Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male reproductive system

Nisarg R Desai, Kavindra K Kesari, Ashok Agarwal, Nisarg R Desai, Kavindra K Kesari, Ashok Agarwal

Abstract

Hazardous health effects stemming from exposure to radiofrequency electromagnetic waves (RF-EMW) emitted from cell phones have been reported in the literature. However, the cellular target of RF-EMW is still controversial. This review identifies the plasma membrane as a target of RF-EMW. In addition, the effects of RF-EMW on plasma membrane structures (i.e. NADH oxidase, phosphatidylserine, ornithine decarboxylase) and voltage-gated calcium channels are discussed. We explore the disturbance in reactive oxygen species (ROS) metabolism caused by RF-EMW and delineate NADH oxidase mediated ROS formation as playing a central role in oxidative stress (OS) due to cell phone radiation (with a focus on the male reproductive system). This review also addresses: 1) the controversial effects of RF-EMW on mammalian cells and sperm DNA as well as its effect on apoptosis, 2) epidemiological, in vivo animal and in vitro studies on the effect of RF-EMW on male reproductive system, and 3) finally, exposure assessment and dosimetry by computational biomodeling.

Figures

Figure 1
Figure 1
The figure shows various cellular targets of radiofrequency electromagnetic waves (RF-EMW). Acute (short term) exposure to RF-EMW can stimulate plasma membrane NADH oxidase which can increase reactive oxygen species (ROS) formation. Increase in ROS can stimulate endothelial growth factor (EGF) receptor which in turn activates extra cellular signal regulated kinase (ERK) pathway. ERK pathway consist of subsequent activation of Ras, Raf proteins and mitogen-activated protein kinase (MAPK). MAPK pathway has tumor promoting role. Chronic exposure to ROS can activate various stress kinase (p38 MAP kinase). Activation of p38 MAP kinase can stimulate ERK pathway and also lead to phosphorylation of heat shock proteins (Hsp) which inhibits apoptosis. Inhibition of apoptosis might promote carcinogenesis by prolonging survival of cell with damaged DNA. Hsp also stabilizes endothelial stress fiber and alters secretion of bFGF. This can lead to increase in permeability of blood testis barrier and causes infertility. RF-EMW can also promote cancer by stimulating ornithine decarboxylase (ODC), a rate limiting enzyme in polyamine synthesis pathway as well as by interfering with plasma membrane calcium channels.

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