Investigation of the effects of distance from sources on apoptosis, oxidative stress and cytosolic calcium accumulation via TRPV1 channels induced by mobile phones and Wi-Fi in breast cancer cells

Possible molecular pathways of mobile phones and Wi-Fi on oxidative stress and apoptosis through cytosolic calcium accumulation (via TRPV1 channels) in MCF-7 cancer cells. It is likely that EMR-mediated Ca2 + entry via TRPV1 channels in the MCF-7 cancer cells involves accumulation of ROS and opening of mitochondrial permeability transition (MPT) that consequently leads to mitochondrial dysfunction. When the low oxidative stress and Ca2 + are just enough to lead to the mitochondrial membrane pores, physiological cell functions may be induced. As the oxidative damage and Ca2 + entry increase, molecules such as cytochrome c may be released from mitochondria and trigger apoptosis. At the extreme, oxidative stress and Ca2 + entry cause severe MPT or even the rupture of the mitochondrial membrane, substantial swelling of the mitochondria with rupture of the outer membrane and release of apoptosis-inducing factors such as caspase-3 and -9.272