2025-02-27 中国科学院(CAS)
<関連情報>
- https://english.cas.cn/newsroom/research_news/phys/202503/t20250304_903030.shtml
- https://www.sciencedirect.com/science/article/pii/S2213231725000746
- https://www.sciencedirect.com/science/article/pii/S2667325824002838
酸化還元不均衡がマウスの磁気特性と機能変化を引き起こす Redox imbalance drives magnetic property and function changes in mice
Chuanlin Feng, Lei Zhang, Xiaoyuan Zhou, Shiyu Lu, Ruowen Guo, Chao Song, Xin Zhang
Redox Biology Available online: 21 February 2025
DOI:https://doi.org/10.1016/j.redox.2025.103561
Abstract
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.
代謝性疾患マウス脾臓における内因性鉄のバイオミネラリゼーション Endogenous iron biomineralization in the mouse spleen of metabolic diseases
Ruowen Guo, Lei Zhang, Dongsheng Song, Biao Yu, Chao Song, Hanxiao Chen, Wenjing Xie, Chuanlin Feng, Guofeng Cheng, Kejun Hu, Jialiang Jiang, Zhe Qu, Haifeng Du, Xin Zhang
Fundamental Research Available online: 25 July 2024
DOI:https://doi.org/10.1016/j.fmre.2024.07.004
Graphical abstract
Abstract
As the most abundant essential trace element in our human bodies, iron plays essential roles in multiple physiological and pathological conditions, including oxygen transport, cancer, diabetes, Alzheimer’s and Parkinson’s diseases. Although it has been shown that iron can form particles in some bacteria, migrating birds and fish, whether iron biomineralization can also occur in mammals is still debated. Here we demonstrate that iron metabolism abnormalities in diseased mice can directly lead to endogenous iron biomineralization and particle formation in the spleen. Excessive iron accumulation leads to endogenous particle formation with an averaged size of ∼800 nm. In the spleens of severely diabetic mice, they accumulate in the red pulp region, where the red blood cells are recycled. This directly changes the magnetic property of the spleens and results in spleen damage in a gradient high magnetic field. Therefore, our findings not only demonstrate the existence of endogenous iron biomineralization in metabolic diseases, but also set up a direct link among iron accumulation, magnetic property and magnetic responses of animal organs, which may also be applied in other iron metabolism-related diseases including cancer and Alzheimer’s disease.
