Browsing by Subject "neurotoxicity"
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Item Is attempting suicide an adverse effect of oxybutynin in a child with enuresis nocturna? [1](Lippincott Williams and Wilkins, 2001) Coskun S.; Yüksel H.; Onag A.[No abstract available]Item Repeated epidural injections of ketamine with preservative benzethonium chloride produce evidence for neurotoxicity in rabbits(2003) Yentur E.A.; Mirzai I.T.; Mirzai H.; Ates U.; Baka M.; Yurtseven M.Background and objectives: In this study, we investigated whether repeated doses of 1% ketamine with preservative benzethonium chloride, administered into the epidural space of the rabbit, caused direct neurotoxicity. Methods: Twelve rabbits were randomly assigned to two groups (ketamine and control). After the animals were anesthetized, lumbar epidural catheters were placed for repeated epidural drug delivery. The ketamine group received 1% ketamine with preservative benzethonium chloride (0.5 ml) and the control group received isotonic saline (0.5 ml) once a day for 14 consecutive days. The day after the last injection, the animals were reanaesthetized, the left and right ventricles were cannulated and perfused with 2% glutaraldehyde, 1% formaldehyde mixture, in 0.1 mol/l phosphate buffer. Then, laminectomy was performed. A five centimetre segment of the spinal cord was removed and examined by light and electron microscopy to observe possible histological changes. Microscopic examinations were performed by coding each animal by a neuro-histologist who was blinded as to the source of each specimen. Results: Ketamine-treated rabbits showed significant histological changes at light and electron microscopy findings compared with the control group (p < 0.05). Conclusions: These changes suggested a neurotoxic effect of ketamine with preservative benzethonium chloride following chronic epidural administration.Item The Effects of Methotrexate on the Development of Neural Tube Defects in the Chick Embryo(2003) Vatansever H.S.; Umur A.Ş.; Inan V.S.; Selçuki M.During chick development, one of the earliest differentiated tissues is the neural tube. After 24 h of incubation, a chick egg starts to differentiate and 30-48 h after incubation the neural plate is closed from head to tail to form the neural tube. If factors controlling the neural tube's closing are disrupted, this consequently causes neural tube closure defects during this time. In this study, the effect of methotrexate on the developing neural tube was investigated during early chick development. For this research, 40 specific pathogen free (SPF) white Leghorn type chick embryos were used. They were incubated for 30 h at 37.8 ± 2°C. Methotrexate, which inhibits the dihydrofolate reductase enzyme by a competitive mechanism, was injected within therapeutic dosage limits (10 mg/m2, 20 mg/m2, 40 mg/m2) in ovo. Ten eggs were injected with 0.9% NaCl and used as a control group. All groups, after the injection, were incubated for 48 and 72 h. They were then dissected and the embryos were fixed in 10% (v/v) formalin for 2 h. The embryos were embedded in paraffin wax and 5 μ serial sections were taken. Sections were stained with haematoxylin and then observed under light microscopy. While 20 mg/m2 or 40 mg/m2 methotrexate embryos were not alive when they were opened at 48 h incubation, 10 mg/m 2 methotrexate embryos maintained normal development after 48 and 72 h incubation. However, there was developmental retardation in the methotrexate injected group when compared with the control group with development of the brain being retarded; the volume of brain vesicles was lower than in the control group. Our results suggested that methotrexate, an antimetabolite of folic acid, caused neural tube closure defects when injected at therapeutic dosage levels. Folic acid is essential for normal development of the nervous system; therefore, folate antagonists might be more harmful to the central nervous system than to other parts of the developing body.Item Treatment of mucocutaneous manifestations of behcet's disease; [Behçet hastaliǧi mukokutanöz bulgularinda tedavi̇](2011) Inanr I.; Saçar H.Behçet's disease (BD) is a chronic recurrent vasculitis with an unclear etiology. In addition to typical oral, genital and ocular lesions, it involves many organs and systems mainly vascular articular, vascular and neurological ones. Mucocutaneous manifestations are the most frequent and have an important role in diagnosis. In this article, treatment alternatives for mucocutaneous involvement of BD are reviewed.Item Neurotoxic effect of statins on mouse neuroblastoma NB2a cell line(2011) Vural K.; Tuglu M.I.Objective: Evidences from cell culture experiments suggest a link between cholesterol and nervous system disease. Statins may have neurotoxic or neuroprotective effects, but these effects remain controversial. Therefore, the present study was aimed to investigate the possible toxicity of statins on a neurite outgrowth in mouse neuroblastoma NB2a cell line. Materials and Methods: We have utilized d-cAMP-induced terminally differentiated NB2a cells in culture as an experimental model to study the effects of statins. The cell survival and proliferation were studied by MTT. Measurement of neurite outgrowth was done by neurotoxicity screening test. NB2a cell differentiation was achieved by serum free medium plus 0.5 mM dibutyryl cAMP. Cells were incubated for 24 hours at 37°C. After this period, lovastatin, mevastatin and atorvastatin were added to wells at different concentrations (1, 3, 10, 100 μM). Approximately 100 cells were chosen for each sample and examined randomly 24 hours later, from 10 different fields. Total length of neurite was photographed microscopically and measured by image analyze software. Changes in neurite lengths were expressed as % inhibition compared to that of the control group. Results: Results showed that three statins at high concentrations induced neurite inhibition, inhibited proliferation and reduced the viability of differentiated neuroblastoma NB2a cells. Conclusions: Our results suggest that statins could act as a neurotoxic agent at high doses depending upon their concentrations. These results require further investigation at ultra structural and molecular levels to understand long term side effects for clinical safety of statins.Item Neurotoxic effect of povidone-iodine on the rat spine using a laminectomy-durotomy model(2012) Akcay E.; Ersahin Y.; Ozer F.; Duransoy Y.K.; Camlar M.; Atci I.; Yagci A.; Ozer O.Objective The efficacy and safety of povidone-iodine in wound dressing and irrigation of some operative cavities were established by many in vitro and in vivo experimental reports and clinical series. However, its use in defective tissue in neural structures has not been confirmed yet. The aim of the present study was to histopathologically investigate its effect on neural tissues when applied on the upper side of defective dura. Methods Wistar rats were randomly divided into two experimental groups: control and povidone-iodine groups. In the control group, durotomy was performed following laminectomy, and the spinal cord was covered with a dry sponge. In the study group, the same procedure was performed, but open duras were covered with a sponge that had been wetted with 0.1 % povidone-iodine solution. Three weeks after surgery, all experimental animals were sacrificed, and histopathological evaluations were conducted. Results Myelin changes were absent or minimal in all cases of the control group but were present as markedly increased myelin degeneration in nearly all cases in the study group. Axonal degeneration and hypoxic neuronal damage were absent in the control group, whereas they were marked in half of the study group. No statistically significant differences were established in Schwann cell proliferation, venous congestion, and lymphocytic proliferation between the two groups. Conclusions Based on the present study, 0.1 % povidone-iodine solution cannot be recommended for wound dressing for neural structures such as myelomeningocele cases because of possible damage to underlying neural tissues. © Springer-Verlag 2012.Item The protective effect of metformin against the noise-induced hearing loss(Springer Verlag, 2018) Kesici G.G.; Öcal F.C.A.; Gürgen S.G.; Erdem Ş.R.; Öğüş E.; Erbek H.S.; Özlüoğlu L.N.Objective: To test the protective effect of metformin against noise-induced hearing loss. Methods: 24 rats were included in the study. The first group was exposed to noise only, the second group took metformin, the third group was exposed to noise and took metformin, and the fourth group was neither exposed to noise nor took metformin as control group. After measurement of baseline DPOAE and ABR of rats, the metformin group and the metformin + noise group received 300 mg/kg/day metformin via gavage for 10 days. On the 11th day, group 1 and group 3 were exposured to white noise at 105 dB SPL for 15 h. After noise exposure, DPOAE and ABR measurements of all rats were repeated on days 1st, 7th, and 21st. At the end of the study, all animals were sacrificed and cochlear tissues were separated for immunohistochemical assessments. Results: ABR threshold values and DPAOE measurements of groups 1 and 3 were deteriorated on the 1st day after noise, while deterioration in group 1 continued on 7th and 21st days, but normalized on 7th day in group 3. After immune staining, a significant immunoreaction was observed in the noise group, while the reaction in the noise + metformin group was close to the control group. Conclusion: Metformin has a protective effect on noise-induced hearing loss in rats. As a conclusion, it is determined that metformin protects from permanent threshold shift in rats. It can be considered a good alternative for protecting noise-induced hearing loss. © 2018, Springer-Verlag GmbH Germany, part of Springer Nature.Item The neuroprotective effect of pioglitazone on NB2a mouse neuroblastoma cell culture; [Pioglitazonun NB2a fare nöroblastoma hücre kültürüdeki nöroprotektif etkisi](Veteriner Fakultesi Dergisi, 2019) Vural K.; Seyrek O.Pioglitazone (PGT) is a PPAR-γ activator that has neuroprotective properties via different mechanisms. It is thought to be neuroprotective in both acute and chronic use. Chlorpyrifos (CPS) is an Organophosphate insecticide that leads to attention deficit and cognitive problems in children and its neurotoxic effects are well known. This study aims to investigate the neuroprotective effects of PGT on CPS neurotoxicity in NB2a cell in the culture medium. We investigated the cell viability and proliferation using MTT assay and the percentage of neurite inhibition was analysed by measuring neurite outgrowth. Apoptosis was evaluated using the apoptotic index in TUNEL staining. Cell proliferation was found to be significantly reduced by CPS (25 µM), and this concentration-based reduction was prevented by PGT. Neurite outgrowth was inhibited by CPS (25 µM), whereas PGT significantly reversed neurite inhibition at and above 10 μM concentrations. The apoptotic index, which was increased using CPS (25 µM), was observed to reduce using PGT, depending on the concentration. Organophosphate is harmful to human health, and to our knowledge, there is no treatment. In individuals exposed to chlorpyrifos toxicity, acute toxic effects on neurons may be prevented or treated by PGT. © 2019, Veteriner Fakultesi Dergisi. All rights reserved.Item The Effect of Monosodium Glutamate on Neuronal Signaling Molecules in the Hippocampus and the Neuroprotective Effects of Omega-3 Fatty Acids(American Chemical Society, 2021) Gürgen S.G.; Sayln O.; Çeti˙n F.; Sarsmaz H.Y.; Yazlcl G.N.; Umur N.; Yücel A.T.Monosodium glutamate (MSG) is a flavoring substance added to many ready-to-eat foods and has known neurotoxic effects. This study was performed in order to examine the potential toxic effect of MSG on neurons in various regions of the hippocampus in prepubertal rats. It also investigated the protective effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on brain-derived neurotropic factor (BDNF), n-methyl-d-aspartate receptor (NMDA-R), and neuropeptide-Y (NPY) expression in the brain, using immunohistochemical and biochemical methods. Six female prepubertal Wistar albino rats were used in each group. Group 1, the control group, received 0.9% saline solution subcutaneously (sc) on days 1, 3, 5, 7, and 9. Group 2 received 4 mg/g MSG sc on days 1, 3, 5, 7, and 9. Group 3 received MSG + EPA (4 mg/g sc on days 1, 3, 5, 7, and 9. Oral 300 mg/kg for 9 d), while Group 4 received MSG + DHA (4 mg/g sc on days 1, 3, 5, 7, and 9 and 300 mg/kg orally for 9 d, respectively). At the end of the ninth day the hippocampal regions of the brain were removed and either fixed for immunohistochemical staining or stored at -80 °C for biochemical parameter investigation. BDNF, NMDA-R, and NPY expression results were evaluated using immunohistochemistry and an enzyme-linked immunosorbent assay. According to our findings, neurons in the control group hippocampal CA1 and DG regions exhibited strong BDNF, NPY, and NMDA-R reactions, while an expression in both regions decreased in the MSG group (p < 0.00). However, in the MSG-EPA and MSG-DHA groups, BDNF, NPY, and NMDA-R immunoreactions in neurons in the same region were similar to those of the control group (p = 0.00). No significant difference was observed in terms of expression in hippocampal neurons between the MSG-EPA and MSG-DHA groups (p > 0.00). In conclusion, since MSG caused a decrease in BDNF, NMDA-R, and NPY neural signaling molecules in the CA1 and DG regions of the hippocampus of prepubertal rats compared to the control group, care is required over the consumption of MSG, since it may affect memory-related neurons in these age groups. In addition, we concluded that the use of omega-3 fatty acids such as EPA and DHA in addition to MSG may protect against the neurotoxic effects of MSG. © 2021 American Chemical Society.Item Surface Area of Graphene Governs Its Neurotoxicity(American Chemical Society, 2023) Taşdemir Ş.; Morçimen Z.G.; Doǧan A.A.; Görgün C.; Şendemir A.Due to their unique physicochemical properties, graphene and its derivatives are widely exploited for biomedical applications. It has been shown that graphene may exert different degrees of toxicity in in vivo or in vitro models when administered via different routes and penetrated through physiological barriers, subsequently being distributed within tissues or located within cells. In this study, in vitro neurotoxicity of graphene with different surface areas (150 and 750 m2/g) was examined on dopaminergic neuron model cells. SH-SY5Y cells were treated with graphene possessing two different surface areas (150 and 750 m2/g) in different concentrations between 400 and 3.125 μg/mL, and the cytotoxic and genotoxic effects were investigated. Both sizes of graphene have shown increased cell viability in decreasing concentrations. Cell damage increased with higher surface area. Lactate dehydrogenase (LDH) results have concluded that the viability loss of the cells is not through membrane damage. Neither of the two graphene types showed damage through lipid peroxidation (MDA) oxidative stress pathway. Glutathione (GSH) values increased within the first 24 and 48 h for both types of graphene. This increase suggests that graphene has an antioxidant effect on the SH-SY5Y model neurons. Comet analysis shows that graphene does not show genotoxicity on either surface area. Although there are many studies on graphene and its derivatives on their use with different cells in the literature, there are conflicting results in these studies, and most of the literature is focused on graphene oxide. Among these studies, no study examining the effect of graphene surface areas on the cell was found. Our study contributes to the literature in terms of examining the cytotoxic and genotoxic behavior of graphene with different surface areas. © 2023 American Chemical Society. All rights reserved.Item Effects of Oxytocin on Glutamate Mediated Neurotoxicity in Neuroblastoma Cell Culture(Turkish Neuropsychiatric Society, 2024) Gürbüz Özgür B.; Vural K.; Tuğlu M.İ.Introduction: We aimed to investigate the effects of oxytocin on neurite growth, cell viability, cell proliferation and apoptosis to demonstrate its neuroprotective effect on glutamate induced neurotoxicity in human neuroblastoma SH-SY5Y cell culture. Method: The effect of oxytocin on the toxic effects of glutamate in human neuroblastoma SH-SY5Y cell line with the Neurotoxicity Screening Test (NTT), apoptotic effects by Terminal Transferase dUTP Nick End Labeling (TUNEL) method and cell viability test by 3-(4.5-dimethylthiazol-2-yl)-2.5-diphenyltetrazolium bromide (MTT) method. In the NTT test; Neurotoxicity was induced by adding glutamate at a concentration of 32 µM to the cell culture. Oxytocin was added at 1, 3, 10, 30 and 100 µM concentrations and its effect on neurite elongation was investigated. It was demonstrated by TUNEL method that application of glutamate caused apoptosis. Afterwards, when glutamate and different doses of oxytocin were given, antiapoptotic effect was evaluated with the apoptotic index. Results: Glutamate was found to have a dose-dependent neurotoxic effect and reduced neurite elongation by 50% at a concentration of 32 μM. It was shown that the inhibition of neurite elongation caused by glutamate decreased in a dose-dependent manner by applying oxytocin. Especially oxytocin was found to significantly reduce neurite inhibition and show a neuroprotective effect starting from 10 µM concentrations. The concentration at which glutamate reduces cell proliferation by 50% was determined as 54 µM in MTT. Subsequently, it was observed that the adverse effect of glutamate on cell proliferation significantly decreased with oxytocin administration, depending on the dose. Conclusion: It was found that different concentrations of glutamate have a significant toxic effect on cell proliferation and viability, glutamate inhibits neurite elongation in a dose-dependent manner; oxytocin reduces neurite inhibition caused by glutamate, has a neuroprotective effect, increases cell viability and has antiapoptotic effects. © 2023 by Turkish Association of Neuropsychiatry.