New View on the Impact of the Low-Frequency Electromagnetic Field (50 Hz) on Stress Responses: Hormesis Effect.

INTRODUCTION: Low-frequency electromagnetic field (50 Hz) (EMF) can modify crucial neuronal processes. Existing data indicate that exposure to EMF may represent a mild stressor and contribute to disturbances of the hypothalamic-pituitary-adrenal (HPA) axis. The important regulatory pathways controlling HPA axis activity include two types of corticosteroid receptors: mineralocorticoid receptors (MRs) and glucocorticoid receptors. They are particularly abundant in the hippocampus, a key locus of HPA axis feedback control. The research aimed at determining whether (1) EMF exhibits hormesis, it means bidirectional action depending on EMF intensity (1 or 7 mT) and (2) repeated EMF exposure changes stress response to subsequent stress factors. METHODS: The exposure (7 days, 1 h/day) of adult rats to EMF (1 mT and 7 mT) was repeated 3 times. HPA axis hormones and their receptors were analysed after each following exposure. Moreover, the impact of EMF exposure on hormonal and behavioural responses to subsequent stress factor - open-field test was evaluated. RESULTS: Our data suggest that exposure to EMF can establish a new "set-point" for HPA axis activity. The direction and dynamics of this process depend on the intensity of EMF and the number of exposures. EMF of 1 mT induced an adaptive stress response, but 7 mT EMF caused sensitization. Consequently, EMF changed the vulnerability of the organism to a subsequent stress factor. We have also shown the increase in MR mRNA abundance in the hippocampus of 1 mT EMF-exposed rats, which can represent the possible neuroprotective response and suggest therapeutic properties of EMFs.

How to Improve the Antioxidant Defense in Asphyxiated Newborns-Lessons from Animal Models.

Oxygen free radicals have been implicated in brain damage after neonatal asphyxia. In the early phase of asphyxia/reoxygenation, changes in antioxidant enzyme activity play a pivotal role in switching on and off the cascade of events that can kill the neurons. Hypoxia/ischemia (H/I) forces the brain to activate endogenous mechanisms (e.g., antioxidant enzymes) to compensate for the lost or broken neural circuits. It is important to evaluate therapies to enhance the self-protective capacity of the brain. In animal models, decreased body temperature during neonatal asphyxia has been shown to increase cerebral antioxidant capacity. However, in preterm or severely asphyxiated newborns this therapy, rather than beneficial seems to be harmful. Thus, seeking new therapeutic approaches to prevent anoxia-induced complications is crucial. Pharmacotherapy with deferoxamine (DFO) is commonly recognized as a beneficial regimen for H/I insult. DFO, via iron chelation, reduces oxidative stress. It also assures an optimal antioxidant protection minimizing depletion of the antioxidant enzymes as well as low molecular antioxidants. In the present review, some aspects of recently acquired insight into the therapeutic effects of hypothermia and DFO in promoting neuronal survival after H/I are discussed.

Does global warming intensify cost of antipredator reaction? A case study of freshwater amphipods.

Global warming is a worldwide phenomenon affecting the functioning of diverse ecosystems, including fresh waters. Temperature increase affects physiology and behaviour of ectotherms due to growing energetic demands necessary to sustain increased metabolic rate. Anti-predator responses may resemble temperature-induced changes in organisms, suggesting synergism between these factors. To check how temperature shapes physiological and behavioural responses of ectotherms to predation risk, we exposed amphipods: Dikerogammarus villosus and Gammarus jazdzewskii to fish kairomones at 10, 17 or 24 °C. Animals were placed in tanks where temperature was gradually adjusted to the desired test temperature and acclimated under such conditions for 3 subsequent days. Then they were exposed to the predator cue (the Eurasian perch kairomone) for 35 min to test their acute responses. We measured metabolic rate (as respiration), antioxidant defence (CAT: catalase activity, TAS: total antioxidant status), oxidative molecules (TOS: total oxidative status), oxidative damage (TBARS: thiobarbituric acid reactive substances) and behaviour (locomotor activity). Amphipods increased respiration with raising temperature and when exposed to predation risk (all temperatures). Only G. jazdzewskii exhibited increased TOS when exposed to 24 °C or to predation risk at all temperatures. Antioxidant defence increased with raising temperature (CAT, TAS) and decreased under predation risk (CAT). Cellular damage increased in G. jazdzewskii under predation risk at 10 and 24 °C, but raised temperature itself did not generate any damage. Amphipods reduced locomotor activity at 24 °C. Thus, at elevated temperatures, amphipods minimized their cellular damage at the cost of increased antioxidant defence and lower locomotor activity (potentially disadvantageous under higher energetic demands). Under predation risk, the performance of antioxidant systems was reduced, probably due to energy allocation into anti-predatory mechanisms, leading to increased cellular damage at suboptimum temperatures. Thus, negative consequences of elevated temperature for organisms may be amplified by changes in behaviour (compromising food acquisition) and non-consumptive predator effects.

Continuity of chronic predation risk determines changes in prey physiology.

Prey reconfigure their physiology to avoid costs of prolonged predator pressure. However, these changes might not occur under periodic predation risk, with repeating acute phases. To test the effect of predation risk continuity on changes in prey physiology, we exposed amphipods: Dikerogammarus villosus and Gammarus jazdzewskii to periodic and constant predation cue. After one week, we measured: cellular defence systems: total antioxidant status (TAS), heat shock proteins (Hsp70); intracellular damage marker: lipid peroxidation (TBARS); condition index: glycogen concentration. Predator presence reduced TAS level in G. jazdzewskii independent of its continuity and in D. villosus after periodic exposure. Amphipods showed downregulation of Hsp70 when exposed to periodic (D. villosus) or constant (G. jazdzewskii) predation risk. Exposure to predators reduced TBARS level in D. villosus (irrespective of the continuity) and G. jazdzewskii (periodic exposure). Glycogen concentration in both species was not affected by predator presence. Thus, the continuity of the predator cue shaped prey physiology reconfiguration, optimizing costs of physiological adjustments under challenging conditions. Nevertheless, the lack of negative consequences of the prolonged exposure to the predator cue, whether constant or periodic, shows that amphipods can thrive under chronic predation risk, which is a constant part of the wild environment.