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长期射频电磁场对 C57BL/6 小鼠衰老大脑氧化应激和神经炎症的影响。

Impact of Long-Term RF-EMF on Oxidative Stress and Neuroinflammation in Aging Brains of C57BL/6 Mice.

机构信息

Division of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul 01812, Korea.

Primate Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk 56216, Korea.

出版信息

Int J Mol Sci. 2018 Jul 19;19(7):2103. doi: 10.3390/ijms19072103.

Abstract

The expansion of mobile phone use has raised questions regarding the possible biological effects of radiofrequency electromagnetic field (RF-EMF) exposure on oxidative stress and brain inflammation. Despite accumulative exposure of humans to radiofrequency electromagnetic fields (RF-EMFs) from mobile phones, their long-term effects on oxidative stress and neuroinflammation in the aging brain have not been studied. In the present study, middle-aged C57BL/6 mice (aged 14 months) were exposed to 1950 MHz electromagnetic fields for 8 months (specific absorption rate (SAR) 5 W/kg, 2 h/day, 5 d/week). Compared with those in the young group, levels of protein (3-nitro-tyrosine) and lipid (4-hydroxy-2-nonenal) oxidative damage markers were significantly increased in the brains of aged mice. In addition, levels of markers for DNA damage (8-hydroxy-2'-deoxyguanosine, p53, p21, γH2AX, and Bax), apoptosis (cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase 1 (PARP-1)), astrocyte (GFAP), and microglia (Iba-1) were significantly elevated in the brains of aged mice. However, long-term RF-EMF exposure did not change the levels of oxidative stress, DNA damage, apoptosis, astrocyte, or microglia markers in the aged mouse brains. Moreover, long-term RF-EMF exposure did not alter locomotor activity in aged mice. Therefore, these findings indicate that long-term exposure to RF-EMF did not influence age-induced oxidative stress or neuroinflammation in C57BL/6 mice.

摘要

手机使用的普及引发了人们对于射频电磁场(RF-EMF)暴露对氧化应激和脑炎症可能产生的生物学效应的关注。尽管人类长期暴露于射频电磁场(RF-EMFs)中,但尚未研究手机射频电磁场长期暴露对衰老大脑中的氧化应激和神经炎症的影响。在本研究中,我们使用 14 月龄的 C57BL/6 小鼠作为中年组进行研究,将其置于 1950MHz 电磁场中(比吸收率(SAR)为 5W/kg,每天 2 小时,每周 5 天)进行 8 个月的暴露。与年轻组相比,老年组小鼠大脑中的蛋白质(3-硝基酪氨酸)和脂质(4-羟基-2-壬烯醛)氧化损伤标志物水平显著增加。此外,老年组小鼠大脑中的 DNA 损伤标志物(8-羟基-2'-脱氧鸟苷、p53、p21、γH2AX 和 Bax)、细胞凋亡标志物(cleaved caspase-3 和 cleaved poly(ADP-ribose)polymer 1(PARP-1))、星形胶质细胞标志物(GFAP)和小胶质细胞标志物(Iba-1)的水平也显著升高。然而,长期射频电磁场暴露并未改变老年小鼠大脑中氧化应激、DNA 损伤、细胞凋亡、星形胶质细胞或小胶质细胞标志物的水平。此外,长期射频电磁场暴露并未改变老年小鼠的运动活动能力。因此,这些发现表明,长期射频电磁场暴露不会影响 C57BL/6 小鼠的年龄诱导的氧化应激或神经炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d73/6073444/11b2267f9fd7/ijms-19-02103-g001.jpg

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