Neurotoxicology and teratology最新文献

{"title":"The relationships of prenatal cocaine exposure, postnatal lead exposure, and victimization to aggressive behavior/delinquency in adolescence","authors":"Khoa Duc Le ,&nbsp;Jeffrey Albert ,&nbsp;June-Yung Kim ,&nbsp;Sonia Minnes ,&nbsp;Meeyoung O. Min ,&nbsp;Lynn T. Singer","doi":"10.1016/j.ntt.2025.107518","DOIUrl":"10.1016/j.ntt.2025.107518","url":null,"abstract":"<div><h3>Introduction</h3><div>Prenatal cocaine exposure (PCE) can alter the monoaminergic neurotransmitter system in the fetal brain related to emotional and behavioral regulation. PCE has been associated with high rates of aggression and delinquency, risk for victimization, and multiple environmental stressors associated with a disadvantaged environment, including postnatal lead exposure. While postnatal lead exposure has also been linked to aggressive behavior/delinquency, little is known about the combined impacts of PCE and lead on behavior, nor how they interact with environmental stressors such as victimization.</div></div><div><h3>Objectives</h3><div>Assess the relationships of PCE, postnatal lead levels, and victimization to adolescent self-report of aggressive behavior/delinquency, controlling for other prenatal drug exposures and the quality of the caregiving environment.</div></div><div><h3>Methods</h3><div>At age 17, 336 adolescents (50 % PCE, 46 % male) reported their aggressive behavior/delinquency (AGG) on the Problem-Oriented Screening Instrument for Teenagers, and type of lifetime victimization on the Juvenile Victimization Questionnaire. Blood lead levels were measured at 2–4 years, and the Home Observation for the Measurement of the Environment – Early Adolescence at 15 years. Binomial logistic, multiple regression and mediation analyses examined group differences and relationships among variables.</div></div><div><h3>Results</h3><div>PCE, victimization (child maltreatment and peer/sibling victimization), and postnatal lead levels were each associated with higher AGG. Girls with PCE reported higher AGG than non-exposed girls while boys did not differ, and all adolescents with PCE reported more child maltreatment and peer/sibling victimization. Child maltreatment partially mediated the relationship between PCE and aggressive behavior/delinquency.</div></div><div><h3>Conclusions</h3><div>Recognition of the higher rates of maltreatment and peer/sibling victimization with PCE is important for intervention efforts, as each contributes to higher AGG. As PCE may be associated differentially with higher AGG in girls, gender-focused interventions should be considered while addressing the increased impact of victimization and postnatal lead levels on AGG in both PCE and NCE boys and girls.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107518"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529023","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":"Neurodevelopmental impacts of betamethasone administered in the late preterm period: An experimental study in CD-1 mice","authors":"Isabelle Hardy ,&nbsp;Anthony Gagnon ,&nbsp;Erika-Kate Croft ,&nbsp;Luc Tremblay ,&nbsp;Réjean Lebel ,&nbsp;Marie-Ève Roy-Lacroix ,&nbsp;Larissa Takser ,&nbsp;Annie Ouellet ,&nbsp;Denis Gris","doi":"10.1016/j.ntt.2025.107523","DOIUrl":"10.1016/j.ntt.2025.107523","url":null,"abstract":"<div><div>The safety of antenatal corticosteroid administration during the late preterm period is currently questioned. This experimental study conducted in a CD-1 mouse model aimed to determine if exposure to betamethasone in the late preterm period 1) induces behavioral changes in adulthood and 2) alters cerebral anatomy. In the prenatal group, four gravid mice were randomly assigned to receive 0.1 mg of betamethasone (around 1.82 mg/kg based on an average body weight of 55 g) or an equivalent volume of phosphate buffered saline (PBS) on gestation day 18, and yielded a total of 43 pups. This model was selected to test the impact of cumulative exposure to exogenous and endogenous steroids. In the postnatal group, six gravid mice yielded a total of 69 pups which were randomly assigned to receive betamethasone or PBS. Pups in the intervention group received 0.03 mg of betamethasone subcutaneously on postnatal day 5, at which time mouse brain development is equivalent to that of humans at 34–36 weeks' gestation. To evaluate objective 1, pups were subjected to behavioral tests on postnatal days 21–50. On postnatal day 60, structural magnetic resonance imaging (MRI) was performed to assess objective 2. Outcomes were compared between treatment groups using linear mixed models including random effects for litter and a fixed term for the interaction of treatment and sex. We used a statistical significance threshold of <em>p</em> &lt; 0.05. Male mice exposed to betamethasone ante- or postnatally engaged in more social contact than those exposed to PBS (interaction of betamethasone and male sex: prenatal β = 0.09, 95 % CI (0.02, 0.17), <em>p</em> = 0.02; postnatal β = 0.08, 95 %CI (0.01, 0.14), <em>p</em> = 0.03), while female mice engaged in less social contact. MRI showed that male mice exposed to betamethasone prenatally had larger habenulas and smaller amygdala than those exposed to PBS (interaction of betamethasone and male sex: habenula β = 0.01, 95 %CI (0.004, 0.02), <em>p</em> = 0.01, amygdala β = −1.43, 95 %CI (−2.67, −0.21), <em>p</em> = 0.03), while female mice had larger amygdala and smaller habenulas. Postnatal exposure to betamethasone was associated with lower combined volume of the parietal cortex and hypothalamus (interaction of betamethasone and male sex: β = −0.32, 95 %CI (−0.58, −0.03), <em>p</em> = 0.04). No other significant differences in behavioral outcomes or brain volumes were identified. These results suggest that exposure to betamethasone in the late preterm period is associated with small but significant sex-specific disruptions of the limbic system, associated with social behavior disturbances.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107523"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626778","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":"Pregnancy protects nervous tissues against the neurotoxicity of intrathecal bupivacaine in rabbits","authors":"Ju-Feng Ma ,&nbsp;Jing Zhang ,&nbsp;Rui He ,&nbsp;Ju-Hui Niu ,&nbsp;Shen Yang","doi":"10.1016/j.ntt.2025.107519","DOIUrl":"10.1016/j.ntt.2025.107519","url":null,"abstract":"<div><h3>Background</h3><div>Local anesthetics have been associated with spinal neurotoxicity, including the risk of persistent neurological injury. Pregnancy is known to increase the sensitivity of nervous tissue to local anesthetics, potentially elevating the risk of neurological deficits in obstetric patients following spinal block. This study aimed to investigate the effects of pregnancy on the neurotoxicity of intrathecal bupivacaine.</div></div><div><h3>Methods</h3><div>Pregnant and non-pregnant rabbits were administered three injections of either 0.375 % or 0.75 % bupivacaine, or normal saline, at 48-h intervals (average volume: 200 μl). Seven days after the first injection, electron microscopic scores (EMS), spinal neuronal apoptotic rates, intracellular Ca²⁺ concentrations, and mitochondrial membrane potential were evaluated.</div></div><div><h3>Results</h3><div>The EMS indicated more severe neurotoxicity in non-pregnant rabbits compared to pregnant rabbits in the bupivacaine-treated groups (median [Q1-Q3]: 23 [21–26] vs. 21 [18.5–24], <em>P</em> = 0.045). Pregnant rabbits exhibited significantly lower apoptosis rates and intracellular Ca²⁺ concentrations, along with a higher mitochondrial membrane potential compared to their non-pregnant counterparts (0.99 % ± 1.33 % vs. 2.03 % ± 2.09 %, <em>P</em> &lt; 0.01; 240 ± 104 vs. 257 ± 112, <em>P</em> &lt; 0.01; 84.1 % ± 6.1 % vs. 69.9 % ± 15.4 %, <em>P</em> &lt; 0.01).</div></div><div><h3>Conclusion</h3><div>These findings indicated that pregnancy protects nervous tissue against the toxicity of intrathecal bupivacaine.</div><div><strong>Conclusion:</strong> These findings suggest that pregnancy confers a protective effect on nervous tissue against the neurotoxicity induced by intrathecal bupivacaine.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107519"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529022","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":"Pregnancy outcomes following maternal exposure to favipiravir: A Terafar case series","authors":"Nusret Uysal ,&nbsp;Baris Karadas ,&nbsp;Secil Karaca Kurtulmus ,&nbsp;Merve Tor ,&nbsp;Ismail Yilmaz ,&nbsp;Nihal Olgac Dundar ,&nbsp;Yusuf C. Kaplan","doi":"10.1016/j.ntt.2025.107524","DOIUrl":"10.1016/j.ntt.2025.107524","url":null,"abstract":"<div><h3>Objective</h3><div>To assess pregnancy outcomes following maternal favipiravir exposure, with a particular focus on congenital malformations and neonatal development.</div></div><div><h3>Methods</h3><div>A case series, including data from pregnancies with favipiravir exposure between 2020 and 2021, was conducted at Izmir Katip Celebi University Teratology Information Center. Pregnant women and their infants were evaluated through structured interviews, ultrasonography, neonatal follow-ups, and developmental assessments. Congenital malformations were classified per EUROCAT criteria, and development was assessed using the Denver Developmental Screening Test-III.</div></div><div><h3>Results</h3><div>Of 45 pregnancies, 37 resulted in live births (including 1 set of twins), seven were electively terminated, and one ended in intrauterine death. Among the 28 infants with first-trimester exposure, 7.1 % (<em>n</em> = 2) had major malformations (congenital ichthyosis and hydronephrosis) and an additional 7.1 % (n = 2) had minor malformations (pleural effusion, patent foramen ovale). A review of exposure windows relative to critical developmental periods did not indicate a consistent or conclusive temporal association with the observed anomalies. Preterm birth and low birth weight rates were 9.6 % and 6.4 %, respectively. Neonatal jaundice occurred in 32.2 % of neonates. Developmental screening was normal in most cases, with one infant—who did not have any congenital malformations—exhibiting mild language delay.</div></div><div><h3>Conclusion</h3><div>Our study does not indicate a major teratogenic signal regarding favipiravir exposure in pregnancy, though the higher elective termination rate suggests increased risk perception. While study limitations prevent definitive conclusions, our findings may be of value to clinicians in counseling pregnant women regarding favipiravir exposure.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107524"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144656127","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":"Introduction to \"Effects of stress exposure during development on neurobehavioral and neuroendocrine function\".","authors":"Jerrold S Meyer, Sonya Sobrian, Gregg D Stanwood","doi":"10.1016/j.ntt.2025.107520","DOIUrl":"10.1016/j.ntt.2025.107520","url":null,"abstract":"","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":" ","pages":"107520"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560607","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":"Micro(nano)plastics in the brain: Epigenetic perturbations in progression to neurodegenerative diseases","authors":"Mou Mondal ,&nbsp;Apoorva Chouksey ,&nbsp;Vikas Gurjar ,&nbsp;Rajnarayan Tiwari ,&nbsp;Rupesh K. Srivasatava ,&nbsp;Pradyumna Kumar Mishra","doi":"10.1016/j.ntt.2025.107521","DOIUrl":"10.1016/j.ntt.2025.107521","url":null,"abstract":"<div><div>As global plastic production escalates, micro(nano)plastics (MNPs) have become pressing ecological and biomedical concerns. These pollutants are increasingly implicated in the pathogenesis of neurodegenerative diseases. Due to their nanoscale size and surface reactivity, MNPs can cross the blood-brain barrier, accumulating in neural tissues. Once internalized, they disrupt neuronal homeostasis by inducing oxidative stress, mitochondrial dysfunction, and chronic neuroinflammation, key processes in neurodegenerative progression. Mitochondria, central to neuronal energy and redox regulation, are particularly vulnerable, leading to impaired ATP production, elevated ROS, and pro-apoptotic signaling. Recent studies reveal that MNPs also induce epigenetic changes, including aberrant DNA methylation, histone modifications, and dysregulation of non-coding RNAs. These alterations can result in synaptic instability, persistent transcriptional reprogramming, and heightened susceptibility to diseases like Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis. The mitochondrial epigenome is a vital target of MNP-induced disruption, offering potential biomarkers like methylated mtDNA and microRNAs for early diagnosis and prognosis. Understanding the molecular mechanisms behind these epigenetic alterations is essential for developing practical diagnostic tools and therapies. This review provides a comprehensive overview of MNP-induced neurodegeneration, focusing on mitochondrial and epigenetic disruptions. Moreover, it explores emerging biosensing technologies for detecting MNP-induced epigenetic alterations, highlighting the urgent need for further investigation to fully understand the neurotoxic potential of MNPs and develop preventive and therapeutic strategies for mitigating their effects on brain health.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107521"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144595585","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 East Palestine train derailment: A complex environmental disaster","authors":"Lynn T. Singer ,&nbsp;Fredrick Schumacher ,&nbsp;James Fabisiak ,&nbsp;Laura J. Dietz ,&nbsp;Timothy Ciesielski","doi":"10.1016/j.ntt.2025.107522","DOIUrl":"10.1016/j.ntt.2025.107522","url":null,"abstract":"<div><div>This symposium, <em>The East Palestine Train Derailment: A Complex Environmental Disaster</em>, brought together scientists whose research represented initial scientific responses to the community health impacts of the chemical exposures incurred from a disastrous train derailment and subsequent combustion in East Palestine, Ohio in February, 2023. This derailment and burn led to multiple complex toxic exposures to air, soil and water, including vinyl chloride and butyl acrylate. Presenters described the multi-university consortium formed to assist with developing and communicating data-informed summaries to the affected community. Presenters also reported on the immediate health sequelae experienced by the community and the stress and uncertainty regarding long term effects. Plans were reported for several pilot studies funded by the National Institute on Environmental Health Sciences in immediate response to the disaster. Fredrick Schumacher, PhD outlined the aims of The <em>Healthy Futures Research Study</em>: <em>Linking Somatic Mutation Rate with Baseline Exposure in East Palestine</em> that plans to use somatic mutation rate (SMR) to measure the biological impact of environmental exposures based on proximity to the train derailment and residents’ clinical symptomatology. James Fabisiak, PhD shared plans for their study<em>, East Palestine Community-Engaged Environmental Exposure, Health Data, and Biospecimen Bank</em> that will measure chemical contaminants in indoor air and water in homes<strong>,</strong> monitor liver damage in residents and identify parents’ concerns about children’s health and development. As part of that study, Laura Dietz, PhD noted the major psychosocial stressors experienced by the community, particularly the psychological effects on children which the study will try to identify through parental report. Timothy Ciesielski, MD, PhD summarized the difficulties of drawing conclusions related to health and safety risk from the toxicants released through currently available government databases and his experience trying to provide the community with reliable and valid information in the context of working across state lines and multiple state and federal agencies.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107522"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668073","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":"Salvianolic acid A enhances sedative effect of diazepam through the GABAergic pathway: In vivo, molecular docking, and pharmacokinetics approaches","authors":"Imam Hossen Rakib ,&nbsp;Mohd Shahnawaz Khan ,&nbsp;Arusha Ayub ,&nbsp;Md. Sakib Al Hasan ,&nbsp;Mohammed Alfaifi ,&nbsp;Md. Shimul Bhuia ,&nbsp;Emon Mia ,&nbsp;Noshin Tasnim Yana ,&nbsp;Md. Nasimul Haque Shipon ,&nbsp;Muhammad Torequl Islam","doi":"10.1016/j.ntt.2025.107517","DOIUrl":"10.1016/j.ntt.2025.107517","url":null,"abstract":"<div><div>Salvianolic acid A (SAL A), a polyphenolic compound derived from <em>Salvia miltiorrhiza</em>, exhibits several neuroprotective effects, but its sedative potential is unexamined. This study explores the sedative effects of SAL A and its potential to modulate the impacts of diazepam (DZP) in a thiopental sodium (TS)-induced sleep model in <em>Swiss</em> albino mice. Mice received intraperitoneal (i.p.) doses of SAL A (5 and 10 mg/kg) and DZP (2 mg/kg), followed by TS (20 mg/kg), with sleep latency and duration recorded. Molecular docking and in silico analyses evaluated SAL A’s interaction with the GABA_A receptor (α1 and β2 subunits) (PDB ID: <span><span>6X3X</span><svg><path></path></svg></span>) and its pharmacokinetic properties. Results revealed that SAL A significantly (<em>p</em> &lt; 0.05) reduced sleep latency and prolonged sleep duration dose-dependently, with 10 mg/kg showing the strongest effect (latency: 14.29 ± 3.09 min; duration: 175.71 ± 18.97 min; Cohen's d = 4.37 and 1.60, respectively). Combined therapy with SAL A-10 and DZP-2 synergistically enhanced sleep duration, with the highest effect sizes observed (<em>d</em> = 5.45 for latency; 4.36 for duration). Molecular docking studies revealed that SAL A showed similar binding affinity (−8.7 kcal/mol) with 6X3X, comparable to DZP. SAL A also exhibited favorable pharmacokinetic properties and low toxicity. These findings suggest SAL A as a potential novel sedative agent with synergistic effects alongside DZP. However, SAL A's poor blood-brain barrier permeability and need for structural optimization highlight the necessity for future mechanistic studies, enhanced delivery methods, and clinical validation to confirm its therapeutic potential for sleep disorders.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107517"},"PeriodicalIF":2.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144502314","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":"Metal exposure in Brazilian children of waste pickers from the largest open garbage dump in Latin America: Use of deciduous teeth as biomarker","authors":"Andrea M. Dantas ,&nbsp;Eliude B. Gomes ,&nbsp;Raquel F. Gerlach ,&nbsp;Airton C. Martins ,&nbsp;Tara R. Zolnikov ,&nbsp;Aline M. Susuki ,&nbsp;Ana C.B. Bezerra ,&nbsp;Fernando Barbosa Jr ,&nbsp;Michael Aschner ,&nbsp;Mariana R. Urbano ,&nbsp;Monica M.B. Paoliello ,&nbsp;Vanessa R.N. Cruvinel","doi":"10.1016/j.ntt.2025.107516","DOIUrl":"10.1016/j.ntt.2025.107516","url":null,"abstract":"<div><div>Environmental exposures to metals is a concern for public health, due to their association with various adverse health outcomes, especially in children. The aim of this study was to analyze 21 metals (V, Cr, Mn, Co, Ni, Cu, Zn, As, Se, Rb, Ag, Cd, Ba, Ti, Pb, U, Sn, Mo, Ce, La, and Th) in deciduous teeth of waste pickers' children from an open garbage dump region (<em>Estrutural</em> region- Group 1), and compare them with children living in two other regions in Brasilia (<em>Ceilandia</em> – Group 2, and <em>Plano Piloto</em> – Group 3). Three hundred and two children participated in the study, and a single deciduous whole tooth (dentine plus enamel) was analyzed from each child. Socio-demographic variables, breastfeeding time, visits to the dentist, drinking water consumption, among others, were obtained through a questionnaire provided to the parents or guardians of the children. Metal analyses were performed by Inductively Coupled Plasma Mass Spectrometry (ICP-MS). Significantly higher concentrations of V, Co, Cu, and As were found in children from G1, where most parents were waste pickers, compared to the other two regions (<em>p</em> &lt; 0.01). Pb and Cd concentrations were significantly higher in children from G2 and G3 compared with G1 (p &lt; 0.01). Significantly higher levels of Cr, Mn, Zn and Se were found in children from G2 (p &lt; 0.01), where residents also have very low income, analogous to G1. We found a trend towards an increase in metal concentrations in incisor compared to canine and molar teeth of children in all three groups. This study provides novel data and reinforces the use of deciduous teeth as potential matrix for biomonitoring children's metal exposures.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107516"},"PeriodicalIF":2.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144502315","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 N-acetylcysteine after repeated exposure to ethanol in memory and neurotransmission in zebrafish","authors":"Daiana Alves Spilere,&nbsp;Guilherme Lodetti,&nbsp;Ana Carolina Salvador de Farias,&nbsp;Amanda Gomes Teixeira,&nbsp;Eduardo Ronconi Dondossola,&nbsp;Eduardo Pacheco Rico","doi":"10.1016/j.ntt.2025.107508","DOIUrl":"10.1016/j.ntt.2025.107508","url":null,"abstract":"<div><h3>Introduction</h3><div>In the brain, alcohol metabolites alter the functioning of several neurotransmission systems, such as glutamatergic and cholinergic, in addition to impairing memory and learning. Medications for Alcohol Use Disorders (AUD) cause adverse effects and contraindications. <em>N</em>-acetylcysteine (NAC) has been shown to protect memory and restore acetylcholinesterase (AChE) levels. Additionally, it functions as an antioxidant that works alongside glutathione, which is associated with the glutamatergic synapse. In this context, the current research aimed to examine the neuroprotective effects of NAC in animals that underwent repeated ethanol exposure (REE), along with the impacts on memory and the cholinergic and glutamatergic signaling pathways in zebrafish.</div></div><div><h3>Methods</h3><div>The animals were exposed to 1 % ethanol for 8 days for 20 min daily. They received treatment with NAC after the eighth exposure to ethanol for 10 or 60 min. Euthanasia occurred 24 h after the last exposure. Inhibitory avoidance and object recognition tests were performed. Also, the choline acetyltransferase (ChAT) enzyme activities, AChE activity, and glutamate uptake were evaluated.</div></div><div><h3>Results</h3><div>The results show a significant AChE activity increase in the REE group and a decrease in those exposed to alcohol and treated with NAC for 10 min. No significant differences were found regarding ChAT activity. REE significantly reduced glutamate uptake. All groups except the ethanol group acquired aversive memory in inhibitory avoidance tests. Only the NAC-treated group demonstrated longer new object exploration in the recognition test. The study indicates that REE affects AChE, glutamate uptake, and aversive memory and that a single NAC treatment can mitigate these effects. These findings enhance the understanding of REE mechanisms and NAC's protective properties against ethanol-induced damage in zebrafish.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"110 ","pages":"Article 107508"},"PeriodicalIF":2.6,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294151","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}