Baihuan Feng1, Liping Qiu1, Chunmei Ye1, Liangjing Chen1, Yiti Fu1, Wenjun Sun1,2. 1. a Bioelectromagnetics Key Laboratory , Zhejiang University School of Medicine , Hangzhou , China ; 2. b Institute of Environmental Medicine , Zhejiang University School of Medicine , Hangzhou , China.
Abstract
PURPOSE: To investigate the biological effects of a 50-Hz magnetic field (MF) on mitochondrial permeability. MATERIALS AND METHODS: Human amniotic epithelial cells were exposed to MF (50 Hz, 0.4 mT) for different durations. Mitochondrial permeability, mitochondrial membrane potential (ΔΨm), cytochrome c (Cyt-c) release and the related mechanisms were explored. RESULTS: Exposure to the MF at 0.4 mT for 60 min transiently induced mitochondrial permeability transition (MPT) and Cyt-c release, although there was no significant effect on mitochondrial membrane potential (ΔΨm). Other than decreasing the total Bcl-2 associated X protein (Bax) level, MF exposure did not significantly affect the levels of Bax and B-cell lymphoma-2 (Bcl-2) in mitochondria. In addition, cells exposed to the MF showed increased intracellular reactive oxidative species (ROS) levels and glycogen synthase kinase-3β (GSK-3β) dephosphorylation at 9 serine residue (Ser(9)). Moreover, the MF-induced MPT was attenuated by ROS scavenger (N-acetyl-L-cysteine, NAC) or GSK-3β inhibitor, and NAC pretreatment prevented GSK-3β dephosphorylation (Ser(9)) caused by MF exposure. CONCLUSION: MPT induced by MF exposure was mediated through the ROS/GSK-3β signaling pathway.
PURPOSE: To investigate the biological effects of a 50-Hz magnetic field (MF) on mitochondrial permeability. MATERIALS AND METHODS:Human amniotic epithelial cells were exposed to MF (50 Hz, 0.4 mT) for different durations. Mitochondrial permeability, mitochondrial membrane potential (ΔΨm), cytochrome c (Cyt-c) release and the related mechanisms were explored. RESULTS: Exposure to the MF at 0.4 mT for 60 min transiently induced mitochondrial permeability transition (MPT) and Cyt-c release, although there was no significant effect on mitochondrial membrane potential (ΔΨm). Other than decreasing the total Bcl-2 associated X protein (Bax) level, MF exposure did not significantly affect the levels of Bax and B-cell lymphoma-2 (Bcl-2) in mitochondria. In addition, cells exposed to the MF showed increased intracellular reactive oxidative species (ROS) levels and glycogen synthase kinase-3β (GSK-3β) dephosphorylation at 9 serine residue (Ser(9)). Moreover, the MF-induced MPT was attenuated by ROS scavenger (N-acetyl-L-cysteine, NAC) or GSK-3β inhibitor, and NAC pretreatment prevented GSK-3β dephosphorylation (Ser(9)) caused by MF exposure. CONCLUSION: MPT induced by MF exposure was mediated through the ROS/GSK-3β signaling pathway.
Entities:
Keywords:
GSK-3β; Magnetic field; mitochondrial permeability transition; reactive oxygen species
Authors: Alanna V Van Huizen; Jacob M Morton; Luke J Kinsey; Donald G Von Kannon; Marwa A Saad; Taylor R Birkholz; Jordan M Czajka; Julian Cyrus; Frank S Barnes; Wendy S Beane Journal: Sci Adv Date: 2019-01-30 Impact factor: 14.136