Neurotoxicology最新文献

{"title":"The impact of electronic cigarette aerosol exposure on spatial memory formation: Modulation by orally administered vitamin E","authors":"Aiman A. Yaseen ,&nbsp;Karem H. Alzoubi ,&nbsp;Nour Al-Sawalha ,&nbsp;Omar F. Khabour ,&nbsp;Anan Jarab ,&nbsp;Shirin Ali ,&nbsp;Samina Salim ,&nbsp;Thomas Eissenberg","doi":"10.1016/j.neuro.2024.10.014","DOIUrl":"10.1016/j.neuro.2024.10.014","url":null,"abstract":"<div><div>The use of electronic cigarettes (ECIGs) has grown exponentially among young adolescents. Tobacco smoking, in general and ECIG use in particular, has been linked to disruption of the oxidative system, resulting in organ damage. The current investigation intends to evaluate if orally administered Vitamin E (VitE) can protect from learning and cognitive impairment induced by ECIG aerosol exposure in a rat model. This effect was determined by studying behavioral and molecular targets for potential learning and memory impairment. Adult Wistar rats were assigned to the following groups (N= 12/group): Control, ECIG, VitE, and VitE+ECIG. The animals in the groups ECIG and VitE+ECIG were exposed to ECIG aerosol (1 hr/day, 6 days/week) for four weeks. The control group and VitE group were exposed to fresh air. At the same time, the VitE group and VitE+ECIG group were given Vitamin E 100 mg/kg/ day via gavage for the same period as the exposure. The control group and ECIG group were given the vehicle via gavage. Behavioral assessment was performed using the Radial Arm Water Maze. In addition, molecular measures (BDNF, SOD, GPx, GSH, and GSSG), were measured in rats’ hippocampal tissues. The results showed that VitE prevented ECIG aerosol exposure-induced impairment of spatial short-term and long-term memory formation (p&lt;0.05), decreased BDNF, and activities/levels of GPx, SOD, and GSH (p&lt;0.05). Moreover, VitE protected against GSSG levels increases (p&lt;0.05) associated with ECIG aerosol exposure. In summary, exposure to ECIGs resulted in spatial memory impairments, which could be mitigated by orally administered vitamin E.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 263-271"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564808","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":"Sex differences in β-N-Methylamino-L-alanine effects on zebrafish behavioral response","authors":"Nicoli R. do Amaral ,&nbsp;Murilo S. de Abreu ,&nbsp;Alexander Zanella ,&nbsp;Júlia P. Poletto ,&nbsp;Gabriel P. de Mello ,&nbsp;Marco A. da Croce ,&nbsp;Larissa B. Garbelotto ,&nbsp;Manuela G. Bernardon ,&nbsp;Ana C.V.V. Giacomini","doi":"10.1016/j.neuro.2024.10.010","DOIUrl":"10.1016/j.neuro.2024.10.010","url":null,"abstract":"<div><div>The β-N-methylamino-L-alanine (BMAA) is a neurotoxin produced by cyanobacteria and diatoms and related by triggered neurodegeneration. The exposure to neurotoxins has also been reported by causing emotional and neuroendocrine effects and these effects may be sex-specific. However, the effects of BMAA on emotions and pain, as well as neuroendocrine modulations remain poorly understood. Here, we evaluate potential sex differences in zebrafish behavioral responses to BMAA acute exposure on their anxiety and pain phenotypical behavioral repertoire and their neuroendocrine (cortisol) effects. Overall, sex differences in behavioral responses of adult zebrafish to BMAA exposure were demonstrated, as female fish reacted to it more strongly than males by altering their behavioral phenotype in both the novel tank and writhing -like behavior tests. In addition, sex differences were demonstrated in relation to time response, as male increased the writhing-like behavioral responses immediately after injection of BMAA, while female only 24-h after injection, reinforcing the painful stimulus caused by BMAA. However, the exposure to BMAA elevated the whole-body cortisol levels in both male and female zebrafish. Collectively, these findings emphasize the growing importance of studying sex differences in zebrafish, including the evaluation of neurotoxins effects on emotions and pain in this aquatic experimental model.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 257-262"},"PeriodicalIF":3.4,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567977","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":"Exposure to an environmentally representative mixture of polybrominated diphenyl ethers (PBDEs) alters zebrafish neuromuscular development","authors":"Alec McDermott,&nbsp;Cécilia Bernier,&nbsp;Vanessa Piché,&nbsp;Isabelle Plante ,&nbsp;Shunmoogum A. Patten","doi":"10.1016/j.neuro.2024.10.009","DOIUrl":"10.1016/j.neuro.2024.10.009","url":null,"abstract":"<div><div>Polybrominated diphenyl ethers (PBDEs) are a prevalent group of brominated flame retardants (BFRs) added to several products such as electronics, plastics, and textiles to reduce their flammability. They are reported as endocrine disruptors and neurodevelopmental toxicants that can accumulate in human and wildlife tissues, thus making their ability to leach out of products into the environment a great cause for concern. In this study, zebrafish (<em>Danio rerio</em>) embryos and larvae were exposed to a wide concentration range (1.5, 15, 150 and 300 pM) of a PBDE mixture from one to six days post-fertilization (dpf). Hatching rates, mortality and general morphology were assessed during the exposure period. A delay in hatching was observed at the two highest PBDEs concentrations and mortality rate increased at 6 dpf. By 4 dpf, larvae exposed to 150 pM and 300 pM PBDEs developed an upcurved phenotype. Analysis of motor behavior at 6 dpf revealed that PBDE exposure acutely reduced locomotion. To further analyze these motor deficits, we assessed the neural network density and motor neuron and neuromuscular junctions (NMJ) development by immunostaining and imaging. Acetylated α-tubulin staining revealed a significant loss of neurons in a dose-dependent manner. Synaptic vesicle protein 2 (SV2) and ⍺-bungarotoxin (⍺-BTX) staining revealed a similar pattern, with a significant loss of SV2 and nicotinic acetylcholine receptors, thus preventing the colocalization of presynaptic neurons with postsynaptic neurons. Consistent with these results, the presence of cleaved caspase-3 and acridine orange positive cells showed increased cell death in zebrafish larvae exposed to PBDEs. Our results suggest that exposure to PBDEs leads to deficits in the zebrafish neuromuscular system through neuron death, inducing morphological and motor deficiencies throughout their development. They provide valuable insight into the neurotoxic effects of PBDEs, further highlighting the relevance of the zebrafish model in toxicological studies.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 247-256"},"PeriodicalIF":3.4,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142555036","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}

{"title":"Manifestation of polystyrene microplastic accumulation in brain with emphasis on morphometric and histopathological changes in limbic areas of Swiss albino mice","authors":"Manjyot Kaur,&nbsp;Anju Sharma,&nbsp;Placheril John,&nbsp;Pradeep Bhatnagar","doi":"10.1016/j.neuro.2024.10.008","DOIUrl":"10.1016/j.neuro.2024.10.008","url":null,"abstract":"<div><div>The widespread problem of microplastic (MP) contamination is becoming a major threat to the globe. Although most of the research to date has concentrated on the physiological impacts of MPs exposure, a relatively new field of study is beginning to examine its effects on the behaviour and limbic regions of the brain. In this study, exposure to polystyrene MPs (PS-MPs) for acute and sub-chronic durations negatively affected cognition and induced anxiety-like behaviour in mice. PS-MPs were detected in vital organs of mice, including the brain, which induced neurobehavioural and pathological changes in the limbic system. Furthermore, morphometric analysis revealed a significant decrease in the total cell count in the Dentate Gyrus (DG) and Cornu Ammonis (CA) regions of the hippocampus. Signs of neuronal injury and dystrophic changes were observed in the cortex, amygdala, and hypothalamus, potentially affecting anxiety and fear responses. Our study thus provides insight into the effect of PS-MPs on the neurobiology of the brain’s limbic system and related behavioural alterations.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 231-246"},"PeriodicalIF":3.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470943","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":"Neuroprotective effect of empagliflozin against doxorubicin-induced chemobrain in rats: Interplay between SIRT-1/MuRF-1/PARP-1/NLRP3 signaling pathways and enhanced expression of miRNA-34a and LncRNA HOTAIR","authors":"Merihane M. Nasr ,&nbsp;Sara A. Wahdan ,&nbsp;Reem N. El-Naga ,&nbsp;Rania M. Salama","doi":"10.1016/j.neuro.2024.10.006","DOIUrl":"10.1016/j.neuro.2024.10.006","url":null,"abstract":"<div><div>Chemobrain, a challenging side effect of doxorubicin (DOX)-based chemotherapy, impairs cognitive abilities in cancer survivors. DOX triggers chemobrain via oxidative stress, leading to inflammation and apoptosis. Empagliflozin (EMPA), a sodium glucose co-transporter-2 inhibitor, demonstrated neuroprotective effects by reducing reactive oxygen species (ROS) and inflammation, but its protective mechanisms against DOX-induced chemobrain is not fully known. Thus, this study aimed to investigate EMPA’s neuroprotective effects on DOX-induced chemobrain in rats and to uncover the underlying protective mechanisms. Fifty male Wistar rats were divided into control, EMPA, DOX (2 mg/kg, IP, once/week for 4 weeks), and two treated groups (DOX+ EMPA 5 and 10 mg/kg/day, PO, for 4 weeks). Behavioral tests showed improved memory, motor performance, and reduced anxiety in EMPA-treated groups compared to DOX, with superior results at the higher dose. Histopathological analysis revealed increased intact neurons in the cortex and hippocampus in EMPA-treated groups, with 346.4 % increase in CA3 (p &lt; 0.0001), 19.1 % in dentate gyrus (p = 0.0006), and 362.6 % in cortex (p &lt; 0.0001) in the high-dose EMPA group. Biochemical investigations of the high-dose EMPA group revealed significant decreases in inflammatory and apoptotic markers (JNK/PARP-1/NLRP3/MuRF-1/FOXO-1), increased SIRT-1 protein expression by 389.9 % (p &lt; 0.0001), and reduced miRNA-34a and LncRNA HOTAIR gene expression (50.4 % and 53.4 % respectively, p &lt; 0.0001) relative to DOX group. Conclusively, EMPA demonstrated superior behavioral and histopathological outcomes particularly at higher dose, positioning it as a promising neuroprotective candidate against DOX-induced chemobrain, possibly through modulating SIRT-1, NF-κb, NLRP3, and oxidative stress pathways.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 216-230"},"PeriodicalIF":3.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470944","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":"Investigating tributyltin's toxic effects: Intestinal barrier and neuroenteric disruption in rat’s jejunum","authors":"I.C.C.S. Oliveira ,&nbsp;G.P. Marinsek ,&nbsp;A.R.N. Gonçalves ,&nbsp;B.S. Lopes ,&nbsp;L.V.B. Correia ,&nbsp;R.C.B. Da Silva ,&nbsp;I.B. Castro ,&nbsp;R.B. Mari","doi":"10.1016/j.neuro.2024.10.004","DOIUrl":"10.1016/j.neuro.2024.10.004","url":null,"abstract":"<div><div>The expansion of economic activities in coastal areas has significantly increased chemical contamination, leading to major environmental challenges. Contaminants enter the human body through the food chain, particularly via seafood and water consumption, triggering biomagnification and bioaccumulation processes. The gastrointestinal tract (GIT) acts as a selective barrier, protecting against chemical pollutants and maintaining homeostasis through a complex network of cells and immune responses. This study assessed impact of tributyltin (TBT), a highly toxic organometallic compound used in antifouling coatings for ships, on the GIT and myenteric neural plasticity in young rats. TBT exposure leads to histopathological changes, including epithelial detachment and inflammatory foci, especially at lower environmental doses. The study found that TBT causes significant reductions in villi height, increases in goblet cells and intraepithelial lymphocytes, and disrupts the myenteric plexus, with higher densities of extraganglionic neurons in exposed animals.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 208-215"},"PeriodicalIF":3.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470947","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":"Effects of mixed metal exposures on MRI diffusion features in the medial temporal lobe","authors":"Eun-Young Lee ,&nbsp;Juhee Kim ,&nbsp;Janina Manzieri Prado-Rico ,&nbsp;Guangwei Du ,&nbsp;Mechelle M. Lewis ,&nbsp;Lan Kong ,&nbsp;Jeff D. Yanosky ,&nbsp;Paul Eslinger ,&nbsp;Byoung-Gwon Kim ,&nbsp;Young-Seoub Hong ,&nbsp;Richard B. Mailman ,&nbsp;Xuemei Huang","doi":"10.1016/j.neuro.2024.10.005","DOIUrl":"10.1016/j.neuro.2024.10.005","url":null,"abstract":"<div><h3>Background</h3><div>Environmental exposure to metal mixtures is common and may be associated with increased risk for neurodegenerative disorders including Alzheimer’s disease. This study examined associations of mixed metal exposures with medial temporal lobe (MTL) MRI structural metrics and neuropsychological performance.</div></div><div><h3>Methods</h3><div>Metal exposure history, whole blood metal, MRI R1 (1/T1) and R2* (1/T2*) metrics (estimates of brain Mn and Fe, respectively), and neuropsychological tests were obtained from subjects with/without a history of mixed metal exposure from welding fumes (42 exposed subjects; 31 controls). MTL structures (hippocampus, entorhinal and parahippocampal cortices) were assessed by morphologic (volume or cortical thickness) and diffusion tensor imaging [mean (MD), axial (AxD), radial diffusivity (RD), and fractional anisotropy (FA)] metrics. In exposed subjects, effects of mixed metal exposure on MTL structural and neuropsychological metrics were examined.</div></div><div><h3>Results</h3><div>Compared to controls, exposed subjects displayed higher MD, AxD, and RD throughout all MTL ROIs (p’s&lt;0.001) with no morphological differences. They also had poorer performance in processing/psychomotor speed, executive, and visuospatial domains (p’s&lt;0.046). Long-term mixed metal exposure history indirectly predicted lower processing speed performance via lower parahippocampal FA (p’s&lt;0.023). Higher entorhinal R1 and whole blood Mn and Cu levels predicted higher entorhinal diffusivity (p’s&lt;0.043) and lower <em>Delayed Story Recall</em> performance (p=0.007).</div></div><div><h3>Discussion</h3><div>Mixed metal exposure predicted certain MTL structural and neuropsychological features that are similar to those detected in Alzheimer’s disease at-risk populations. These data warrant follow-up as they may illuminate a potential path for environmental exposure to brain changes associated with Alzheimer’s disease-related health outcomes.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 196-207"},"PeriodicalIF":3.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470946","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":"The inhibitory influence of carvacrol on behavioral modifications, brain oxidation, and general inflammation triggered by paraquat exposure through inhalation","authors":"Reyhaneh Khosravi ,&nbsp;Sima Beigoli ,&nbsp;Sepideh Behrouz ,&nbsp;Sabiheh Amirahmadi ,&nbsp;Parisa Sarbaz ,&nbsp;Mahmoud Hosseini ,&nbsp;Hadi Sarir ,&nbsp;Mohammad Hossein Boskabady","doi":"10.1016/j.neuro.2024.10.003","DOIUrl":"10.1016/j.neuro.2024.10.003","url":null,"abstract":"<div><div>The current study investigated how carvacrol (C) can prevent behavioral and brain oxidative changes, along with systemic inflammation caused by inhaled paraquat (PQ). Control rats exposed to saline solution, whereas six rat groups were subjected to PQ aerosols at a concentration of 54 mg/m³ in 16 days. The PQ-exposed groups received saline (PQ group), C at dosages of 20 (C-L) and 80 mg/kg/day (C-H), dexamethasone at a dosage of 0.03 mg/kg/day, pioglitazone at dose of 5 and 10 mg/kg/day (Pio-L and Pio-H), and a combination of C-L + Pio-L. Various parameters were assessed following the end of the treatment duration. There were marked elevation in total and differential white blood cell counts (WBCs), and malondialdehyde levels in the blood, hippocampus, and cerebral tissue but, thiol, superoxide dismutase (SOD), and catalase (CAT) exhibited a notable decrease (p &lt; 0.05 to p &lt; 0.001). The escape delay and traveled distance exhibited enhancement, however, on the probe day, the duration spent in the target quadrant and the time taken to enter the dark room at 3, 24, 48, and 72 hours post an electrical shock, showed a reduction in the PQ group (P&lt;0.05 to P&lt;0.001). Inhaled PQ-induced changes were significantly improved in C, Pio, Dexa, and C-L + Pio-L treated groups (P&lt;0.05 to P&lt;0.001). The effects of C-L + Pio-L on most measured variables were higher than C-L and Pio-L (P&lt;0.05 to P&lt;0.001). C improved PQ-induced changes similar to dexamethasone and C-L showed additive effects when administered in combination with Pio.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 184-195"},"PeriodicalIF":3.4,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406656","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":"The enigma of mitochondrial epigenetic alterations in air pollution-induced neurodegenerative diseases","authors":"Sayanti Acharyya ,&nbsp;Sruthy Hari Kumar ,&nbsp;Apoorva Chouksey ,&nbsp;Nikita Soni ,&nbsp;Nazim Nazeer ,&nbsp;Pradyumna Kumar Mishra","doi":"10.1016/j.neuro.2024.10.002","DOIUrl":"10.1016/j.neuro.2024.10.002","url":null,"abstract":"<div><div>The incidence of neurodegenerative diseases is a growing concern worldwide, affecting individuals from diverse backgrounds. Although these pathologies are primarily associated with aging and genetic susceptibility, their severity varies among the affected population. Numerous studies have indicated air pollution as a significant contributor to the increasing prevalence of neurodegeneration. Cohort studies have provided compelling evidence of the association between prolonged exposure to different air toxicants and cognitive decline, behavioural deficits, memory impairment, and overall neuronal health deterioration. Furthermore, molecular research has revealed that air pollutants can disrupt the body's protective mechanisms, participate in neuroinflammatory pathways, and cause neuronal epigenetic modifications. The mitochondrial epigenome is particularly interesting to the scientific community due to its potential to significantly impact our understanding of neurodegenerative diseases' pathogenesis and their release in the peripheral circulation. While protein hallmarks have been extensively studied, the possibility of using circulating epigenetic signatures, such as methylated DNA fragments, miRNAs, and genome-associated factors, as diagnostic tools and therapeutic targets requires further groundwork. The utilization of circulating epigenetic signatures holds promise for developing novel prognostic strategies, creating paramount point-of-care devices for disease diagnosis, identifying therapeutic targets, and developing clinical data-based disease models utilizing multi-omics technologies and artificial intelligence, ultimately mitigating the threat and prevalence of neurodegeneration.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 158-183"},"PeriodicalIF":3.4,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142392085","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":"Sex-dependent effects of short-term ethanol, energy drinks and acute noise exposure on hippocampal oxidative balance and glutamate transporter EAAT-1 during rat adolescence","authors":"Sonia Jazmín Molina ,&nbsp;Gonzalo Nahuel Corsi ,&nbsp;Lara Candela Araujo Añon ,&nbsp;Laura Ruth Guelman","doi":"10.1016/j.neuro.2024.10.001","DOIUrl":"10.1016/j.neuro.2024.10.001","url":null,"abstract":"<div><div>It is known that human adolescents often consume ethanol (EtOH) alone or mixed with energy drinks (ED), especially in noisy environments. Although these agents impact the developing brain, their effects after brief exposure or when presented together remain unclear. Given that few animal studies in this subject are available, this research aimed to study the effects of a brief exposure to these stimuli on the oxidative state and EAAT-1 glutamate transporter levels in the developing rat hippocampus (HC). Adolescent Wistar rats were subjected to a two-bottle choice, limited access to drinking in the dark paradigm, for EtOH and EtOH+ED intake, for 4 days, and subsequent acute noise exposure. Next, hippocampal catalase activity, reactive oxygen species (ROS), glutaredoxin-1 (Grx-1) and glutamate transporter EAAT-1 levels were assessed. Results showed sex-dependent alterations after exposure to these stimuli: Females consuming EtOH had higher hippocampal ROS levels, which decreased when combined with noise; males showed reduced ROS levels only after noise exposure. No significant changes occurred in catalase activity, Grx-1, or EAAT-1 levels with EtOH and noise exposure in neither sex. Additionally, ED raised EtOH consumption in both sexes, normalizing ROS levels only in females when combined with EtOH. Finally, ED consumption altered Grx-1 and EAAT-1 levels in both sexes. In summary, brief exposure to these stimuli induced sex-dependent alterations, suggesting differentiated coping strategies between sexes. Whereas ED consumption may have antioxidant effects in some cases, it could also increase excitotoxicity risk. These novel findings raise questions for future research on the underlying corresponding mechanisms.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 147-157"},"PeriodicalIF":3.4,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375732","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}