Redox imbalance drives magnetic property and function changes in mice.

The magnetic properties of substances directly determine their response to an externally applied magnetic field, which are closely associated with magnetoreception, magnetic resonance imaging (MRI), and magnetic bioeffects. However, people's understanding of the magnetic properties of living organisms remains limited. In this study, we utilized NRF2 (nuclear factor erythroid 2-related factor 2) deficient mice to investigate the contribution of redox (oxidation-reduction) homeostasis, in which the key process is the transfer of electron, a direct target of magnetic field and origin of paramagnetism. Our results show that the NRF2-/- mice exhibit significantly altered systemic redox state, accompanied by increased magnetic susceptibility, particularly in the liver and spleen. Further analyses reveal that the levels of paramagnetic reactive oxygen species (ROS) in these tissues are markedly elevated compared to wild-type mice. Moreover, the concentrations of Fe2+ and Fe3+ are significantly elevated in NRF2-/- mice, which are directly correlated with the increased magnetic susceptibility. The disrupted redox balance in NRF2-/- mice not only exacerbates oxidative stress and iron deposition, but also induces impairment to the liver and spleen. The findings highlight the combined effects of ROS and iron metabolism in driving magnetic susceptibility changes, providing valuable theoretical insights for further research into magnetic bioeffects and organ-specific sensitivity to magnetic fields.