Neurotoxicity Research最新文献

{"title":"Caspases and brain-derived Neurotrophic Factor Levels and their Correlations with Psychiatric Symptoms in post-COVID-19.","authors":"Lia D R Broseghini, Camila O Arent, Lucas C Pedro, Laísa N Dos Santos, Flávia S Niero, Gabriel S Mondo, Amanda G Bertollo, Maiqueli Eduarda D Mingoti, Khyani Mathias, Lucineia G Danielski, Tatiana Barichello, João Quevedo, Luciane B Ceretta, Zuleide Maria Ignácio, Fabricia Petronilho, Gislaine Z Réus","doi":"10.1007/s12640-025-00757-z","DOIUrl":"https://doi.org/10.1007/s12640-025-00757-z","url":null,"abstract":"<p><p>The coronavirus disease 2019 (COVID-19) pandemic has brought significant challenges to global health, not only due to respiratory symptoms but also due to its impact on psychiatric disorders. Understanding the biological mechanisms underlying psychiatric manifestations in individuals with COVID-19 is crucial. This study aimed to investigate potential alterations in caspase 3 and 8 levels, as well as brain-derived neurotrophic factor (BDNF) levels, in individuals with COVID-19. The association of these markers with mental health was also assessed. A cross-sectional study was conducted, including individuals with COVID-19 and those without the disease. The stress levels were higher in individuals with COVID-19. Caspase 3 and 8 and BDNF levels were increased in individuals with COVID-19 compared to individuals without COVID-19. No significant differences were found in caspase 3 and 8 and BDNF levels between moderate/severe and asymptomatic/mild symptoms of COVID-19. The results indicate that no significant differences were observed between the diagnosis of anxiety disorders and the levels of markers. However, higher caspase 3 levels in individuals without anxiety and COVID-19 were found. No significant associations between the diagnosis of major depressive disorder or psychiatric symptoms and caspase 3, caspase 8, and BDNF levels were found. The results indicate that, although caspase 3, caspase 8, and BDNF levels are increased in individuals with COVID-19, these elevations are not associated with the severity of COVID-19 symptoms or psychiatric conditions and symptoms in post-COVID-19. These findings suggest that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection may influence cellular activity and neurotrophic markers, but that other factors likely contribute to psychiatric disorders.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 5","pages":"39"},"PeriodicalIF":3.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145252031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Asiatic Acid Attenuated Aluminum Chloride-Induced Tau Pathology, Oxidative Stress and Apoptosis Via AKT/GSK-3β Signaling Pathway in Wistar Rats.","authors":"Mashoque Ahmad Rather, Arokiasamy Justin-Thenmozhi, Thamilarasan Manivasagam, Chidambaram Saravanababu, Gilles J Guillemin, Musthafa Mohamed Essa","doi":"10.1007/s12640-025-00762-2","DOIUrl":"https://doi.org/10.1007/s12640-025-00762-2","url":null,"abstract":"","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 5","pages":"38"},"PeriodicalIF":3.3,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145252009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Naringenin Decreases α-Synuclein Expression and Neuroinflammation in MPTP-Induced Parkinson's Disease Model in Mice.","authors":"Sugumar Mani, Sathiya Sekar, Rajamani Barathidasan, Thamilarasan Manivasagam, Arokiasamy Justin Thenmozhi, Murugan Sevanan, Saravana Babu Chidambaram, Musthafa Mohamed Essa, Gilles J Guillemin, Meena Kishore Sakharkar","doi":"10.1007/s12640-025-00761-3","DOIUrl":"https://doi.org/10.1007/s12640-025-00761-3","url":null,"abstract":"","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 5","pages":"37"},"PeriodicalIF":3.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Telmisartan Ameliorates Astroglial and Dopaminergic Functions in a Mouse Model of Chronic Parkinsonism.","authors":"Sathiya Sekar, Sugumar Mani, Barathidasan Rajamani, Thamilarasan Manivasagam, Arokiasamy Justin Thenmozhi, Abid Bhat, Bipul Ray, Musthafa Mohamed Essa, Gilles J Guillemin, Saravana Babu Chidambaram","doi":"10.1007/s12640-025-00759-x","DOIUrl":"https://doi.org/10.1007/s12640-025-00759-x","url":null,"abstract":"","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 5","pages":"36"},"PeriodicalIF":3.3,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regular Exercise with Panax Ginseng Supplementation Attenuates Arsenic-Induced Muscular Weakness and Neurobehavioral Changes in Mice.","authors":"Sharmin Akter Beauty, Sharon Jahan Sarder, Jakir Hossain, Nesar Uddin, Osman Goni, Rajoana Karim Rimi, Shakhawoat Hossain, Farjana Nikkon, Seiichiro Himeno, Khaled Hossain, Zahangir Alam Saud","doi":"10.1007/s12640-025-00756-0","DOIUrl":"https://doi.org/10.1007/s12640-025-00756-0","url":null,"abstract":"<p><p>Arsenic (As) contamination of groundwater in some parts of Bangladesh has become a major threat to human health. Chronic exposure to As leads to anxiety development, memory impairment, and muscle weakness in humans and experimental animals. Panax ginseng (PG) is an herb utilized for multiple health-related applications. Furthermore, regular exercise (Ex) can reduce the risk of various diseases, and is also effective against heavy metal-associated neurotoxicity. Swiss albino mice were divided into five groups (n = 6) to evaluate the protective effects of Ex and PG (50 mg/kg body weight) supplementation against As-induced (10 mg/kg body weight) muscular weakness and neurobehavioral Changes for 60 days. Mice exposed to As showed weaker muscular strength, impaired memory and increased anxiety-like behavior along with the alteration of biochemical parameters related muscular weakness and neurobehavioral changes compared to control mice. However, As + Ex + PG-exposed mice showed significantly (p < 0.05) better performances in all behavioral tests compared to mice exposed to As alone. Additionally, compared to As-exposed mice, As + Ex + PG-exposed mice showed significantly improved (p < 0.05) activity of acetylcholinesterase (AChE), butyrylcholinesterase (BChE), superoxide dismutase (SOD), and reduced glutathione reductase (rGR) in brain, while serum levels of lactate dehydrogenase (LDH) and creatine kinase (CK) were reduced. Furthermore, levels of nuclear factor erythroid 2-related factor-2 (Nrf2), heme oxygenase-1 (HO-1), and interleukin-10 (IL-10) levels were increased, while interleukin-6 (IL-6) levels were decreased in brain tissue of As + Ex + PG-exposed mice compared to As-exposed mice. The results of this study suggest that Ex with PG supplementation can attenuate As-induced muscle weakness, cognitive disorder and anxiety development, possibly through the up-regulation of the Nrf2-HO-1 pathway in the As-exposure mice.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 5","pages":"34"},"PeriodicalIF":3.3,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intracerebral Administration of Hydrogen Sulfide Impairs Bioenergetics, Redox Status and Mitochondrial Quality Control in Rat Striatum.","authors":"Manuela Bianchin Marcuzzo, Josyane de Andrade Silveira, Camila Vieira Pinheiro, Jaqueline Santana da Rosa, Angela B Zemniaçak, Morgana Brondani, Nathalia Simon Kist, Chrístofer Ian Hernandez Hoffmann, Helgi B Schioth, Alexandre U Amaral, Moacir Wajner, Guilhian Leipnitz","doi":"10.1007/s12640-025-00758-y","DOIUrl":"https://doi.org/10.1007/s12640-025-00758-y","url":null,"abstract":"<p><p>Elevated hydrogen sulfide (sulfide) levels are observed in tissues, including the brain, of patients with ethylmalonic encephalopathy. Clinical manifestations of this disorder involve severe neurological symptoms and abnormalities such as developmental delay, pyramidal and extrapyramidal signs, cortical atrophy and basal ganglia lesions. To elucidate the pathophysiology of basal ganglia alterations, we investigated the effects of sulfide on bioenergetics, redox status and mitochondrial quality control in the striatum of Wistar rats. After placing the rat in a stereotaxic apparatus, a single intrastriatal administration of sulfide (NaHS; 2 or 4 µmol) or PBS (control) was performed. Thirty minutes after the administration, the rats were euthanized, and the striatum was used for the determination of biochemical parameters. Sulfide administration, at both doses, altered the activities of antioxidant enzymes. At the lowest dose, sulfide showed a strong tendency toward increased activity of citrate synthase. Furthermore, the highest dose of sulfide also reduced respiratory chain complex IV activity and mitochondrial respiration with NADH- and FADH₂-linked substrates. Levels of Nrf2, the main factor that regulates the expression of antioxidant defenses, were also reduced by 4 µmol of sulfide. The metabolite further increased the content of MFN1, suggesting mitochondrial fusion. Additionally, sulfide elevated Parkin and TBC1D15 and reduced LC3 levels, indicative of mitophagy dysregulation. The content of markers of mitochondrial mass and fission were not changed. Our study shows that high levels of sulfide in the striatum of rats affect bioenergetics, redox status and mitochondrial quality control. We suggest that these pathomechanisms are involved in the pathophysiology of basal ganglia alterations verified in ethylmalonic encephalopathy.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 5","pages":"35"},"PeriodicalIF":3.3,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: AMPK Inhibition Enhances the Neurotoxicity of Cu(II) in SH-SY5Y Cells.","authors":"Ai-Ping Lan, Xian-Jia Xiong, Jun Chen, Xi Wang, Zhi-Fang Chai, Yi Hu","doi":"10.1007/s12640-025-00755-1","DOIUrl":"https://doi.org/10.1007/s12640-025-00755-1","url":null,"abstract":"","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 5","pages":"33"},"PeriodicalIF":3.3,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144962950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Amelioration of Aluminum Maltolate-Induced Inflammation and Endoplasmic Reticulum Stress-Mediated Apoptosis by Tannoid Principles of Emblica Officinalis in Neuronal Cellular Model.","authors":"Mathiyazahan Dhivya Bharathi, Arokiasamy Justin-Thenmozhi, Thamilarasan Manivasagam, Mashoque Ahmad Rather, Chidambaram Saravana Babu, Musthafa Mohamed Essa, Gilles J Guillemin","doi":"10.1007/s12640-025-00754-2","DOIUrl":"10.1007/s12640-025-00754-2","url":null,"abstract":"","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 4","pages":"32"},"PeriodicalIF":3.3,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha Pinene Affects Intestinal Permeability and Protects the Gastrointestinal System Against Rotenone Toxicity via the Keap1/Nrf2 Pathway in Rats.","authors":"Berna Tezcan Yavuz, Emel Kabartan Cokeli, Cansin Sirin Tomruk, Gulay Hacioglu, Selma Cirrik, Canberk Tomruk","doi":"10.1007/s12640-025-00753-3","DOIUrl":"10.1007/s12640-025-00753-3","url":null,"abstract":"<p><p>Rotenone, often used to experimentally induce Parkinson's disease in rodents, is a well-known neurotoxic pesticide. One of the most common non-motor symptoms in Parkinson's patients is gastrointestinal dysfunction. Therefore, protecting the gastrointestinal system plays an important role in the onset and progression of the disease. In this study, both the effects of Rotenone on the stomach and small intestine and the possible protective role of Alpha Pinene against Rotenone toxicity, were investigated. Sixty adult male Sprague-Dawley rats were randomly divided into five groups as Control, Vehicle, Alpha Pinene (50 mg/kg/day), Rotenone (2 mg/kg/day) and Rotenone + Alpha Pinene. At the end of the 28-day experimental period, the stomach and jejunum tissues were examined using histological (haematoxylin-eosin and alcian blue-PAS stainings), biochemical (malondialdehyde, zonulin and Fatty Acid Binding Protein-2 levels) and molecular (Keap1, Nrf2 and HO-1 mRNA levels) techniques. While the data showed the presence of oxidative stress and impaired intestinal permeability in the stomach and jejunum tissues in the Rotenone group, these symptoms were observed to be alleviated in the Rotenone + Alpha Pinene group. This study reveals that Alpha Pinene may be a valuable herbal organic compound for the protection of the stomach and intestine and the reduction of complaints in diseases affecting the gastrointestinal system such as Parkinson's disease.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 4","pages":"31"},"PeriodicalIF":3.3,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic Changes in Oxidative Stress and Epigenetic Modifications in the Ventral Mesencephalon and Striatum of MPTP-Treated Mice: Implications for Parkinson's Disease Pathogenesis.","authors":"Pablo Gallo-Soljancic, Maria Egle De Stefano, Ana-Maria Gonzalez-Cuello, Emiliano Fernandez-Villalba, Lode Godderis, Maria Trinidad Herrero","doi":"10.1007/s12640-025-00748-0","DOIUrl":"10.1007/s12640-025-00748-0","url":null,"abstract":"<p><p>This study investigates the effects of an acute 1-metil 4-fenil 1,2,3,6-tetraidro-piridina (MPTP) treatment, a known inducer of parkinsonism, on oxidative stress and epigenetic changes in the mouse ventral midbrain (VM) and striatum. Key markers were analyzed at 4, 8, 24, and 48 h post-injections: the hydroxylated form of the purine guanine (8-hydroxy-2'-deoxyguanosine; 8-OHdG), a marker of oxidative stress; the methylated form of cytosine (5-methylcytosine; 5-mC), associated with gene silencing; the hydroxy methylated form of cytosine (5-hydroxymethylcytosine; 5-hmC), involved in demethylation and gene regulation. The results showed a pronounced decrease in 8-OHdG levels in the VM, suggesting a rapid oxidative stress response, whereas the striatum exhibited a less pronounced response, reflecting regional differences in oxidative stress vulnerability DNA methylation patterns revealed complex and biphasic changes in 5-mC levels in the VM, contrasted with a less pronounced response in the striatum, suggesting disrupted methylation homeostasis and regional epigenetic variability. MPTP treatment also significantly reduced in 5-hmC levels in the VM, pointing to impaired active DNA demethylation and compromised epigenetic flexibility. In contrast, the striatum maintained consistently high 5-hmC levels, reflecting compensatory hydroxymethylation mechanisms specific to this region. These findings highlight pronounced regional differences in oxidative stress vulnerability and epigenetic regulation, with the VM showing heightened sensitivity to oxidative damage and impaired epigenetic flexibility. This underscores the importance of understanding the role of oxidative and epigenetic mechanisms in Parkinson's disease pathophysiology, The changes pave the way for novel therapeutic strategies targeting oxidative DNA damage and epigenetic homeostasis.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 4","pages":"30"},"PeriodicalIF":3.3,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12227354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}