Abstract:

TRPV1 channel is activated with pH changes, increasing temperature, free radicals, and oxidative stress, and it may be a good measure for detecting the effect of microwave non-ionizing radiation on cellular and molecular responses. The scoping review study aims to survey the influence of mobile and wireless radiation on the TRPV1 channel mechanism. We systematically considered international databases to recognize related studies, including PubMed, Scopus, Cochrane Library, CINAHL, ISI Web of Science, Science Direct from the start, PROSPERO and EMBASE use headings for scientific topics (Mesh). The hunt covered the period from 1980 until 2019. A total of seven studies comprising 137 cases, three in vitro tests on breast cancer cell line Michigan Cancer Foundation-7 (MCF-7), embryonic kidney HEK293T cells and Rabbit polyclonal anti-TRPV1, and four in vivo experimental studies comprising 21 male and 24 female Wistar Albino rats, were included. Two studies indicated cell phones induced mitochondrial ROS, Oxidative stress-induced in the hippocampus, mitochondrial apoptosis via activation of TRPV1 in HIPPON and DRGN cells. The cytosolic Ca2+ induced by TRPV1 induced oxidative overactions and apoptosis at a distance of 10 cm from the source of the cells. Our review shows that cell phone and wireless radiation have a possible effect on Ca2+ signaling by TRPV1 channel activation. This reaction may induce ROS, Fenton and Haber-Weiss reaction which increase free radicals’ level in the mitochondria.

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