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Big Marsh is a 121-hectares site, representative of many other sites in the Calumet region (near Chicago, IL, USA), which has been significantly altered by the steel industry and decades of legal and illegal dumping and industrial filling. The slag-containing soil at the site has been found to be contaminated with polycyclic aromatic hydrocarbons (PAHs) and heavy metals. Due to the large size of the site to be remedied, and variable distribution of the contaminants throughout the shallow depth at slightly above the risk-based levels, phytoremediation is considered as a green and sustainable remedial option. The objective of this work was to investigate the use of phytoremediation in a three-year field-scale study, specifically determine plant survival and the fate of PAHs and heavy metals in soil and plant roots and stems. Replicate test plots were prepared by laying a thin layer of compost at the ground surface and then tilling and homogenizing the slag-soil fill to a depth of approximately 0.3 m. Nine native and restoration plant species were selected and planted at the site, and their survival and growth were monitored and fate of contaminants in soil and plants were also monitored for three growing seasons. Sequential extraction procedure was performed to determine the fractionation of the heavy metals in soils before and after planting. The results showed a decrease in PAHs concentrations in the soil, probably due to enhanced biodegradation within rhizosphere. No significant decrease in heavy metal concentrations in soil was found, but they were found to be immobilized. Contaminant concentrations were found below detection limits in the plant roots and shoots samples, demonstrating insignificant uptake by the plants. Overall, selected native grasses in combination with compost amendment to the soil proved to be able to survive under the harsh site slag fill conditions, helping to degrade or immobilize the contaminants and reducing the risk of the contaminants to public and the environment. [ABSTRACT FROM AUTHOR]

Purpose: We aimed to determine the effects of different doses of amyloid-beta (Aβ) peptide on learning and memory, and whether the changes in brain oscillations induced by dose-dependent accumulation of Aβ could be used as biomarkers to detect early stages of Alzheimer's disease (AD)., Material and Methods: Male albino Wistar rats aged 3 months were randomly divided into four groups (n ​= ​12/group) obtained by i. h. Injection (to the dorsal hippocampus) of saline or different doses of 0.01 ​μg/μl, 0.1 ​μg/μl, and 1 ​μg/μl of Aβ. After two weeks of recovery period, open field and novel object recognition tests were performed and spontaneous EEG recordings were obtained. Later, hippocampus tissues were collected for Western blot and ELISA analysis., Results: A significant decrement in recognition memory was observed in 0.1 ​μg/μl, and 1 ​μg/μl injected groups. In addition, Aβ accumulation induced significant decrement of the expression of NeuN, SNAP-25, SYP, and PSD-95 proteins, and led to the increment of GFAP expression in hippocampus. Moreover, we detected remarkable alterations in spontaneous brain activity. The hippocampal Aβ levels were negatively correlated with hippocampal gamma power and positively correlated with hippocampal theta power. Also, we observed significant changes in coherence values, indicating the functional connectivity between different brain regions, after the accumulation of Aβ. Especially, there was a significant correlation between changes in frontohippocampal theta coherence and in frontotemporal theta coherence., Conclusions: Our findings indicate that Aβ peptide induces AD-like molecular changes at certain doses, and these changes could be detected by evaluating brain oscillations., Competing Interests: Declaration of competing interest The authors declare no conflict of interests., (Copyright © 2022 Medical University of Bialystok. Published by Elsevier B.V. All rights reserved.)

The aim of this study was to determine the effects of short and long-term RFR exposure on ABR by evaluating lipid peroxidation and antioxidant status in adult rats. Sixty male albino Wistar rats were randomly divided into four groups. S1:1 week sham, S10:10 weeks sham, E1:1 week RFR, E10:10 weeks RFR. Experimental group rats were exposed to RFR 2 h/day, 5 days/week during the test period. Sham rats were kept in the same conditions without RFR. After the experiment, ABRs were recorded from the mastoids of rats using tone burst acoustic stimuli. Biochemical investigations in rat brain and ultrastructural analysis in temporal cortex were performed. ABR wave I latency prolonged in E1-group and shortened in E10-group compared to their shams. TBARS level increased in E1-group, decreased in E10-group, on the contrary, SOD and CAT activities and GSH level decreased in E1-group, increased in E10-group compared to their sham groups. Edema was present in the neuron and astrocyte cytoplasms and astrocyte end-feet in both E1 and E10 groups. Our results suggest that 900 MHz RFR may have negative effects on the auditory system in acute exposure and no adverse effects in chronic exposure without weekends.

Purpose: Accumulation of amyloid beta (Aβ) is thought to be the major cause of the development and progression of Alzheimer's disease (AD). The aim of this study is to elucidate the effects of Aβ 1-42 at increasing concentrations on auditory evoked potentials (AEPs) and to determine possible changes relevant to the accumulation of Aβ 1-42 ., Materials and Methods: In this study, rats were randomized to following groups (n = 10 per group): sham (0.9% NaCl), Aβ-1 (1 μg/μl), Aβ-2 (2 μg/μl), Aβ-3 (3 μg/μl), Aβ-4 (4 μg/μl), Aβ-5 (6 μg/μl), Aβ-6 (8 μg/μl) and Aβ-7 (10 μg/μl) groups obtained by injection of 5 μl per ventricle. Then, AEPs were recorded in freely-moving rats. Latencies and amplitudes of AEPs, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were obtained in response to auditory stimulus. Furthermore, Aβ 1-42 levels were determined in the temporal cortex., Results: Aβ 1-42 levels were significantly higher in the temporal cortex in Aβ groups compared to the sham. In frontal and parietal regions, P1N1 amplitudes were significantly decreased in Aβ-3, 4, 5 and 6 groups, and N1P2 amplitudes were significantly decreased in all Aβ groups, whereas in temporal regions, P1N1 and N1P2 amplitudes were decreased in Aβ-2,3,4,5,6 and 7 compared to the sham. In the evoked gamma power and phase synchronization of gamma responses, we detected significant decrease after Aβ-4 group, whereas a significant decrease in the filtered gamma responses was observed in Aβ groups compared to the sham., Conclusions: AEPs might be used as a biomarker to determine the Aβ 1-42 related neuronal degeneration in the auditory networks., Competing Interests: Declaration of competing interest The authors declare no conflicts of interest., (Copyright © 2020 Medical University of Bialystok. Published by Elsevier B.V. All rights reserved.)

Purpose: There is a growing interest in the usage of radiofrequency radiation (RF) as a noninvasive brain stimulation method. Previously reported data demonstrated that RF exposure caused a change in brain oscillations. Therefore, we aimed to investigate effects of RF on brain oscillation by measuring the auditory response of different brain regions in rats., Materials and Methods: Rats were randomly divided into three groups (n = 12 per each group): Cage control (C), sham rats (Sh), and rats exposed to 2.1 GHz RF for 2 h/day for 7 days. At the end of the exposure, auditory evoked potentials (AEPs) were recorded at different locations in rats. Latencies and amplitudes of AEPs, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were obtained in response to an auditory stimulus. Furthermore, TBARS levels and 4-HNE, GFAP, iNOS, and nNOS expressions were evaluated in all groups., Results: Peak-to-peak amplitudes of AEPs were significantly higher in the RF group compared with the Sh group. There is no significant difference in peak latencies of AEPs between groups. Beside, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were significantly higher in the RF group compared with the Sh group. In addition, the RF group had significantly lower TBARS and 4-HNE levels than the Sh group. There were no significant differences between groups for GFAP, nNOS, and iNOS levels, and between the C and RF groups for all parameters., Conclusions: Our present findings suggest that short-term RF treatment under chosen experimental conditions have statistically significant effect on neuronal networks of rats by probably reducing oxidative damage. However, this effect must be further studied for possible noninvasive brain stimulation.

Alzheimer's disease (AD) is the most prevalent form of dementia and has an increasing incidence. The neuropathogenesis of AD is suggested to be a result of the accumulation of amyloid-β (Aβ) peptides in the brain. To date, Aβ-induced cognitive and neurophysiologic impairments have not been illuminated sufficiently. Therefore, we aimed to examine how spontaneous brain activities of rats changed by injection of increasing Aβ doses into the brain hemispheres, and whether these changes could be used as a new biomarker for the early diagnosis of the AD. Rats were randomized into following groups: sham (Sham) and seven Aβ-treated (i.c.v.) groups in increasing concentrations (from Aβ-1 to Aβ-7). After recovery, EEG recordings were obtained from implanted electrodes from eight electrode locations, and then, spectral and statistical analyses were performed. A significant decrement in gamma activity was observed in all Aβ groups compared with the sham group. In delta activity, we observed significant changes from Aβ-4 to Aβ-7 group compared with sham group. Delta coherence values were decreased from Aβ-4 to Aβ-7 and Aβ-5 to Aβ-7 groups for frontal and temporal electrode pairs, respectively. A gradual increment was observed in Aβ 1-42 level till Aβ-4 group. Positive correlation for global delta power and negative correlation for global gamma power between Aβ 1-42 peptide levels were detected. Consequently, it is conceivable to suggest gamma oscillation might be used to detect early stages of AD. Moreover, changes in delta activity provide information about the onset of major pathologic changes in the progress of AD., (© 2018 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)

The aim of this study was to investigate the possible toxic effects of sulfite on neurons by measuring active avoidance learning in normal and sulfite oxidase (SOX)-deficient aged rats. Twenty-four months of age Wistar rats were divided into four groups: control (C), sulfite-treated group (S), SOX-deficient group (D) and SOX-deficient + sulfite-treated group (DS). SOX deficiency was established by feeding rats with a low molybdenum (Mo) diet and adding 200 ppm tungsten (W) to their drinking water. Sulfite in the form of sodium metabisulfite (25 mg/kg) was given by gavage for six weeks. Active avoidance responses were determined by using an automated shuttle box. Hepatic SOX activity was measured to confirm SOX deficiency. The hippocampus was used for determining the activity of cyclooxygenase (COX) and caspase-3 enzymes and the level of prostaglandin E2 (PGE2) and nitrate/nitrite. SOX-deficient rats had an approximately 10-fold decrease in hepatic SOX activity compared with normal rats. Sulfite did not induce impairment of active avoidance learning in SOX-deficient rats and in normal rats compared with their control groups. Sulfite had no effect on the activity of COX and caspase-3 in the hippocampus. Treatment with sulfite did not significantly increase the level of PGE2 and nitrate/nitrite in the hippocampus.

Sulfite, commonly used as a preservative in foods, beverages, and pharmaceuticals, is a very reactive and potentially toxic molecule which is detoxified by sulfite oxidase (SOX). Changes induced by aging may be exacerbated by exogenous chemicals like sulfite. The aim of this study was to investigate the effects of ingested sulfite on visual evoked potentials (VEPs) and brain antioxidant statuses by measuring superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities. Brain lipid oxidation status was also determined via thiobarbituric acid reactive substances (TBARS) in normal- and SOX-deficient aged rats. Rats do not mimic the sulfite responses seen in humans because of their relatively high SOX activity level. Therefore this study used SOX-deficient rats since they are more appropriate models for studying sulfite toxicity. Forty male Wistar rats aged 24 months were randomly assigned to four groups: control (C), sulfite (S), SOX-deficient (D) and SOX-deficient + sulfite (DS). SOX deficiency was established by feeding rats with low molybdenum (Mo) diet and adding 200 ppm tungsten (W) to their drinking water. Sulfite in the form of sodium metabisulfite (25 mg kg(-1) day(-1)) was given by gavage. Treatment continued for 6 weeks. At the end of the experimental period, flash VEPs were recorded. Hepatic SOX activity was measured to confirm SOX deficiency. SOX-deficient rats had an approximately 10-fold decrease in hepatic SOX activity compared with the normal rats. The activity of SOX in deficient rats was thus in the range of humans. There was no significant difference between control and treated groups in either latence or amplitude of VEP components. Brain SOD, CAT, and GPx activities and brain TBARS levels were similar in all experimental groups compared with the control group. Our results indicate that exogenous administration of sulfite does not affect VEP components and the antioxidant/oxidant status of aged rat brains., (© The Author(s) 2014.)

Acute stress and elevated glucocorticoid hormone levels are well known to impair the retrieval of hippocampus-dependent 'declarative' memory. Recent findings suggest that stress might also impair the retrieval of non-hippocampal memories. In particular, stress shortly before retention testing was shown to impair the retrieval of striatal stimulus-response associations in humans. However, the mechanism underlying this stress-induced retrieval impairment of non-hippocampal stimulus-response memory remains elusive. In the present study, we investigated whether an acute elevation in glucocorticoid levels mediates the impairing effects of stress on retrieval of stimulus-response memory. Male Sprague-Dawley rats were trained on a stimulus-response task in an eight-arm radial maze until they learned to associate a stimulus, i.e., cue, with a food reward in one of the arms. Twenty-four hours after successful acquisition, they received a systemic injection of vehicle, corticosterone (1mg/kg), the corticosterone-synthesis inhibitor metyrapone (35mg/kg) or were left untreated 1h before retention testing. We found that the corticosterone injection impaired the retrieval of stimulus-response memory. We further found that the systemic injection procedure per se was stressful as the vehicle administration also increased plasma corticosterone levels and impaired the retrieval of stimulus-response memory. However, memory retrieval was not impaired when rats were tested 2min after the systemic vehicle injection, before any stress-induced elevation in corticosterone levels had occurred. Moreover, metyrapone treatment blocked the effect of injection stress on both plasma corticosterone levels and memory retrieval impairment, indicating that the endogenous corticosterone response mediates the stress-induced memory retrieval impairment. None of the treatments affected rats' locomotor activity or motivation to search for the food reward within the maze. These findings show that stress may affect memory processes beyond the hippocampus and that these stress effects are due to the action of glucocorticoids., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

In our previous study, the developmental effects of extremely low-frequency electric fields (ELF-EF) on visual and somatosensory evoked potentials in adult rats were studied. There is no study so far examining the effects of 50 Hz electric field (EF) on mismatch negativity (MMN) recordings after exposure of rats during development. Therefore, our present study aimed to investigate MMN and oxidative brain damage in rats exposed to EF (12 kV/m, 1 h/day). Rats were divided into four groups, namely control (C), prenatal (Pr), postnatal (Po), and prenatal+postnatal (PP). Pregnant rats of Pr and PP groups were exposed to EF during pregnancy. Following birth, rats of PP and Po groups were exposed to EF for three months. After exposure to EF, MMN was recorded by electrodes positioned stereotaxically to the surface of the dura, and then brain tissues were removed for histological and biochemical analyses. The MMN amplitude was higher to deviant tones than to standard tones. It was decreased in all experimental groups compared with the C group. 4-Hydroxy-2-nonenal (4-HNE) levels were significantly increased in the Po group with respect to the C group, whereas they were significantly decreased in the PP group compared with Pr and Po groups. Protein carbonyl levels were significantly decreased in the PP group compared with C, Pr, and Po groups. EF decreased MMN amplitudes were possibly induced by lipid peroxidation.

The purpose of our study was to investigate the developmental effects of extremely low frequency electric fields (ELF-EFs) on visual evoked potentials (VEPs) and somatosensory-evoked potentials (SEPs) and to examine the relationship between lipid peroxidation and changes of these potentials. In this context, thiobarbituric acid reactive substances (TBARS) levels were determined as an indicator of lipid peroxidation. Wistar albino female rats were divided into four groups; Control (C), gestational (prenatal) exposure (Pr), gestational+ postnatal exposure (PP) and postnatal exposure (Po) groups. Pregnant rats of Pr and PP groups were exposed to 50 Hz electric field (EF) (12 kV/m; 1 h/day), while those of C and Po groups were placed in an inactive system during pregnancy. Following parturition, rats of PP and Po groups were exposed to ELF-EFs whereas rats of C and Pr groups were kept under the same experimental conditions without being exposed to any EF during 68 days. On postnatal day 90, rats were prepared for VEP and SEP recordings. The latencies of VEP components in all experimental groups were significantly prolonged versus C group. For SEPs, all components of PP group, P2, N2 components of Pr group and P1, P2, N2 components of Po group were delayed versus C group. As brain TBARS levels were significantly increased in Pr and Po groups, retina TBARS levels were significantly elevated in all experimental groups versus C group. In conclusion, alterations seen in evoked potentials, at least partly, could be explained by lipid peroxidation in the retina and brain.