title: The protective effect of autophagy on mouse spermatocyte derived cells exposure to 1800MHz radiofrequency electromagnetic radiation.
abstract: The increasing exposure to radiofrequency (RF) radiation emitted from mobile phone use has raised public concern regarding the biological effects of RF exposure on the male reproductive system. Autophagy contributes to maintaining intracellular homeostasis under environmental stress. To clarify whether RF exposure could induce autophagy in the spermatocyte, mouse spermatocyte-derived cells (GC-2) were exposed to 1800MHz Global System for Mobile Communication (GSM) signals in GSM-Talk mode at specific absorption rate (SAR) values of 1w/kg, 2w/kg or 4w/kg for 24h, respectively. The results indicated that the expression of LC3-II increased in a dose- and time-dependent manner with RF exposure, and showed a significant change at the SAR value of 4w/kg. The autophagosome formation and the occurrence of autophagy were further confirmed by GFP-LC3 transient transfection assay and transmission electron microscopy (TEM) analysis. Furthermore, the conversion of LC3-I to LC3-II was enhanced by co-treatment with Chloroquine (CQ), indicating autophagic flux could be enhanced by RF exposure. Intracellular ROS levels significantly increased in a dose- and time-dependent manner after cells were exposed to RF. Pretreatment with anti-oxidative NAC obviously decreased the conversion of LC3-I to LC3-II and attenuated the degradation of p62 induced by RF exposure. Meanwhile, phosphorylated extracellular-signal-regulated kinase (ERK) significantly increased after RF exposure at the SAR value of 2w/kg and 4w/kg. Moreover, we observed that RF exposure did not increase the percentage of apoptotic cells, but inhibition of autophagy could increase the percentage of apoptotic cells. These findings suggested that autophagy flux could be enhanced by 1800MHz GSM exposure (4w/kg), which is mediated by ROS generation. Autophagy may play an important role in preventing cells from apoptotic cell death under RF exposure stress.
authors.affiliation: Institute of Computing Medicine, Third Military Medical University, Chongqing, 400038, China; Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: liu.kaijun@yahoo.com.
authors.forename: Kaijun
authors.initials: K
authors.lastname: Liu
authors.affiliation: Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: zhangguowei.2009@163.com.
authors.forename: Guowei
authors.initials: G
authors.lastname: Zhang
authors.affiliation: Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: 987137630@qq.com.
authors.forename: Zhi
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: ancyliu521@126.com.
authors.forename: Yong
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: jianyun564@163.com.
authors.forename: Jianyun
authors.initials: J
authors.lastname: Dong
authors.affiliation: Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: momomei198@sina.com.
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Dong
authors.affiliation: Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: jinyiliutmmu@163.com.
authors.forename: Jinyi
authors.initials: J
authors.lastname: Liu
authors.affiliation: Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: caojia1962@126.com.
authors.forename: Jia
authors.initials: J
authors.lastname: Cao
authors.affiliation: Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: aolin117@163.com.
authors.forename: Lin
authors.initials: L
authors.lastname: Ao
authors.affiliation: Institute of Computing Medicine, Third Military Medical University, Chongqing, 400038, China. Electronic address: zhangsx1021@yahoo.com.
authors.forename: Shaoxiang
authors.initials: S
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001343:Autophagy / Q000187:drug effects / Q000528:radiation effects*; D002460:Cell Line; D040421:Cell Phone; D002738:Chloroquine / Q000633:toxicity; D004307:Dose-Response Relationship, Radiation; D060733:Electromagnetic Radiation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D008297:Male; D051379:Mice; D046529:Microscopy, Electron, Transmission; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress / Q000528:radiation effects; D010766:Phosphorylation; D017382:Reactive Oxygen Species / Q000378:metabolism; D013090:Spermatocytes / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects* / Q000648:ultrastructure; D013997:Time Factors; D014162:Transfection
chemical_list: D000975:Antioxidants; C480860:Map1lc3b protein, mouse; D008869:Microtubule-Associated Proteins; D017382:Reactive Oxygen Species; D002738:Chloroquine; D048049:Extracellular Signal-Regulated MAP Kinases
keywords: Autophagy; ROS; Radiofrequency electromagnetic field