Hypomagnetic Field Induces the Production of Reactive Oxygen Species and Cognitive Deficits in Mice Hippocampus

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Abstract

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.

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Oxidative stress refers to elevated intracellular levels of reactive oxygen species (ROS) that cause damage to lipids, proteins and DNA. Oxidative stress has been linked to a myriad of pathologies. However, elevated ROS also act as signaling molecules in the maintenance of physiological functions--a process termed redox biology. In this review we discuss the two faces of ROS--redox biology and oxidative stress--and their contribution to both physiological and pathological conditions. Redox biology involves a small increase in ROS levels that activates signaling pathways to initiate biological processes, while oxidative stress denotes high levels of ROS that result in damage to DNA, protein or lipids. Thus, the response to ROS displays hormesis, given that the opposite effect is observed at low levels compared with that seen at high levels. Here, we argue that redox biology, rather than oxidative stress, underlies physiological and pathological conditions. Copyright © 2014 Elsevier Ltd. All rights reserved.

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Klaus Apel, Heribert Hirt (2004)

Several reactive oxygen species (ROS) are continuously produced in plants as byproducts of aerobic metabolism. Depending on the nature of the ROS species, some are highly toxic and rapidly detoxified by various cellular enzymatic and nonenzymatic mechanisms. Whereas plants are surfeited with mechanisms to combat increased ROS levels during abiotic stress conditions, in other circumstances plants appear to purposefully generate ROS as signaling molecules to control various processes including pathogen defense, programmed cell death, and stomatal behavior. This review describes the mechanisms of ROS generation and removal in plants during development and under biotic and abiotic stress conditions. New insights into the complexity and roles that ROS play in plants have come from genetic analyses of ROS detoxifying and signaling mutants. Considering recent ROS-induced genome-wide expression analyses, the possible functions and mechanisms for ROS sensing and signaling in plants are compared with those in animals and yeast.

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Oxidative Stress: Harms and Benefits for Human Health

Gabriele Pizzino, Natasha Irrera, Mariapaola Cucinotta … (2017)

Oxidative stress is a phenomenon caused by an imbalance between production and accumulation of oxygen reactive species (ROS) in cells and tissues and the ability of a biological system to detoxify these reactive products. ROS can play, and in fact they do it, several physiological roles (i.e., cell signaling), and they are normally generated as by-products of oxygen metabolism; despite this, environmental stressors (i.e., UV, ionizing radiations, pollutants, and heavy metals) and xenobiotics (i.e., antiblastic drugs) contribute to greatly increase ROS production, therefore causing the imbalance that leads to cell and tissue damage (oxidative stress). Several antioxidants have been exploited in recent years for their actual or supposed beneficial effect against oxidative stress, such as vitamin E, flavonoids, and polyphenols. While we tend to describe oxidative stress just as harmful for human body, it is true as well that it is exploited as a therapeutic approach to treat clinical conditions such as cancer, with a certain degree of clinical success. In this review, we will describe the most recent findings in the oxidative stress field, highlighting both its bad and good sides for human health.