Hypomagnetic Field Induces the Production of Reactive Oxygen Species and Cognitive Deficits in Mice Hippocampus.
Lanxiang TianYukai LuoAisheng ZhanJie RenHuafeng QinYongxin PanPublished in: International journal of molecular sciences (2022)
Previous studies have found that hypomagnetic field (HMF) exposure impairs cognition behaviors in animals; however, the underlying neural mechanisms of cognitive dysfunction are unclear. The hippocampus plays important roles in magnetoreception, memory, and spatial navigation in mammals. Therefore, the hippocampus may be the key region in the brain to reveal its neural mechanisms. We recently reported that long-term HMF exposure impairs adult hippocampal neurogenesis and cognition through reducing endogenous reactive oxygen species (ROS) levels in adult neural stem cells that are confined in the subgranular zone (SGZ) of the hippocampus. In addition to adult neural stem cells, the redox state of other cells in the hippocampus is also an important factor affecting the functions of the hippocampus. However, it is unclear whether and how long-term HMF exposure affects ROS levels in the entire hippocampus (i.e., the dentate gyrus (DG) and ammonia horn (CA) regions). Here, we demonstrate that male C57BL/6J mice exposed to 8-week HMF exhibit cognitive impairments. We then found that the ROS levels of the hippocampus were significantly higher in these HMF-exposed mice than in the geomagnetic field (GMF) group. PCR array analysis revealed that the elevated ROS levels were due to HMF-regulating genes that maintain the redox balance in vivo, such as Nox4 , Gpx3 . Since high levels of ROS may cause hippocampal oxidative stress, we suggest that this is another reason why HMF exposure induces cognitive impairment, besides the hippocampal neurogenesis impairments. Our study further demonstrates that GMF plays an important role in maintaining hippocampal function by regulating the appropriate endogenous ROS levels.
Keyphrases
- reactive oxygen species
- cerebral ischemia
- cognitive impairment
- neural stem cells
- subarachnoid hemorrhage
- blood brain barrier
- dna damage
- brain injury
- cell death
- prefrontal cortex
- oxidative stress
- induced apoptosis
- genome wide
- high fat diet induced
- adipose tissue
- cell cycle arrest
- gene expression
- randomized controlled trial
- dna methylation
- mild cognitive impairment
- metabolic syndrome
- wild type
- young adults
- ischemia reperfusion injury
- diabetic rats
- skeletal muscle
- endoplasmic reticulum stress