Hanna Kletkiewicz

Global warming and the increased frequency of unpredictable weather events may disrupt the proper timing of seasonal adjustments of a phenotype. This may lead to the deterioration of the animal’s condition and shorten its lifespan. We tested whether warm spells in winter affect the baseline and stress-induced cortisol level and leukocyte relative telomere length in two winter phenotypes of Siberian hamster, Phodopus sungorus , responding and non-responding to short photoperiod. We found that both phenotypes increased cortisol levels in winter and that warm spells augmented this response. Under stable cold conditions, non-responding individuals were more vulnerable to short-term stress than responding ones. However, telomere length increased, suggesting that animals have a high potential to cope with stress and prevent telomere shortening or that these two variables are not directly related. In responding individuals, the higher incidence of torpor also prevented telomeres shortening. These results indicate that both phenotypes, responding and non-responding to short photoperiod, can overcome the challenges posed by an unpredictably changing environment.

Cannabidiol (CBD) is a non-psychotomimetic phytocannabinoid derived from Cannabis sativa. It has therapeutic effects in different paradigms of brain injury, acting as a neuroprotectant. As oxidative stress is a primary risk factor for brain damage after neonatal hypoxia, we tested the effect of CBD on oxidative status and non-protein-bound iron accumulation in the immature brain after hypoxia. Moreover, we tested whether cannabidiol affects the accumulation of hypoxia-inducible factor-1 alpha (HIF-1α) which plays a key role in the regulation of cellular adaptation to hypoxia and oxidative stress. We used 7-day-old mice randomly assigned to hypoxic or control groups. Immediately after hypoxia or control exposure, pups were randomly assigned to a vehicle or CBD treatment. 24 h later, they were decapitated and the brains were immediately removed and stored for further biochemical analyses. We found that CBD reduced lipid peroxidation and prevented antioxidant depletion. For the first time, we also demonstrated that CBD upregulated HIF-1α protein level. This study indicates that CBD may effective agent in attenuating the detrimental consequences of perinatal asphyxia.

Insecticides are dedicated to impair the insect organisms, but also have an impact on other, non-target organisms, including humans. In this way, they became important risk factor for disturbance of physiological homeostasis and can be involved in the development of diseases or in deterioration of existing conditions. The influence of sublethal doses of various insecticides on vertebrates’ and invertebrates’ organisms has been previously observed. In this paper, we have evaluated the impact of exposure to extremely low dose of neurotoxin, bendiocarb (0.1 nM), a commonly used carbamate insecticide on a model organism in neurobiology—Periplaneta americana. The assessment was performed on all levels of animal organism from molecular (oxidative stress parameters: phosphorylation level of proteins, cAMP level, protein kinase A and C levels, and octopamine) to physiological (heart beat and gas exchange tests) and behavioral (motor skills assay, grooming test). Exposure to such a low level of bendiocarb did not cause direct paralysis of insects, but changed their grooming behavior, decreased heart rate, and increased gas exchange. We also observed the increased parameters of oxidative stress as well as stressogenic response to 0.1 nM bendiocarb exposure. Exposure to a trace amount of bendiocarb also increased sensitivity to effective doses of the same insecticide, thus acts as preconditioning. These results force us to reconsider the possible risk from frequent/continuous exposure to traces of pesticide residues in the environment to human health.

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.

Studies reported evidence for opposite effects of extremely low‐frequency electromagnetic field (EMF): harmful, including the oxidative stress induction, and beneficial, such as the activation of antioxidant defense. People's exposure to EMF is often repeated or prolonged, and it is important to consider the cumulative effect of such kind of exposure on the organism. If changes evoked by repeated exposure to EMF are permanent, responsiveness to other stress factors can be modified. The aims of our study were (1) to evaluate changes in the levels of oxidative stress and antioxidant defense markers in the prefrontal cortex of adult rats after repeated exposure to 1 and 7 mT EMF and (2) to assess whether repeated EMF exposure can modify oxidative/antioxidative status in response to other stress factors. Rats were exposed to EMF 1 h/day for 7 days, one, twice, or three times. After each exposure, 8‐isoprostanes, protein carbonyl groups, and the total antioxidant capacity were assessed. Part of the animals, after EMF treatment, was exposed to another stress factor—open field. Results showed that repeated exposure changed the oxidative/antioxidative status depending on the intensity of the EMF and the number of exposures. 1 mT EMF created weak changes in the oxidative status in the brain; however, 7 mT EMF moved the balance to a clearly higher level. The changes in the oxidative status after 1 mT EMF were enough to reduce, and after 7 mT EMF to intensify oxidative processes in response to the next stress. We concluded that the organism might adapt to “weak” EMF, while “strong” EMF exceeds the adaptive capacity of the organism and sensitizes it to subsequent stress, and thus may modulate vulnerability to diseases. Our results also provide new insights into the possible therapeutic properties of the magnetic field, as 1 mT EMF appears to have a potentially protective impact on the brain.

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.

Anoxia during delivery is a complication that can disturb infant brain development leading to various types of neurological disorders. Our studies have shown that increased body temperature of newborn rats of both sexes intensifies the postanoxic oxidative stress and prevents triggering the endogenous adaptive response such as HIF‐1α activation. Currently, brain‐derived neurotrophic factor‐BDNF is considered to be a modulator of neuronal plasticity. In the developing brain, mature BDNF and its precursor exhibit prosurvival action through the TrkB receptor and proapoptotic functions binding to p75^NTR, respectively. The aim of our experiments was to check the effects of body temperature on the postanoxic level of BDNF and on the expression of its receptors as well as on the marker of apoptosis—caspase‐3 in the rat brain. Two‐day‐old Wistar Han rats (male/female ratio, 1:1) were exposed to anoxia in 100% nitrogen atmosphere for 10 min in different thermal conditions, which allowed them to regulate their rectal temperature at the following levels: normothermic—33°C; hyperthermic—37°C; and extremely hyperthermic—39°C. Thermal conditions during neonatal anoxia affected the level of proBDNF, BDNF as well as their receptors and caspase‐3 in the forebrain. The increased BDNF protein level followed by decreased caspase‐3 protein level was probably dependent on body temperature under anoxic conditions and was observed only in rats maintaining decreased body temperature. The positive effect of BDNF was not observed under hyperthermic conditions. Moreover, BDNF level changes correlated with body temperature probably affected the learning and spatial memory in juvenile rats.