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

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.

Interleukin-12p35 deficiency enhances mitochondrial dysfunction and aggravates cardiac remodeling in aging mice

“…In contrast to AIF, PARP is mainly a DNA repair enzyme existing in the nucleus, and activated PARP can prevent DNA damage and inhibit apoptosis [28]. In a recent study, expression of activated PARP was also observed to increase in aging brain tissue, which was consistent with our results and closely related to both DNA damage and apoptosis of brain cells [29]. Moreover, activated PARP, which is an anti-apoptotic protein, is increased in aging heart and brain.…”

NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential

“…351,352 The DNA oxidative damage and protein oxidation in the aged human brain are associated with declined antioxidant enzyme activities. 353,354 Agerelated increase in oxidative stress and cell senescence leads cells/ tissues to be more prone to undergo necroptosis, thereby releasing DAMPs that trigger the chronic inflammation observed with aging. 355 The pro-inflammatory cytokines, in turn, augment both mitochondrial and NOX-generated ROS, contributing to further accumulation of oxidative damage (Fig.…”

Impact of Long-Term use of Mobile Phones on the Prostate in Human users

“…As people are continuously exposed to RF-EMFs from cell phone use in everyday life, which has been amplified over the years, it is important to note that many males carry cell phones in their trouser pockets. Clipping cell phones to the belts while using hands-free devices exposes the urinogenital organs to a higher power density of the mobile phone radiation than a cell phone would in the 'Standby mode' in a trouser pocket (Jeong et al, 2018). It is therefore important to investigate the effect of long-term use of mobile phones on the prostate.…”