Table 4.

Extremely low-frequency (less than 3 kHz) magnetic field effects on reactive oxygen species (ROS) levels.

system	magnetic field	references
ROS
ageing via ROS involvement in brain of mongolian gerbils	0.1/0.25/0.5 mT, 50 Hz	Selakovi et al. [273]
hippocampus mitochondria via increasing H2O2 in mice	8 mT, 50 Hz	Duan et al. [274]
neural differentiation/H2O2 elevation in mesenchymal stem cells	1 mT, 50 Hz	Park et al. [275]
H2O2 production in neuroblastoma cell	2 ± 0.2 mT, 75 ± 2 Hz	Osera et al. [276]
pro-Parkinson’s disease toxin MPP+/H2O2 increase in SH-SY5Y cells	1 mT, 50 Hz	Benassi et al. [277]
rat peritoneal neutrophils-oxidative burst	0.1 mT, 60 Hz	Roy et al. [278]
cortical synaptosomes of Wistar rats-oxidative stress	0.7 mT, 60 Hz	Túnez et al. [279]
pro-oxidant effects of H2O2 in human neuroblastoma cells	2 mT, 75 Hz	Falone et al. [280]
reducing hypoxia/inflammation damage ROS-mediated in neuron-like and microglial cells	1.5 ± 0.2 mT, 75 Hz	Vincenzi et al. [281]
mouse brain-antioxidant defense system	1.2 mT, 60 Hz	Lee et al. [282]
rat-cortical neurons-redox and trophic response/reducing ROS	1 mT, 50 Hz	DiLoreto et al. [283]
human monocytes-cell activating capacity/ROS modulation	1 mT, 50 Hz	Lupke et al. [284]
HL-60 leukaemia cells-proliferation/DNA damage implicating ROS	1 mT, 50 Hz	Wolf et al. [285]
human monocytes-alteration of 986 genes/modulating ROS	1 mT, 50 Hz	Lupke et al. [286]
prostate cancer cells-apoptosis through ROS	0.2 mT, 60 Hz	Koh et al. [287]
K562 cells-O·−2 formation and HSP70 induction	0.025–0.1 mT, 50 Hz	Mannerling et al. [288]
K562 Cells-differentiation via increasing O·−2 production	5 mT, 50 Hz	AySe et al. [289]
K562 leukaemia cell-number of apoptotic cells via increasing O·−2 production	1 mT, 50 Hz	Garip & Akan [290]
PC12 cells-H2O2 increase	1 mT, 50 Hz	Morabito et al. [291]
carcinoma cells-cisplatin via increasing H2O2	1 mT, 50 Hz	Bułdak et al. [292]
human carcinoma cells-morphology and biochemistry implicating ROS	0.1 mT, 100&217 Hz	Sadeghipour et al. [293]
rats- DNA strand breaks in brain cells by modulating ROS	0.1–0.5 mT, 60 Hz	Lai & Singh [294]
cardiomyocytes-injury treatment implicating ROS	4.5 mT, 15 Hz	Ma et al. [295]
genomic instability/oxidative processes in human neuroblastoma cells	100 μT, 50 Hz	Luukkonen et al. [296]
expression of NOS and O·−2 in human SH-SY5Y cells	1 mT, 50 Hz	Reale et al. [297]
ROS-related autophagy in mouse embryonic fibroblasts	2 mT, 50 Hz	Chen et al. [298]
healing via reducing ROS production in artificial skin wounds	<40 μT, 100 Hz	Ferroni et al. [299]
apoptosis via oxidative stress in human osteosarcoma cells	1 mT, 50 Hz	Yang et al. [300]
increase O·−2 in erythro-leukemic cells	1 mT, 50 Hz	Patruno et al. [301]
Genomic instability/H2O2 increase in SH-SY5Y cells	100 μT, 50 Hz	Kesari et al. [302]
NOX-produced ROS in hAECs	0.4 mT, 50 Hz	Feng et al. [303]
mitochondrial permeability via increasing H2O2 in human aortic endothelial cells	0.4 mT, 50 Hz	Feng et al. [304]
apoptotic via mitochondrial O·−2 release in human aortic endothelial cells	0.4 mT, 50 Hz	Feng et al. [305]
antioxidant activity implicating H2O2 in human keratinocyte cells	25 − 200 μT, 1–50 Hz	Calcabrini et al. [306]
antioxidative defense mechanisms via ROS in human osteoblasts	2 − 282 μT, 16 Hz,	Ehnert et al. [307]
astrocytic differentiation implicating ROS in human bone stem cells	1 mT, 50 Hz	Jeong et al. [308]
reduce mitochondrial O·−2 production in human neuroblastoma cells	100 μT, 50 Hz	Höytö et al. [309]
ROS production in human cryptochrome	1.8 mT, <100 Hz	Sherrard et al. [222]
proliferation by decreasing intracellular ROS levels in human cells	10 mT, 60 Hz	Song et al. [310]
cytotoxic effect in by raising intracellular ROS in human GBM cells	1–58 mT, 350 Hz	Helekar et al. [311]