Yanyang Li , Binwei Yao , Junqi Men , Yueyue Pang , Jingchao Gao , Yanxin Bai , Hui Wang , Jing Zhang , Li Zhao , Xinping Xu , Ji Dong , Congsheng Li , Ruiyun Peng
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引用次数: 0
Abstract
The effect of multi-frequency electromagnetic environments on male reproduction has attracted the medical community’s interest. Studies have investigated the effects and mechanisms of single-frequency microwave exposure on male reproduction, but comparative research on high-power microwave (HPM) composite and single exposure remains scarce. This study aimed to examine the effects and mechanisms of combined 1.5 GHz and 4.3 GHz microwave exposure on male reproduction. Male Wistar rats were exposed to 1.5 GHz (L-band) and 4.3 GHz (C-band) electromagnetic radiation for 15 minutes. The four groups were: sham, 10 mW/cm² L-band, 10 mW/cm² C-band, and 5 mW/cm² L-band and 5 mW/cm² C-band compound. Assessments were made on the pathological structures of testes, sperm viability, serum sex hormones, oxidative stress, and energy metabolism levels after radiation. Exposure to 1.5 GHz and 4.3 GHz microwaves individually resulted in testicular tissue damage and reduced sperm quality. There was little difference between the damage caused by HPM composite and single exposure. The exposed groups showed histological and ultrastructural changes, with reduced spermatozoa viability, motility parameters, and serum testosterone, luteinizing hormone, follicle-stimulating hormone, and serum inhibin-B on days 1 and 7 after exposure. These tended to recover partially by day 14. Adenosine triphosphate content and lactate dehydrogenase and succinate dehydrogenase activities in the exposed testicular tissue decreased, corresponding to decreased superoxide dismutase activity and increased malondialdehyde content. Both single and combined exposure to L- and C-band HPM affect the male reproductive system. Exposure to single and compound HPM shows no significant difference in risks, with oxidative stress and energy metabolism disturbances playing key roles.
期刊介绍:
Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine.
All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.