Neurotoxicology最新文献

{"title":"Parental preconceptual α-cypermethrin exposure alters embryonic brain transcriptomics in mice: Implications for autism spectrum disorder and stress vulnerability","authors":"Benjamin Hing ,&nbsp;Robert Taylor ,&nbsp;Samuel Eliasen ,&nbsp;Hanna E. Stevens","doi":"10.1016/j.neuro.2025.07.010","DOIUrl":"10.1016/j.neuro.2025.07.010","url":null,"abstract":"<div><div>Pyrethroid insecticides are widely used in agriculture and households, and their exposure can affect neurodevelopment. Few studies have evaluated how preconception parental exposure could also affect this process. To address this knowledge gap, adult C57Bl6/J mice were gavaged daily with α-cypermethrin at a human relevant low (0.3 mg/kg) or high (10 mg/kg) dose in corn oil for four weeks prior to conception. Offspring embryonic day 16 dorsal forebrain was extracted for transcriptomic analysis. In offspring forebrains of exposed compared to unexposed parents, there was increasing number of differentially expressed genes (DEGs) from paternal (least) to maternal to both parent exposure (most). A dose dependent effect was observed in offspring forebrain for paternal and maternal preconceptual exposures. Maternal and both parent exposures led to upregulated genes in offspring brain for biological processes involved in translation with predicted activation of <em>EIF4E</em>, a gene associated with autism. In contrast, paternal exposure upregulated cell cycle related DNA damage signaling processes. After any parent exposure, there was upregulation of biological processes involved in mitochondria function and oxidative stress and a downregulation of neuronal and synaptic processes with predicted inhibition of <em>BDNF</em> signaling. Weighted gene correlation network analysis identified modules associated with different parent exposures that were over-represented with DEGs and had similar functional signatures as DEG-related pathways. Importantly, DEGs in offspring forebrain after any parent exposure were over-represented with genes related to autism spectrum disorder (ASD) and stress vulnerability. The study highlights the potential contribution of preconception parental pyrethroid exposure to aberrant brain functioning.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 181-196"},"PeriodicalIF":3.9,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760608","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":"C. elegans as a powerful model for neurotoxicity assessment","authors":"Daniel José Barbosa ,&nbsp;Inês C. Santos ,&nbsp;Tatiana Moyisyeyenko ,&nbsp;Cristina Mendes ,&nbsp;Ana Filipa Sobral","doi":"10.1016/j.neuro.2025.07.009","DOIUrl":"10.1016/j.neuro.2025.07.009","url":null,"abstract":"<div><div>The small nematode <em>Caenorhabditis elegans</em> (<em>C. elegans</em>) has emerged as a valuable tool in neurotoxicology due to its well-characterized nervous system, genetic tractability, and high conservation of molecular pathways with humans. These characteristics allow to study cellular and molecular mechanisms triggered by neurotoxic substances. In <em>C. elegans,</em> behavioral, molecular, neurophysiological, and neuronal morphology assays, together with genetic models targeting dopaminergic, glutamatergic, GABAergic, and cholinergic neurons, as well as models for mitochondrial dysfunction and oxidative stress, are valuable for elucidating mechanisms of neurotoxicity. Additionally, <em>C. elegans</em> is widely used for high-throughput neurotoxicity screenings, with automated systems enhancing scalability and accuracy. Despite its advantages, <em>C. elegans</em> has some limitations for translating data to humans, including the absence of a blood-brain barrier and complex brain regions, as well as differences in metabolism. However, it remains a strong model for neurotoxic screening and mechanistic studies. This review offers a broader, updated perspective by addressing not only classical neurotoxicants (<em>e.g.,</em> heavy metals, pesticides) but also increasingly relevant substances like microplastics and industrial chemicals, psychotropic medications, and drugs of abuse. It also provides a detailed overview of diverse <em>C. elegans</em> behavioral, molecular, and neurophysiological neurotoxicity assays, and genetic models for neurotransmitter signaling, mitochondrial dysfunction, and oxidative stress. Importantly, it also discusses the relevance of <em>C. elegans</em> within regulatory frameworks such as adverse outcome pathways (AOPs), a connection largely overlooked in prior reviews. These features address gaps in the current literature and distinguish this work from existing reviews on the topic.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 85-110"},"PeriodicalIF":3.9,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144724807","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":"Prenatal and early childhood exposure to phthalates and neurodevelopment in 42 months old children","authors":"Liron Cohen-Eliraz ,&nbsp;Asher Ornoy ,&nbsp;Eliana Ein-Mor ,&nbsp;Moriah Bar-Nitsan ,&nbsp;Ronit Calderon-Margalit ,&nbsp;Tammy Pilowsky-Peleg","doi":"10.1016/j.neuro.2025.07.007","DOIUrl":"10.1016/j.neuro.2025.07.007","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Increased prevalence of neurodevelopmental syndromes raises concerns regarding risks from environmental exposures. Phthalates are a class of chemicals widely used in daily products. It has been suggested that prenatal and early childhood exposure to phthalates are associated with disruption of developmental outcomes, cognitive and psychomotor functions.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Aims&lt;/h3&gt;&lt;div&gt;To estimate the association between prenatal and early childhood exposure to phthalates and neurodevelopmental outcomes.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Women were recruited at 11–18 weeks of gestation and provided spot urine samples, analyzed for phthalate metabolites (DEHP, DiNP, MBzBP). Children (n = 102) were examined at 42 months of age, using a broad developmental assessment and standard maternal reports, regarding cognitive, developmental and behavioral problems (WPPSI-III, NIH-toolbox, NEPSY-II, CBCL, ASQ-3 questionnaires), and provided spot urine samples (n = 47). To explore the associations between tertiles or continuous levels of metabolites and developmental outcomes, multivariate general linear models (GLM) were used.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;DEHP and DiNP metabolites were above the level of detection (&gt;LOD) in more than 97 % of maternal specimens and MBzBP was detected in 88 % of maternal specimens. Increased DEHP levels were associated with problem solving scores among boys (scores: 53.24 &lt;u&gt;+&lt;/u&gt; 2.34, 54&lt;u&gt;.&lt;/u&gt;29 &lt;u&gt;+&lt;/u&gt; 2.45, and 43.54 &lt;u&gt;+&lt;/u&gt; 3.26 for low, medium and high DEHP tertiles, respectively; p = 0.029), and fine motor problems (47.58 &lt;u&gt;+&lt;/u&gt; 2.93, 49&lt;u&gt;.&lt;/u&gt;75 &lt;u&gt;+&lt;/u&gt; 3.07, and 32.01 &lt;u&gt;+&lt;/u&gt; 4.07 for low, medium and high DEHP tertiles, respectively; p = 0.003) and attention problems among girls (Flanker scores: 112.53 &lt;u&gt;+&lt;/u&gt; 14.28, 110&lt;u&gt;.&lt;/u&gt;3 &lt;u&gt;+&lt;/u&gt; 12.93, and 98.83 &lt;u&gt;+&lt;/u&gt; 12.65 for low, medium and high DEHP tertiles, respectively; p = 0.007). Moreover, in girls, a potential U-shaped association was found between levels of exposure to MBzBP and problem solving (54.55 &lt;u&gt;+&lt;/u&gt; 6.87, 44&lt;u&gt;.&lt;/u&gt;69 &lt;u&gt;+&lt;/u&gt; 14.88, and 54.62 &lt;u&gt;+&lt;/u&gt; 6.60 for low, medium and high MBzBP tertiles, respectively; p = 0.015), fine motor problems (56.36 &lt;u&gt;+&lt;/u&gt; 5.04, 42&lt;u&gt;.&lt;/u&gt;50 &lt;u&gt;+&lt;/u&gt; 15.49, and 51.92 &lt;u&gt;+&lt;/u&gt; 8.04 for low, medium and high MBzBP tertiles, respectively; p = 0.007), and verbal abilities (Vocabulary scores: 11.46 &lt;u&gt;+&lt;/u&gt; 3.01, 8.25 &lt;u&gt;+&lt;/u&gt; 3.43, and 11.53 &lt;u&gt;+&lt;/u&gt; 2.69 for low, medium and high MBzBP tertiles, respectively; p = 0.007). Early childhood exposure was associated with fine motor scores and DEHP and MBzBP postnatal exposure (DEHP: β = −0.010, Cl: −0.016, −0.004, p = 0.003; MBzBP: β = −0.321, Cl: −0.499, −0.144, p = 0.001). Most associations became nonsignificant after FDR correction for multiple comparisons.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;This study suggests associations between prenatal exposure to phthalates and early childhood motor and cognitive abilities, wi","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 74-84"},"PeriodicalIF":3.4,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144704597","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":"Long-term mercury exposure and cognitive functions in a First Nation community in Northern Ontario, Canada","authors":"Donna Mergler ,&nbsp;Aline Philibert ,&nbsp;Jennifer Laura Lee ,&nbsp;Myriam Fillion ,&nbsp;Judy Da Silva","doi":"10.1016/j.neuro.2025.07.005","DOIUrl":"10.1016/j.neuro.2025.07.005","url":null,"abstract":"<div><div>Prenatal, childhood, and current mercury (Hg) exposure through fish consumption have each been associated with cognitive deficits, but little information exists on the consequences of long-term exposure among adults. Since 1962, Grassy Narrows First Nation has been exposed to Hg from an industrial discharge. Average Hair Hg (HHg) concentrations, initially very high, decreased over time and stabilized in the 1990’s. Montreal Cognitive Assessment (MoCA) test outcomes were analyzed in 85 persons aged 32–75 y (median: 53 y) with respect to retrospective year-based HHg measurements between 1970 and 1997 and current blood Hg. Since the MoCA has not been clinically validated for Indigenous populations, residuals of age- and education-adjusted scores were used (MoCA-r scores). Lower MoCA-r scores were observed among persons in the higher quartile of maximum HHg compared to those in the lower quartile (p = 0.007). Clustering of the test items yielded 3 clusters representing verbal fluency and abstraction, cognitive flexibility and working memory, and visuospatial functioning. To model the evolution of HHg over time, longitudinal mixed effect models (LMEM) were performed with persons with ≥ 10 repeated year-based HHg measurements. Higher long-term past HHg was associated with lower MoCA-r and all cluster scores. No association was observed between MoCA-r or cluster scores and blood Hg, which reflects recent exposure. The findings suggest that legacy exposure can affect cognitive functioning decades later, even when average current concentrations have decreased to below recommended guidelines. Prospective studies could provide information on the rate of decline and the possible future impact of current exposure.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 145-154"},"PeriodicalIF":3.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718158","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":"Kisspeptin-10 protects against HIV-1 Tat-induced blood-brain barrier dysfunction and neuroinflammation via RhoA/ROCK pathway: Implications for HAND therapy","authors":"Chao Cheng,&nbsp;Dong Xiong,&nbsp;Fengwei Zheng,&nbsp;Tianze Wang,&nbsp;Weixin Li","doi":"10.1016/j.neuro.2025.07.008","DOIUrl":"10.1016/j.neuro.2025.07.008","url":null,"abstract":"<div><div>This study investigated the effects of Kisspeptin-10 (Kp-10) on HIV-1 Tat-induced blood-brain barrier (BBB) permeability and oxidative stress using both <em>in vivo</em> and <em>in vitro</em> models. <em>In vivo</em>, one hour after intraperitoneal administration of 50 nmol/kg (DSS)*6-Kp-10, mice were intravenously injected with HIV-1 Tat (100 μg/kg). Markers of oxidative stress, inflammatory cytokines, and BBB integrity were then evaluated. <em>In vitro</em>, bEnd.3 cells were treated with HIV-1 Tat and Kp-10, and endothelial permeability, Claudin-5 expression, and RhoA/ROCK signaling were assessed. HIV-1 Tat increased oxidative stress in the cortical tissue of mice, as evidenced by elevated malondialdehyde (MDA) and reduced levels of catalase (CAT) activity, glutathione peroxidase (GSH-Px) activity, and total antioxidant capacity (T-AOC). These effects were attenuated by Kp-10 administration. Additionally, Kp-10 suppressed the expression of pro-inflammatory cytokines, including interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-α), in response to HIV-1 Tat. Notably, Kp-10 mitigated HIV-1 Tat-induced BBB dysfunction by upregulating Claudin-5 expression in the cortical tissue of mice. <em>In vitro</em>, bEnd.3 cells were treated with HIV-1 Tat in the presence of Kp-10 at various concentrations. Our results demonstrated that Kp-10 prevented HIV-1 Tat-induced increases in trans-endothelial permeability and reductions in transepithelial electrical resistance (TEER) by upregulating Claudin-5 expression. Furthermore, Kp-10 inhibited the activation of the RhoA/Rho-associated protein kinase (RhoA/ROCK) signaling pathway in bEnd.3 cells. Overexpression of the RhoA-GTP Q63L mutant abolished the protective effects of Kp-10, suggesting that these effects are mediated through the RhoA/ROCK axis. These findings suggest that Kp-10 might be a potential therapeutic agent for HIV-associated neurocognitive disorders (HAND).</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 111-121"},"PeriodicalIF":3.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718157","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":"Impact of a high-fat diet on spatial learning and memory: The role of sex, APOE genotype, and postnatal chlorpyrifos exposure","authors":"Laia Guardia-Escote ,&nbsp;Judit Biosca-Brull ,&nbsp;Jordi Blanco ,&nbsp;Maria Cabré ,&nbsp;Pia Basaure ,&nbsp;Cristian Pérez-Fernández ,&nbsp;Fernando Sánchez-Santed ,&nbsp;José L. Domingo ,&nbsp;Maria Teresa Colomina","doi":"10.1016/j.neuro.2025.07.004","DOIUrl":"10.1016/j.neuro.2025.07.004","url":null,"abstract":"<div><div>Environmental factors, such as exposure to neurotoxicants and diet, play a critical role in shaping cognitive function, particularly in genetically susceptible individuals. Chlorpyrifos (CPF), an organophosphate pesticide, and high-fat diets (HFD) have been independently associated with cognitive impairment, yet their combined effects remain poorly understood. Apolipoprotein E (<em>APOE)</em> genotype influences vulnerability to cognitive decline, with the <em>ε4</em> allele being a major risk factor for neurodegenerative diseases. This study assessed the interplay between <em>APOE</em> genotype, sex, early-life CPF exposure, and HFD on spatial learning and memory. Male and female C57BL/6, apoE3- and apoE4-targeted replacement (TR) mice were orally exposed to CPF during postnatal days 10–15 and subsequently subjected to a HFD for 8 weeks. At the end of the HFD challenge, body weight gain was calculated, and spatial learning and memory assessed using the Morris Water Maze test. Results indicate that HFD-driven weight gain was influenced by sex and <em>APOE</em> genotype. All groups acquired the spatial learning task, but postnatal CPF exposure affected performance in certain groups. Retention was more variable in females, suggesting increased susceptibility to environmental exposures. Notably, apoE4-TR females showed improved memory retention following either CPF exposure or HFD, whereas apoE4-TR males exhibited impaired long-term memory after HFD exposure. These findings highlight the complex interactions between genetic and environmental factors. Understanding these dynamics is essential for developing targeted nutritional and public health strategies to mitigate cognitive decline. Importantly, dietary recommendations should not be generalized but tailored to individual profiles to optimize cognitive health and disease prevention.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 42-52"},"PeriodicalIF":3.4,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626785","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":"cth-2/mpst-1-dependent H2S deficiency enhances acrylonitrile acute toxicity in Caenorhabditis elegans","authors":"Bobo Yang ,&nbsp;Michael Aschner ,&nbsp;Rongzhu Lu","doi":"10.1016/j.neuro.2025.07.002","DOIUrl":"10.1016/j.neuro.2025.07.002","url":null,"abstract":"<div><div>Acrylonitrile (AN) is a toxic, colorless to pale-yellow liquid extensively used in industrial production and has been linked to neurotoxicity. Though our previous study showed a correlation between AN-induced neurotoxicity and gasotransmitter hydrogen sulfide (H₂S) in mammalian cells, experimental evidence on overall animal toxicity and specific neurological injury is still limited. We aimed to further explore the molecular association between H₂S and AN-induced acute toxicity in <em>Caenorhabditis elegans (C. elegans)</em> by using its genetic advantages, and provide experimental evidence for the validation of H₂S donors as AN antidote. In the present study, we demonstrated that acute AN exposure resulted in toxicity as evidenced by changes in death rate, locomotor behavior, brood size, dopaminergic neuron morphology, and oxidative stress. Notably, AN inhibited the H₂S content, which was double-examined by methylene blue spectrophotometry and lead acetate paper assay. Furthermore, AN significantly decreased 3-mercaptopyruvate sulphurtransferase (3-MPST)-mediated H₂S synthesizing activity and the transcription level of the corresponding coding gene <em>mpst-1</em> but had no effect on the cystathionine β synthetase (CBS)/cystathionine γ lyase (CSE)-mediated H₂S synthesizing activity using L-cysteine as a common substrate and the mRNA levels of H₂S oxidative metabolism enzymes. <em>cth-2</em> and <em>mpst-1</em> mutations significantly downregulated the H₂S content and the corresponding H₂S synthesizing activity, and further enhanced the AN-induced toxicity response including lethality, brood size and lifespan. In contrast, H₂S donor GYY4137 significantly attenuated the AN-damaged survival rate, body bends, and dopaminergic neuron morphology. Our findings demonstrated that the reduction of H₂S mediates the acute toxicity of AN.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 64-73"},"PeriodicalIF":3.4,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626784","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 role of nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and Nrf2 signalling in methanol-induced on brain, eye, and pancreas toxicity in rats","authors":"Meriam NN Rezk ,&nbsp;Mariem Maher Shafek Keryakous ,&nbsp;Michael A. Fawzy ,&nbsp;Fatma El-Zahraa A. Abd El-Aziz ,&nbsp;Asmaa F.A. Dawood ,&nbsp;Hanan D. Yassa ,&nbsp;Nermeen N. Welson","doi":"10.1016/j.neuro.2025.07.003","DOIUrl":"10.1016/j.neuro.2025.07.003","url":null,"abstract":"<div><div>Toxic methyl alcohol is widely employed in industry, and it is highly toxic. Only 15 cc ingestion can result in irreversible blindness. The mechanism of toxicity is still a matter of debate. This study was conducted to investigate the incorporation of nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and Nrf2 signaling pathways in the toxicity of the brain, eye, and pancreas following ingestion of methyl alcohol and the possible protective role of PPAR-γ modulators. Twenty-four adult Wister albino rats were divided into four groups of six rats each: a control group, a pioglitazone group, a methanol group, and a combined pioglitazone and methanol group. Oxidative stress markers, random blood sugar, insulin, and pancreatic function measurements were evaluated. Western blot analysis for PPAR-γ and Nrf2 protein expressions was performed. Histopathological examination was performed for eye, brain, and pancreas tissues, and the results were compared. PPAR-γ seemed to be incorporated in the development of organ toxicity associated with methyl alcohol ingestion. The protective role of PPAR-γ modulators was achieved through the improvement of assessed pathways. Therefore, damage can be dramatically improved through incorporating PPAR-γ agonists in the management plan of methyl alcohol toxicity.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 53-63"},"PeriodicalIF":3.4,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619441","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":"Toluene, styrene and methyl-ethyl-ketone inhalation: Effects on the power of cortical oscillations in rats","authors":"E. Bernal Meléndez ,&nbsp;T. Venet ,&nbsp;A. Thomas ,&nbsp;S. Boucard ,&nbsp;L. Guenot ,&nbsp;L. Merlen ,&nbsp;S. Grossmann ,&nbsp;E. Joubert ,&nbsp;M. Mascherin ,&nbsp;S. Viton ,&nbsp;L. Wathier ,&nbsp;F. Cosnier ,&nbsp;B. Pouyatos","doi":"10.1016/j.neuro.2025.07.001","DOIUrl":"10.1016/j.neuro.2025.07.001","url":null,"abstract":"<div><div>Exposure to volatile organic solvents, in both industrial workers and animal models, has a depressant effect on the central nervous system and alters behavior. However, the specific impact on brain activity during acute exposure has not been extensively studied. Here, we assessed how acute exposure to three common industrial solvents - toluene, styrene and methyl-ethyl-ketone (MEK) - affected the power of brain oscillations in rats. Rats (n = 14/group) were implanted with cortical electrodes which were connected to a removable headstage during exposure, to wirelessly transmit digitized electrocorticographic (ECoG) signals. Signals were continuously recorded while the rats inhaled solvent vapors (1000 ppm) for 6 h, with a 1-h control period before and after (breathing filtered air). Experiments were repeated for four successive days. In addition to brain oscillations, post-rotatory nystagmus (PRN) and sensory-motor coordination were tested following air/solvent exposure. MEK had no significant effects on the parameters tested. Styrene decreased the power of overall brain activity, but had no effect on motor activity. Toluene increased the power of fast oscillations (30–90 Hz) within minutes and further over time; concomitantly, the power of slow waves (2–12 Hz) decreased. Motor activity was slightly increased by toluene. Both toluene and styrene increased the number and duration of saccades measured by PRN. Dose-response experiments with styrene (n = 16 rats) revealed significant changes in oscillation power even at 50 ppm. These findings suggest that ECoG can be used to assess solvent effects on brain activity in real-time, surpassing the sensitivity of traditional sensorimotor tests.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 31-41"},"PeriodicalIF":3.4,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144605952","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":"Impact of early adolescent lead exposure on brain function and response: Findings from a Chinese cohort","authors":"Olivia M. Halabicky ,&nbsp;Naixue Cui ,&nbsp;Jianghong Liu","doi":"10.1016/j.neuro.2025.06.007","DOIUrl":"10.1016/j.neuro.2025.06.007","url":null,"abstract":"<div><h3>Purpose</h3><div>While the detrimental effects of lead exposure on cognition have been well documented, less research has focused on pre-adolescent populations. The purpose of this study was to understand the relationship between adolescent lead exposure and measures of brain functionality.</div></div><div><h3>Methods</h3><div>In a Chinese early adolescent cohort (N = 258 (50.1 % female) mean age 11.51 years) we examined associations between blood lead levels (BLLs) and P300 event-related potential elicited by three types of stimuli during an auditory oddball task.</div></div><div><h3>Results</h3><div>Mean BLLs in adolescence were 3.17 mcg/dl. In ANOVAs comparing BLL groups above and below the mean, those with greater BLLs had significantly prolonged novelty P300 latency (F=4.67; p = 0.032). In linear models adjusted for age, sex, BLLs at 3–5 years, child IQ, residence location, parent's education, and father’s smoking during pregnancy, increasing BLLs were associated with a 20.21 ms increase in target latency (95 % CI 3.73, 36.69). In sex stratified analyses, a 1 mcg/dl increase in BLLs was associated with a 26.64 ms increase in novel latency in males only (95 % CI 3.49, 49.78).</div></div><div><h3>Discussion</h3><div>Our results suggest a modest association between early adolescent lead exposure and detriments in neurophysiology, particularly related to novelty P300 in males and target P300 in the overall sample. Future research can consider how P300 alterations influence child and adolescent developmental trajectories and test ERP measures as a mediator between early life environmental exposures and later health decision making.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"110 ","pages":"Pages 23-30"},"PeriodicalIF":3.4,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144597418","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}