Effects of static magnetic field on the sulfate metabolic pathway involved in Magnetospirillum magneticum AMB-1 cell growth and magnetosome formation.

AIMS: Magnetotactic bacteria (MTB) can use their unique intracellular magnetosome organelles to swim along the Earth's magnetic field. They play important roles in the biogeochemical cycles of iron and sulfur. Previous studies have shown that the applied magnetic fields could affect the magnetosome formation and antioxidant defense systems in MTB. However, the molecular mechanisms by which magnetic fields affect MTB cells remain unclear. We aim to better understand the dark at 28°C-29°C for 20 h, as shownthe interactions between magnetic fields and cells, and the mechanism of MTB adaptation to magnetic field at molecular levels. METHODS AND RESULTS: We performed microbiological, transcriptomic, and genetic experiments to analyze the effects of a weak static magnetic field (SMF) exposure on the cell growth and magnetosome formation in the MTB strain Magnetospirillum magneticum AMB-1. The results showed that a 1.5 mT SMF significantly promoted the cell growth but reduced magnetosome formation in AMB-1, compared to the geomagnetic field. Transcriptomic analysis revealed decreased expression of genes primarily involved in the sulfate reduction pathway. Consistently, knockout mutant lacking adenylyl-sulfate kinase CysC did no more react to the SMF and the differences in growth and Cmag disappeared. Together with experimental findings of increased reactive oxidative species in the SMF-treated wild-type strain, we proposed that cysC, as a key gene, can participate in the cell growth and mineralization in AMB-1 by SMF regulation. CONCLUSIONS: This study suggests that the magnetic field exposure can trigger a bacterial oxidative stress response involved in AMB-1 growth and magnetosome mineralization by regulating the sulfur metabolism pathway. CysC may serve as a pivotal enzyme in mediating sulfur metabolism to synchronize the impact of SMF on both growth and magnetization of AMB-1.

Cognitive improvement via a modulated rhythmic pulsed magnetic field in D-galactose-induced accelerated aging mice.

Rhythmic physical stimulations have emerged as effective noninvasive intervention strategies in the treatment of pathological cognitive deficits. Transcranial magnetic stimulation (TMS) can regulate neural firing and improve the learning and memory abilities of rodents or patients with cognitive deterioration. However, the effects of elaborate magnetic stimulation with low intensity during aging or other neurological disordering processes on cognitive decline remain unclear. In this study, we developed an elaborate modulated pulsed magnetic field (PMF) stimulation with a complex pattern in the theta repeated frequency and gamma carrier frequency and then determined the effects of this rhythmic PMF on the cognitive function of accelerated aging mice established by chronic subcutaneous injection of D-galactose (D-gal). The results of the Morris water maze (MWM) test showed that mice treated with modulated PMF displayed shorter swimming distance and latency time in the spatial exploration acquisition trial and exhibited a significant preference in the target presumptive platform area in the probe trial, all of which indicated the enhancement in spatial learning and memory abilities upon PMF stimulation of the accelerated aging mice. The novel object recognition (NOR) test results showed a similar tendency as the MWM results although without statistical significance. Further determination of histological structures demonstrated that the cognitive function-related hippocampal CA3 neurons degenerated upon D-gal injection, which could also be partially rescued by PMF application. In comparison with the high-intensity TMS approach, low-intensity magnetic stimulation could be much safer and allow deeper penetration without adverse effects such as seizure. In summary, modulated PMF, even with low intensity, could effectively improve rodent cognitive functions impaired by D-gal-induced accelerated aging, which might provide a new safe therapeutic strategy for cognitive deficits as well as other neurological disorders.