Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signaling pathway in mouse spermatogenic cells in vitro and thus may affect male fertility

Sołek, Przemysław; Majchrowicz, Lena; Błoniarz, Dominika; Krotoszynska, Ewelina; Koziorowski, Marek

doi:10.1016/j.tox.2017.03.015

Cited by 33 publications

(12 citation statements)

References 34 publications

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“…As a tumor suppressor gene, p53 is kept at a low expression level normally; when the cells encounter stressful situations, p53 is activated and cell growth is arrested by p53 blocking the cell cycle, and even apoptosis is triggered. Consistent with the results of this study, Xing et al found that 24 h of exposure to microwaves increased the levels of p53 protein [34]; Solek et al believed that pulsed electromagnetic field induced an increase in the p53 protein level, resulting in p53/p21-dependent apoptosis [35]. However, in contrast to those results, there are negative findings: Hirose et al demonstrated that 2.1425 GHz EMR caused no significant difference in expression levels of p53 between the exposure group and the control group [36]; Silva et al indicated that no effect on p53 expression was found [37].…”

Section: Discussionsupporting

confidence: 90%

Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells

Song

Liang

et al. 2020

IJERPH

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To investigate the effect of 1800 MHz electromagnetic radiation (EMR) on apoptosis, we exposed NIH/3T3 cells at 1800 MHz with a specific absorption rate (SAR) of 2 W/kg intermittently for 12, 24, 36, and 48 h. After exposure, Cell Counting Kit-8 (CCK-8) and flow cytometry were used to detect cell viability and apoptosis; the expression of p53, a molecule with the key role in apoptosis, was measured by real-time qPCR, western blot, and immunofluorescence; and images of the structure of the mitochondria, directly reflecting apoptosis, were captured by electron microscopy. The results showed that the viability of cells in the 12, 36, and 48 h exposure groups significantly decreased compared with the sham groups; after 48 h of exposure, the percentage of late apoptotic cells in the exposure group was significantly higher. Real-time qPCR results showed that p53 mRNA in the 48 h exposure group was 1.4-fold of that in the sham group; significant differences of p53 protein fluorescence expression were observed between the exposure groups and the sham groups after 24 h and 48 h. The mitochondrial swelling and vesicular morphology were found in the electron microscopy images after 48 h exposure. These findings demonstrated 1800 MHz, SAR 2 W/kg EMR for 48 h may cause apoptosis in NIH/3T3 cells and that this apoptosis might be attributed to mitochondrial damage and upregulation of p53 expression.

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Section: Discussionsupporting

confidence: 90%

Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells

Song

Liang

et al. 2020

IJERPH

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“…Exposure of in vitro mouse spermatogenesis pathway cell lines (GC-1 spg and GC-2 spd) to 50 or 120 Hz ELF-MF determined an increase in superoxide anion production, which was associated to activation of the intrinsic apoptotic pathway and proliferation inhibition, although after a 48-hour postexposure recovery, an increased activation of NF- κ B, a transcription factor involved in the maintenance of redox balance, was found [ 147 , 148 ]. These effects were abolished by medium supplementation with Aloe arborescens's juice [ 148 ].…”

Section: Emf Effects In Male Reproductive System and Fertilitymentioning

confidence: 99%

Role of Mitochondria in the Oxidative Stress Induced by Electromagnetic Fields: Focus on Reproductive Systems

Santini

Cordone

Falone

et al. 2018

Oxidative Medicine and Cellular Longevity

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Modern technologies relying on wireless communication systems have brought increasing levels of electromagnetic field (EMF) exposure. This increased research interest in the effects of these radiations on human health. There is compelling evidence that EMFs affect cell physiology by altering redox-related processes. Considering the importance of redox milieu in the biological competence of oocyte and sperm, we reviewed the existing literature regarding the effects of EMFs on reproductive systems. Given the role of mitochondria as the main source of reactive oxygen species (ROS), we focused on the hypothesis of a mitochondrial basis of EMF-induced reproductive toxicity. MEDLINE, Web of Science, and Scopus database were examined for peer-reviewed original articles by searching for the following keywords: “extremely low frequency electromagnetic fields (ELF-EMFs),” “radiofrequency (RF),” “microwaves,” “Wi-Fi,” “mobile phone,” “oxidative stress,” “mitochondria,” “fertility,” “sperm,” “testis,” “oocyte,” “ovarian follicle,” and “embryo.” These keywords were combined with other search phrases relevant to the topic. Although we reported contradictory data due to lack of uniformity in the experimental designs, a growing body of evidence suggests that EMF exposure during spermatogenesis induces increased ROS production associated with decreased ROS scavenging activity. Numerous studies revealed the detrimental effects of EMFs from mobile phones, laptops, and other electric devices on sperm quality and provide evidence for extensive electron leakage from the mitochondrial electron transport chain as the main cause of EMF damage. In female reproductive systems, the contribution of oxidative stress to EMF-induced damages and the evidence of mitochondrial origin of ROS overproduction are reported, as well. In conclusion, mitochondria seem to play an important role as source of ROS in both male and female reproductive systems under EMF exposure. Future and more standardized studies are required for a better understanding of molecular mechanisms underlying EMF potential challenge to our reproductive system in order to improve preventive strategies.

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“… 5 Pulsed or continuous electromagnetic field induces apoptosis of the spermatogenic cells in mouse through p53/p21-mediated apoptotic signaling pathway and thus results in male fertility. 6 Similarly, decrease of p53 levels affects germ cell homeostasis during spermatogenesis. 7 Deficiency of the Magea gene cluster leads to small testes and high rates of apoptosis during the first wave of spermatogenesis, but the Magea gene cluster regulates male germ cell apoptosis without affecting the fertility in mice.…”

Section: Introductionmentioning

confidence: 99%

Mkrn2 deficiency induces teratozoospermia and male infertility through p53/PERP-mediated apoptosis in testis

et al. 2020

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The apoptosis that occurs in the immature testis under physiological conditions is necessary for male germ cell development, whereas improper activation of apoptosis can impair spermatogenesis and cause defects in reproduction. We previously demonstrated that in mice, the makorin-2 ( Mkrn2 ) gene is expressed exclusively in the testis and its deletion leads to male infertility. To understand the potential molecular mechanism, in this study, we found that levels of apoptosis in the testis were abnormally high in the absence of Mkrn2 . To identify specific gene(s) involved, we performed digital gene expression profiling (DGE) and pathway analysis via gene set enrichment analysis (GSEA) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, and we found that MKRN2 inhibits p53 apoptosis effector related to PMP22 (PERP) expression and that levels of the protein in sperm samples have an inverse correlation with infertility levels. GSEA additionally indicated that PERP is a negative regulator of spermatogenesis and that its ectopic expression induces male infertility. Further, Gene Expression Omnibus (GEO) dataset analysis showed that p53, upstream of PERP, was upregulated in oligoasthenoteratozoospermia (OAT). These observations suggest that Mkrn2 is crucial for protecting germ cells from excessive apoptosis and implicate Mkrn2 -based suppression of the p53/PERP signaling pathway in spermatogenesis and male fertility.

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Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signaling pathway in mouse spermatogenic cells in vitro and thus may affect male fertility

Cited by 33 publications

References 34 publications

Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells

Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells

Role of Mitochondria in the Oxidative Stress Induced by Electromagnetic Fields: Focus on Reproductive Systems

Mkrn2 deficiency induces teratozoospermia and male infertility through p53/PERP-mediated apoptosis in testis

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