesis, which resulted in loss of post-meiotic germ cells apparent from testis histology and low sperm count in RFR-exposed animals. Histological alterations such as sloughing of immature germ cells into the seminiferous tubule lumen, epithelium depletion and maturation arrest were also observed. However, all these changes showed recovery to varied degrees following the post-exposure period indicating that the adverse effects of RFR on mice germ cells are detrimental but reversible. To conclude, RFR exposure-induced oxidative stress causes DNA damage in germ cells, which alters cell cycle progression leading to low sperm count in mice. AUTHORS' ABSTRACT: Pandey and Giri 2018 (IEEE #6997): Increasing male infertility of unknown aetiology can be associated with environmental factors. Extensive use of mobile phones has exposed the general population to unprecedented levels of radiofrequency radiations (RFRs) that may adversely affect male reproductive health. Therefore, the present study investigated the effect of RFR Global System for Mobile communication (GSM) type, 900 MHz and melatonin supplementation on germ cell development during spermatogenesis. Swiss albino mice were divided into four groups. One group received RFR exposure for 3 h twice/day for 35 days and the other group received the same exposure but with melatonin (N-acetyl-5-methoxytryptamine) (MEL; 5 mg/kg bw/day). Two other groups received only MEL or remain unexposed. Sperm head abnormality, total sperm count, biochemical assay for lipid peroxides, reduced glutathione, superoxide dismutase activity and testis histology were evaluated. Additionally, flow cytometric evaluation of germ cell subtypes and comet assay were performed in testis. Extensive DNA damage in germ cells of RFR-exposed animals along with arrest in pre-meiotic stages of spermatogenesis eventually leading to low sperm count and sperm head abnormalities were observed. Furthermore, biochemical assays revealed excess free radical generation resulting in histological and morphological changes in testis and germ cells morphology, respectively. However, these effects were either diminished or absent in RFR-exposed animals supplemented with melatonin. Hence, it can be concluded that melatonin inhibits pre-meiotic spermatogenesis arrest in male germ cells through its anti-oxidative potential and ability to improve DNA reparative pathways, leading to normal sperm count and sperm morphology in RFR-exposed animals.
Findings		Effects
Status		Completed With Publication
Principal Investigator		Assam University, Silchar, Assam, India.
Funding Agency		?????
Country		INDIA
References		Pandey, N et al. Toxicol Ind Health., (2017) 33:373-384 Pandey, N et al. Toxicol Ind Health., (2018) 34:315-327
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