Science Advances 30 Jan 2019:
Vol. 5, no. 1, eaau7201
Biological systems are constantly exposed to electromagnetic fields (EMFs) in the form of natural geomagnetic fields and EMFs emitted from technology. While strong magnetic fields are known to change chemical reaction rates and free radical concentrations, the debate remains about whether static weak magnetic fields (WMFs; <1 mT) also produce biological effects. Using the planarian regeneration model, we show that WMFs altered stem cell proliferation and subsequent differentiation via changes in reactive oxygen species (ROS) accumulation and downstream heat shock protein 70 (Hsp70) expression. These data reveal that on the basis of field strength, WMF exposure can increase or decrease new tissue formation in vivo, suggesting WMFs as a potential therapeutic tool to manipulate mitotic activity.
However, recent evidence indicates that WMFs can affect biological systems in multiple ways. WMF exposure increased intracellular calcium concentrations and the rate of cellular development in satellite cells, and caused embryo mortality as well as altered vertebrae development in roach embryos (10, 11). Cell-dependent effects from WMFs were seen in rat renal versus cortical astrocyte cells, with decreased levels of apoptosis, proliferation, and necrosis in renal cells but increases in all three in astrocyte cells (12). WMFs were also found to produce transient induction of the membrane permeability transition and increased cytosolic cytochrome c levels in human amniotic cells via an increase in reactive oxygen species (ROS) (13).
A theoretical basis exists for the effects of WMFs on the concentration of free radicals such as ROS, as outlined in (14–16). Traditionally viewed as harmful, ROS can trigger cell death and thus are highly regulated by antioxidant enzymes such as superoxide dismutase (SOD), but ROS are also beneficial—acting as regulatory mediators (17), assisting in muscle repair (18), and modulating cell signaling (19). More recently, ROS signaling has been shown to regulate new tissue growth, as such in zebrafish where ROS production triggers apoptosis-induced compensatory proliferation required for regeneration (20)