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The current study aimed to investigate the role of fucoidan in the oxidative and apoptotic effects of sulfoxaflor, a neonicotinoid sulfoximine insecticide, in the brain of Swiss albino mice (Mus musculus). Sulfoxaflor and fucoidan were administered to mice at doses of 15 mg/kg/day (1/50 oral LD50) and 50 mg/kg/day, respectively, by oral gavage for 24 h or 7 days. The tGSH, TBARS and protein levels, and GPx, GR, and GST enzyme activities were determined by spectrophotometric methods. Caspase-3 gene expression level was determined by RT-PCR. Data analysis showed that brains of sulfoxaflor-treated mice exhibited higher TBARS levels; GPx, GR, and GST enzyme activities; and caspase-3 expression levels, as well as lower levels of tGSH. Co-administration of fucoidan and sulfoxaflor reduced the TBARS levels, increased tGSH levels, and increased GPx, GR, and GST enzyme activities. Fucoidan also decreased the sulfoxaflor-induced up-regulation of caspase-3 mRNA expression. Results of the present study showed that sulfoxaflor caused oxidative stress by inducing lipid peroxidation and altering GSH-dependent antioxidants in the brain of mice. In addition, sulfoxaflor may trigger apoptotic cell death shown by the up-regulation of caspase-3. Fucoidan treatment modulated all the aforementioned alterations in the brain of mice. It was concluded that fucoidan might have antioxidant effects that support the GSH-dependent antioxidant system and can play a modulator role in oxidative stress and caspase-3 expression in the brain of sulfoxaflor treated-mice.

Low-frequency pulsed magnetic field (LF-PMF) application is a non-invasive, easy, and inexpensive treatment method in pain management. However, the molecular mechanism underlying the effect of LF-PMF on pain is not fully understood. Considering the obvious dysregulations of gene expression observed in certain types of voltage-gated sodium channels (VGSCs) in pain conditions, the present study tested the hypothesis that LF-PMF shows its pain-relieving effect by regulating genes that code VGSCs proteins. Five experimental rat groups (Control, Streptozotocin-induced experimental painful diabetic neuropathy (PDN), PDN Sham, PDN 10 Hz PMF, and PDN 30 Hz PMF) were established. After the pain formation in PDN groups, the magnetic field groups were exposed to 10/30 Hz, 1.5 mT PMF for 4 weeks, an hour daily. Progression of pain was evaluated using behavioral pain tests during the entire experimental processes. After the end of PMF treatment, SCN9A (NaV1.7 ), SCN10A (NaV1.8 ), SCN11A (NaV1.9 ), and SCN3A (NaV1.3 ) gene expression level changes were determined by analyzing real-time polymerase chain reaction results. We found that 10 Hz PMF application was more effective than 30 Hz on pain management. In addition, NaV1.7 and NaV1.3 transcriptions were upregulated while NaV1.8 and NaV1.9 were downregulated in painful conditions. Notably, the downregulated expression of the genes encoding NaV1.8 and NaV1.9 were re-regulated and increased to control level by 10 Hz PMF application. Consequently, it may be deduced that 10 Hz PMF application reduces pain by modulating certain VGSCs at the transcriptional level. © 2021 Bioelectromagnetics Society.

Large conductance calcium-activated potassium (BK) channels play a crucial role in the repolarization and after-hyperpolarization phases of the cell membrane. The channel openers are also used in treatment of some diseases, including hypo/hyperkalemic periodic paralysis. However, little is known about the effects of BK channels and the channel activators on membrane potentials in skeletal muscle. In addition, the effects of reactive oxygen species (ROS) on BK channels in skeletal muscle are also unknown. Therefore, the aim of this study was to determine the effects of BK channel openers and ROS on membrane potentials in skeletal muscle fibers. For this purpose, resting membrane potentials and action potentials (AP) of frog gastrocnemius muscles were recorded in the presence of commonly used BK channel openers NS1619 and NS11021, H2O2 (a type of ROS), and both using intracellular microelectrode technique. The channel activators significantly and dose-dependently decreased amplitude and increased rise time of AP but did not impact repolarization. The presence of H2O2 plus NS1619 or NS11021 resulted in significant change because the channel openers completely reversed the deleterious effects of hydrogen peroxide on the repolarization phase of AP in skeletal muscle fibers. In the present study, the contributions of BK channel activation and the modulatory role of H2O2 on membrane potentials was demonstrated in skeletal muscle fibers, for the first time. Moreover, it should be noted that BK channel openers should be used in the treatment of reactive oxygen species-induced skeletal muscle diseases.

Pulsed magnetic fields (PMFs) have significant therapeutic effects on many disorders. However, the effects of PMF on vascular homeostasis remain unclear. Therefore, in the present study, we investigated the role of in vivo PMF in maintaining vascular homeostasis during H2O2-induced oxidative stress. For this purpose, rats were exposed to PMF (40 Hz, 1.5 mT) for 1 h for a period of 30 days, following which their thoracic aortas were excised. H2O2 was exogenously applied to the aortic rings. Constrictions were measured in a tissue bath using an electrophysiological technique. Bcl-2 and endothelial nitric oxide synthase (eNOS) protein levels were determined by Western blotting. We found lesser H2O2-induced vasoconstriction in the PMF group than in the control group in endothelium-intact (E+) rings. As H2O2 also induces apoptosis, after incubation with H2O2 (40 min) to induce early apoptosis, we added KCl and measured KCl-induced contractions. All the groups, endothelium intact or denuded (E-) showed decreased responses; however, we still observed the effect of PMF in the E+ group due to increased endothelial activity. In addition, PMF increased the expression of the eNOS protein, which might be a key target of PMF. Our results suggest that in vivo application of PMF protects vascular responses through endothelium-mediated mechanisms during oxidative stress. Therefore, PMF might play a protective role against vascular diseases.

Astrocytes are greatly impacted by oxidative stress, which can also be related to neurodegenerative diseases. Therefore, preventing the production of reactive oxygen species (ROS) is crucial for maintaining healthy cells. Large conductance Ca2+-activated big potassium (BK) channel openers are effective in eliminating the effects of oxidative stress. The present study aims to determine if NS11021, a BK channel opener, protects the astrocytes from harmful effects of hydrogen peroxide (H2O2), which is an oxidative stress inducer. For this purpose, primary astrocyte cultures were incubated with H2O2, NS11021, and Iberiotoxin both separately and together. H2O2 decreased cell viability by approximately 50% and increased the number of ROS-positive astrocytes. However, NS11021, but not Iberiotoxin, reversed the deleterious effects of H2O2 on cell viability and decreased ROS production. Moreover, dysregulations in Cyclin D1/CDK6/p21 gene expressions under conditions of oxidative stress were regulated again by the opener. To the best of our knowledge, this study has been the first to reveal that NS11021 reversed the deleterious effects of H2O2 on cell viability by regulating ROS production in astrocytes. Its effect may also be related to the regulation of cell cycle at the transcriptional level. NS11021 may also be used as an agent for the treatment of oxidative-stress related dysfunction of astrocytes.

Low-frequency pulsed magnetic field (LF-PMF) application is a non-invasive, easy, and inexpensive treatment method in pain management. However, the molecular mechanism underlying the effect of LF-PMF on pain is not fully understood. Considering the obvious dysregulations of gene expression observed in certain types of voltage-gated sodium channels (VGSCs) in pain conditions, the present study tested the hypothesis that LF-PMF shows its pain-relieving effect by regulating genes that code VGSCs proteins. Five experimental rat groups (Control, Streptozotocin-induced experimental painful diabetic neuropathy (PDN), PDN Sham, PDN 10 Hz PMF, and PDN 30 Hz PMF) were established. After the pain formation in PDN groups, the magnetic field groups were exposed to 10/30 Hz, 1.5 mT PMF for 4 weeks, an hour daily. Progression of pain was evaluated using behavioral pain tests during the entire experimental processes. After the end of PMF treatment, SCN9A (NaV

WOS: 000495863700013 This paper reports the range extension of Kyphosus vaigiensis in the northeastern (NE) Mediterranean. On 18 November, 2018, a single specimen of K. vaigiensis was caught in Iskenderun Bay (36 degrees 45.6' N, 35 degrees 40.8' E) by a recreational fisherman and reported through a social media application. The specimen was identified using morphological and molecular methods. Its occurrence and distribution in the NE Mediterranean were investigated based on interviews with fishers.

Voltage-gated sodium channel genes and associated proteins have been cloned and studied in many mammalian and invertebrate species. However, there is no data available about the sodium channel gene(s) in the crayfish, although the animal has frequently been used as a model to investigate various aspects of neural cellular and circuit function. In the present work, by using RNA extracts from crayfish abdominal ganglia samples, the complete open reading frame of a putative sodium channel gene has firstly been cloned and molecular properties of the associated peptide have been analyzed. The open reading frame of the gene has a length of 5793 bp that encodes for the synthesis of a peptide, with 1930 amino acids, that is 82 % similar to the a-peptide of a sodium channel in a neighboring species, Cancer borealis. The transmembrane topology analysis of the crayfish peptide indicated a pattern of four folding domains with several transmembrane segments, as observed in other known voltage-gated sodium channels. Upon analysis of the obtained sequence, functional regions of the putative sodium channel responsible for the selectivity filter, inactivation gate, voltage sensor, and phosphorylation have been predicted. The expression level of the putative sodium channel gene, as defined by a qPCR method, was measured and found to be the highest in nervous tissue.

Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder and the most common form of dementia in people over the age of 65. The predominant genetic risk factor for AD is the ε4 allele encoding apolipoprotein E (ApoE4). The secreted glycoprotein Reelin, which is a physiological ligand for the multifunctional ApoE receptors Apolipoprotein E receptor 2 (Apoer2) and very low-density lipoprotein receptor (Vldlr), enhances synaptic plasticity. We have previously shown that the presence of ApoE4 renders neurons unresponsive to Reelin by impairing the recycling of the receptors, thereby decreasing its protective effects against amyloid β (Aβ) oligomer-induced synaptic toxicity in vitro. Here, we show that when Reelin was knocked out in adult mice, these mice behaved normally without overt learning or memory deficits. However, they were strikingly sensitive to amyloid-induced synaptic suppression, and had profound memory and learning disabilities at very low amounts of amyloid deposition. Our findings highlight the physiological importance of Reelin in protecting the brain against Aβ-induced synaptic dysfunction and memory impairment.