Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
National Egyptian Center of Environmental and Toxicological Research (NECTER), Faculty of Medicine, Cairo University, Cairo, Egypt.
Toxicol Appl Pharmacol. 2019 May 1;370:117-130. doi: 10.1016/j.taap.2019.03.009. Epub 2019 Mar 13.
The exponentially increasing use of electromagnetic field (EMF)-emitting devices imposes substantial health burden on modern societies with particular concerns of male infertility. Limited studies have addressed the modulation of this risk by protective agents. We investigated the hazardous effects of rat exposure to EMF (900 MHz, 2 h/day for 8 weeks) on male fertility and evaluated the possible protective effect of the polyamine, spermine, against EMF-induced alterations. Exposure to EMF significantly decreased sperm count, viability and motility, and increased sperm deformities. EMF-exposed rats exhibited significant reductions in serum inhibin B and testosterone along with elevated activin A, follicle-stimulating hormone, luteinizing hormone and estradiol concentrations. Testicular steroidogenic acute regulatory protein (StAR), c-kit mRNA expression and testicular activities of the key androgenic enzymes 3β- and 17β-hydroxysteroid dehydrogenases were significantly attenuated following exposure to EMF. Exposure led to testicular lipid peroxidation, decreased catalase and glutathione peroxidase activities and triggered nuclear factor-kappa B p65, inducible nitric oxide synthase, cyclooxygenase-2 and caspase-3 overexpression. EMF-exposed rats showed testicular DNA damage as indicated by elevated comet parameters. Spermine administration (2.5 mg/Kg/day intraperitoneally for 8 weeks) prevented EMF-induced alterations in the sperm and hormone profiles, StAR and c-kit expression and androgenic enzyme activities. Spermine hampered EMF-induced oxidative, inflammatory, apoptotic and DNA perturbations. Histological and histomorphometric analysis of the testes supported all biochemical findings. In conclusion, rat exposure to EMF disrupts sperm and hormone profiles with underlying impairment of steroidogenesis and spermatogenesis. Spermine confers protection against EMF-associated testicular and reproductive aberrations, at least in part, via antioxidant, anti-inflammatory and anti-apoptotic mechanisms.
电磁场(EMF)发射设备的使用呈指数增长,给现代社会带来了巨大的健康负担,尤其是男性不育问题。有限的研究已经探讨了保护剂对这种风险的调节作用。我们研究了大鼠暴露于电磁场(900MHz,每天 2 小时,持续 8 周)对男性生育能力的危害作用,并评估了多胺精胺对电磁场诱导的改变的可能保护作用。暴露于电磁场会显著降低精子数量、活力和运动能力,并增加精子畸形。暴露于电磁场的大鼠血清抑制素 B 和睾酮水平显著降低,同时激活素 A、卵泡刺激素、黄体生成素和雌二醇浓度升高。睾丸甾体生成急性调节蛋白(StAR)、c-kitmRNA 表达和关键雄激素酶 3β-和 17β-羟甾脱氢酶的睾丸活性在暴露于电磁场后显著减弱。暴露导致睾丸脂质过氧化、过氧化氢酶和谷胱甘肽过氧化物酶活性降低,并触发核因子-κB p65、诱导型一氧化氮合酶、环氧化酶-2 和半胱天冬酶-3 的过度表达。暴露于电磁场的大鼠显示出睾丸 DNA 损伤,彗星参数升高。精胺(每天 2.5mg/Kg 腹腔内注射,持续 8 周)给药可防止 EMF 引起的精子和激素谱、StAR 和 c-kit 表达以及雄激素酶活性的改变。精胺阻止了 EMF 引起的氧化、炎症、凋亡和 DNA 改变。睾丸的组织学和组织形态学分析支持所有生化发现。总之,大鼠暴露于电磁场会破坏精子和激素谱,导致类固醇生成和精子发生受损。精胺通过抗氧化、抗炎和抗凋亡机制对电磁场相关的睾丸和生殖异常提供保护。