Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1944094 | Biochimica et Biophysica Acta (BBA) - Biomembranes | 2015 | 10 Pages |
Abstract
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 Ca2Â + 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 Ca2Â + are just enough to lead to the mitochondrial membrane pores, physiological cell functions may be induced. As the oxidative damage and Ca2Â + entry increase, molecules such as cytochrome c may be released from mitochondria and trigger apoptosis. At the extreme, oxidative stress and Ca2Â + 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
Keywords
TRPV1TrpTRPM2HBSSEGTAEMRDMSOROS[Ca2 +]iElectromagnetic radiationMobile phoneOxidative stressApoptosisDimethyl sulfoxideBreast cancerGlobal System for Mobile CommunicationsCalcium signalingRadiofrequencyHank's buffered salt solutiontransient receptor potentialTransient receptor potential vanilloid 1CaPGSMCapsaicinReactive oxygen species
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Authors
Bilal ÃiÄ, Mustafa NazıroÄlu,