Neurotoxicology and teratology最新文献

{"title":"The effects of developmental sub-chronic low-level lead exposure on microglia and a test of possible mitigation by apigenin in C57BL/6J young mice","authors":"Gisel Flores-Montoya,&nbsp;Zichen Tian,&nbsp;Ayasa Michii,&nbsp;Sze Ying Chan,&nbsp;Natalie Sanchez","doi":"10.1016/j.ntt.2024.107406","DOIUrl":"10.1016/j.ntt.2024.107406","url":null,"abstract":"<div><div>Developmental chronic low-level lead (Pb) exposure disrupts central nervous system function and diminishes neurocognition. Microglial cell activation might contribute to these deficits. The present study evaluated the effects of developmental sub-chronic low-level lead exposure on microglial cells and the possible effectiveness of a natural anti-inflammatory intervention with apigenin to mitigate these effects. From PND 0 to 28, 87 C57BL/6 J mice were exposed to one of six treatment conditions: 0 ppm Pb; 30 ppm Pb; 430 ppm Pb; 30 ppm Pb + 400 ppm apigenin; 430 ppm Pb + 400 ppm apigenin; or 400 ppm apigenin, via dams' drinking water. Following sacrifice, brain tissue was harvested and microglial cells were labeled via immunohistochemistry and counted within the dentate gyrus (DG) using unbiased stereology methods. It was hypothesized that developmental sub-chronic low-level lead exposure would increase microglial cell numbers within the DG and that apigenin treatment may mitigate these effects. A significant effect of treatment group was found and post-hoc analyses revealed that Pb-exposure generated an increased number of microglial cells as compared to controls. Interestingly, the 30 ppm Pb with apigenin treatment group did not generate microglial cell numbers different from the control group unexposed to Pb. These results suggested that developmental sub-chronic low-level lead exposure increased microglial cell activation within the DG and that, at low-levels of Pb exposure, apigenin treatment may mitigate these effects. These results provided the groundwork for studies that could identify an effective intervention to alleviate the effects of developmental chronic low-level lead exposure in child neurocognition.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"107 ","pages":"Article 107406"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786316","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 notice to “Screening for novel central nervous system biomarkers in veterans with Gulf War Illness” [Neurotoxicology and Teratology 61 (2017) 36–46]","authors":"Mohamed B. Abou-Donia ,&nbsp;Lisa A. Conboy ,&nbsp;Efi Kokkotou ,&nbsp;Eric Jacobson ,&nbsp;Eman M. Elmasry ,&nbsp;Passent Elkafrawy ,&nbsp;Megan Neely ,&nbsp;Cameron R. Dale Bass ,&nbsp;Kimberly Sullivan","doi":"10.1016/j.ntt.2024.107423","DOIUrl":"10.1016/j.ntt.2024.107423","url":null,"abstract":"","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"107 ","pages":"Article 107423"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927044","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":"Corrigendum to “Stickler A, Hawkey AB, Gondal A, Natarajan S, Mead M, Levin ED. Embryonic exposures to cadmium and PAHs cause long-term and interacting neurobehavioral effects in zebrafish” [Neurotoxicol Teratol. 2024 Mar-Apr;102:107339. doi: 10.1016/j.ntt.2024.107339. Epub 2024 Mar 6]","authors":"E.D. Levin","doi":"10.1016/j.ntt.2024.107405","DOIUrl":"10.1016/j.ntt.2024.107405","url":null,"abstract":"","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"106 ","pages":"Article 107405"},"PeriodicalIF":2.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142780544","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":"Editorial: Passing the torch: The next chapter for Neurotoxicology and Teratology","authors":"Gale A. Richardson ,&nbsp;Gregg Stanwood","doi":"10.1016/j.ntt.2024.107398","DOIUrl":"10.1016/j.ntt.2024.107398","url":null,"abstract":"","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"106 ","pages":"Article 107398"},"PeriodicalIF":2.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470820","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 buprenorphine/naloxone exposure and neonatal neurobehavioral functioning: A preliminary report","authors":"Martha L. Velez ,&nbsp;Krystle McConnell ,&nbsp;Nancy Spencer ,&nbsp;Lina M. Montoya ,&nbsp;Lauren M. Jansson","doi":"10.1016/j.ntt.2024.107400","DOIUrl":"10.1016/j.ntt.2024.107400","url":null,"abstract":"<div><h3>Introduction</h3><div>Although prescription of buprenorphine/naloxone during pregnancy is gaining acceptance, buprenorphine monotherapy is more often used due to the scarce knowledge of the effects of the combined medications on the fetus and neonate. Evaluation of neurobehavioral functioning of neonates prenatally exposed to buprenorphine/naloxone is lacking. The NICU Network Neurobehavioral Scale (NNNS) has been used to evaluate neurobehavioral functioning, stress responses, and regulatory capacities of neonates at risk for altered development due to prenatal stressors. This pilot study presents a descriptive analysis of the neurobehavioral functioning among neonates exposed in utero to buprenorphine/naloxone, as well as maternal characteristics and factors present during their pregnancy.</div></div><div><h3>Methods</h3><div>Participants were pregnant parents receiving comprehensive treatment for opioid use disorder (OUD) and obstetric care, choosing buprenorphine/naloxone treatment with singleton, uncomplicated pregnancies. Participants provided confidential urine specimens for legal and illegal psychoactive substances according to protocol. Maternal psychiatric disorders and psychiatric medications as well as weekly dosing records were obtained for the duration of study participation. The NNNS was administered to 16 full-term neonates on days 3,14 and 30 of life.</div></div><div><h3>Results</h3><div>Mean summary scores for 12 neurobehavioral domains (attention, arousal, self-regulation, handling, quality of movement, excitability, lethargy, non-optimal reflexes, asymmetrical reflexes, hypertonia, hypotonia and stress/abstinence syndrome) are presented for neonates prenatally exposed to buprenorphine/naloxone at three time points during the first month of life. Several maternal factors that can influence the functioning of the neonate were presented in this sample including smoking cigarettes (94 %), a psychiatric diagnosis (87.5 %), positive urinalysis for legal or illegal substances during treatment (56.2 %).</div></div><div><h3>Conclusions</h3><div>This report provides preliminary information regarding the neurobehavioral functioning of neonates exposed to buprenorphine/naloxone over the first month of life, including consideration of maternal factors. However, future research with a larger sample and controlling for different neonate and maternal factors is necessary to confirm these preliminary findings.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"106 ","pages":"Article 107400"},"PeriodicalIF":2.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567631","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":"Trans-Ferulic acid reduces the sedative activity of diazepam in thiopental sodium-induced sleeping mice: A potential GABAergic transmission","authors":"Md. Shimul Bhuia ,&nbsp;Md. Sakib Al Hasan ,&nbsp;Raihan Chowdhury ,&nbsp;Siddique Akber Ansari ,&nbsp;Irfan Aamer Ansari ,&nbsp;Muhammad Torequl Islam","doi":"10.1016/j.ntt.2024.107403","DOIUrl":"10.1016/j.ntt.2024.107403","url":null,"abstract":"<div><div><em>trans</em>-Ferulic acid (TFA), a bioactive compound found in many plants, has been recognized for its diverse pharmacological activities, including potential neurological benefits. Previous studies suggest that TFA exerts anxiolytic effects <em>via</em> GABAergic pathways. This study aimed to investigate the sedative effects of TFA and its possible molecular mechanisms through <em>in vivo</em> and <em>in silico</em> approaches. Adult <em>Swiss</em> mice were randomly divided into six groups (<em>n</em> = 7): control (vehicle), standard (DZP: Diazepam at 3 mg/kg, p.o.), three test groups (TFA at 25, 50, and 75 mg/kg, p.o.), and a combination group (TFA: 50 mg/kg with DZP: 3 mg/kg, p.o.). Thirty minutes post-treatment, thiopental sodium (TS) at 40 mg/kg was administered to induce sedation, and latency as well as duration of sleep, were observed for up to 4 h. <em>In silico</em> studies were conducted with GABA_A receptor subunits (α1 and β2) to elucidate the possible molecular interactions. The results demonstrated that TFA significantly reduced latency and extended sleep duration in a dose-dependent manner compared to the control. Additionally, TFA combined with DZP further significantly (<em>p</em> &lt; 0.001) enhanced these effects. <em>In silico</em> analysis revealed that TFA and DZP exhibited strong binding affinities with the GABA_A receptor subunits (α1 and β2) in the identical binding sites, with binding energies of −6.8 and − 8.7 kcal/mol, respectively. Collectively, TFA exerted a mild sedative effect in TS-induced sleeping mice and modulated the activity of DZP, likely through interactions with GABA_A receptors. TFA showed promising activity as a potential candidate for managing sleep disorders such as insomnia.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"106 ","pages":"Article 107403"},"PeriodicalIF":2.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639166","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":"Bisphenol F-induced precocious genesis of aggressive neurobehavioral response is associated with heightened monoamine oxidase activity and neurodegeneration in zebrafish brain","authors":"Suvam Bhoi ,&nbsp;Prerana Sarangi ,&nbsp;Lilesh Kumar Pradhan ,&nbsp;Pradyumna Kumar Sahoo ,&nbsp;Bhabani Sankar Sahoo ,&nbsp;Sai Aparna ,&nbsp;Sangeeta Raut ,&nbsp;Saroj Kumar Das","doi":"10.1016/j.ntt.2024.107402","DOIUrl":"10.1016/j.ntt.2024.107402","url":null,"abstract":"<div><div>The production and use of plastics and plastics products has increased dramatically in recent decades. Moreover, their unprotected disposal into ambient life sustaining environment poses a significant health risk. Bisphenol F (BPF) an alternative to bisphenol A (BPA) has been extensively employed for making of plastics. Recent reports have documented the neurotoxic potential of BPF through induction of altered neurochemical profile, microglia-astrocyte-mediated neuroinflammation, oxidative stress, transformed neurobehavioral response, cognitive dysfunction, etc. In the present study, our approach was to understand the underlying mechanism of BPF-persuaded genesis of aggressive neurobehavioral response in zebrafish. The basic findings advocated a temporal transformation in native explorative behaviour and progressive induction of aggressive behavioural response in zebrafish following exposure to BPF. Our neurobehavioral findings supported the argument of oxidative stress-mediated neuromorphological transformation in the periventricular grey zone (PGZ) of the zebrafish brain. In line with earlier reports, our findings also showed that heightened monoamine oxidase (MAO) activity and downregulation in tyrosine hydroxylase expression in the zebrafish brain is associated with the precocious genesis of aggressive neurobehavioral response in zebrafish brain. Our findings also shed light on BPF-instigated apoptotic neuronal death as revealed by augmented chromatin condensation and cleaved caspase-3 expression. Further observation showed that the downregulation of NeuN (a marker of post-mitotic mature neuron) expression provided substantial neurotoxicity, leading to neurodegeneration in the PGZ region of the zebrafish brain. These basic findings grossly advocate that BPF acts as a potent neurotoxicant in transmuting native neurobehavioral response through the induction of oxidative stress, heightened MAO activity and neuromorphological transformation in the zebrafish brain.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"106 ","pages":"Article 107402"},"PeriodicalIF":2.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504798","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":"Lasting effects of adolescent social instability stress on dendritic morphology in the nucleus accumbens in female and male Long Evans rats","authors":"Ashutosh Patel ,&nbsp;Abdulhai Aljaabary ,&nbsp;YiJie Yuan ,&nbsp;Pardis Asgari ,&nbsp;Craig D.C. Bailey ,&nbsp;Cheryl M. McCormick","doi":"10.1016/j.ntt.2024.107401","DOIUrl":"10.1016/j.ntt.2024.107401","url":null,"abstract":"<div><div>Social instability stress (SS) in adolescence in rats leads to long-lasting changes in social behaviour and reward-related behaviour relative to control rats. Given the role of the nucleus accumbens (NAc) in such behaviours, we investigated the morphology of medium spiny neurons (MSNs), which are most neurons in the NAc, in adult female and male rats exposed to SS in adolescence. Irrespective of sex, SS rats had increased number of dendritic spines in both the core and shell regions of the NAc (2.3 % and 18.1 % increase, respectively). In the core, SS rats had a 16 % reduction in the total dendritic lengths of MSNs, whereas in the shell, SS rats had a greater dendritic length closer to the soma, and particularly in SS female rats, whereas the opposite was found farther from the soma (SS 10.6 % &gt; CTL overall). Although the extent to which such structural changes may underlie the enduring effects of SS in adolescence requires investigation, the results add to evidence that changes to the social environment in adolescence can determine adult neuronal structural.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"106 ","pages":"Article 107401"},"PeriodicalIF":2.6,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504799","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":"Prenatal tobacco and tobacco-Cannabis co-exposure and unpredictability in maternal anger/hostility: Implications for toddler reactivity","authors":"Madison R. Kelm ,&nbsp;Pamela Schuetze ,&nbsp;Rina D. Eiden","doi":"10.1016/j.ntt.2024.107399","DOIUrl":"10.1016/j.ntt.2024.107399","url":null,"abstract":"<div><div>Tobacco and cannabis are frequently used together during pregnancy. However, relatively little is known about how co-use and related maternal risk factors impact toddler reactivity. One understudied risk factor is maternal experience of anger/hostility, despite evidence suggesting that individuals who use substances experience more anger/hostility. In addition, mood unpredictability in anger/hostility (MUA), a relatively novel construct, may be particularly important for mothers who use substances as they attempt to cut down or quit during pregnancy and may also impact toddler reactivity. Importantly, prenatal exposures may also impact toddler outcomes via continued postnatal exposure and infant reactivity. We examined a conceptual model linking prenatal tobacco and tobacco-cannabis co-use, maternal anger/hostility, and unpredictability in anger/hostility with toddler reactivity in a sample (<em>N</em> = 247 at recruitment, 190 at toddler age; <em>N</em> = 247 for model testing) of dyads recruited during the first trimester of pregnancy into a tobacco group (use of combustible cigarettes; including sub-group of women who also used cannabis) and a non-substance use group. Results indicated a direct effect of prenatal co-exposure on blunted toddler reactivity for males only. Mothers who used substances prenatally had the highest levels of anger/hostility and MUA. Prenatal anger/hostility and MUA were associated with higher reactivity at infancy which in turn, was associated with higher toddler reactivity. Prenatal co-exposure and higher prenatal maternal anger/hostility was associated with continued postnatal exposure to cannabis which in turn, was associated with higher reactivity at toddlerhood. Results highlight the importance of examining prenatal co-exposure and continued postnatal cannabis exposure as well as associated maternal risk factors such as anger/hostility and MUA for toddler developmental outcomes.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"106 ","pages":"Article 107399"},"PeriodicalIF":2.6,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470821","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":"Oxidative stress as a potential mechanism linking gestational phthalates exposure to cognitive development in infancy","authors":"Kaegan E Ortlund ,&nbsp;Susan L. Schantz ,&nbsp;Andréa Aguiar ,&nbsp;Francheska M. Merced-Nieves ,&nbsp;Megan L. Woodbury ,&nbsp;Dana E. Goin ,&nbsp;Antonia M. Calafat ,&nbsp;Ginger L. Milne ,&nbsp;Stephanie M. Eick","doi":"10.1016/j.ntt.2024.107397","DOIUrl":"10.1016/j.ntt.2024.107397","url":null,"abstract":"<div><h3>Background</h3><div>Gestational exposure to phthalates, endocrine disrupting chemicals widely used in consumer products, has been associated with poor recognition memory in infancy. Oxidative stress may represent one pathway linking this association. Hence, we examined whether exposure to phthalates was associated with elevated oxidative stress during pregnancy, and whether oxidative stress mediates the relationship between phthalate exposure and recognition memory.</div></div><div><h3>Methods</h3><div>Our analysis included a subset of mother-child pairs enrolled in the Illinois Kids Development Study (IKIDS, <em>N</em> = 225, recruitment years 2013–2018). Concentrations of 12 phthalate metabolites were quantified in 2nd trimester urine samples. Four oxidative stress biomarkers (8-isoprostane-PGF_2α, 2,3-dinor-5,6-dihydro-8-isoPGF_2α, 2,3-dinor-8-isoPGF_2α, and prostaglandin-F_2α) were measured in 2nd and 3rd trimester urine. Recognition memory was evaluated at 7.5 months, with looking times to familiar and novel stimuli recorded via infrared eye-tracking. Novelty preference (proportion of time looking at a novel stimulus when paired with a familiar one) was considered a measure of recognition memory. Linear mixed effect models were used to estimate associations between monoethyl phthalate (MEP), sum of di(2-ethylhexyl) phthalate metabolites (ΣDEHP), sum of di(isononyl) phthalate metabolites (ΣDINP), and sum of anti-androgenic phthalate metabolites (ΣAA) and oxidative stress biomarkers. Mediation analysis was performed to assess whether oxidative stress biomarkers mediated the effect of gestational phthalate exposure on novelty preference.</div></div><div><h3>Results</h3><div>The average maternal age at delivery was 31 years and approximately 50 % of participants had a graduate degree. A natural log unit increase in ΣAA, ΣDINP, and ΣDEHP was associated with a statistically significant increase in 8-isoPGF_2α, 2,3-dinor-5,6-dihydro-8-isoPGF_2α, and 2,3-dinor-8-isoPGF_2α. The association was greatest in magnitude for ΣAA and 2,3-dinor-5,6-dihydro-8-isoPGF_2α (β = 0.45, 95 % confidence interval = 0.14, 0.76). The relationship between ΣAA, ΣDINP, ΣDEHP, and novelty preference was partially mediated by 2,3-dinor-8-isoPGF_2α.</div></div><div><h3>Conclusions</h3><div>Gestational exposure to some phthalates is positively associated with oxidative stress biomarkers, highlighting one mechanistic pathway through which these chemicals may impair early cognitive development.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"106 ","pages":"Article 107397"},"PeriodicalIF":2.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372381","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}