Neurotoxicology最新文献

{"title":"Saroglitazar, a PPAR α/γ agonist alleviates 3-Nitropropionic acid induced neurotoxicity in rats: Unveiling the underlying mechanisms","authors":"Madhuri Suma Jakkamsetti ,&nbsp;Aravinda Sai Kolusu ,&nbsp;Suma Rongala ,&nbsp;Bhanu Prakash Arakareddy ,&nbsp;Lakshmi Prashanthi Nori ,&nbsp;Pavan Kumar Samudrala","doi":"10.1016/j.neuro.2024.09.004","DOIUrl":"10.1016/j.neuro.2024.09.004","url":null,"abstract":"<div><div>Saroglitazar (SGZ), a peroxisomal proliferated activated receptor α/γ agonist showed neuroprotective effects in various neurodegenerative disorders like Alzheimer’s and Parkinson’s. However, no studies were performed on Huntington’s, so the goal of the current study is to examine the effect of SGZ on Huntington’s disease like symptoms induced by 3-Nitropropionic acid. In this protocol, twenty-four rats were divided into four groups, each group consisting of 6 animals. Group 1: The control group received 1 % CMC 10 mg/kg, p.o. for 14 days. Groups 2, 3, and 4 received 3-NP 15 mg/kg, i.p. from Day 1 to Day 7. Groups 3 and 4 received SGZ 5 mg/kg, p.o. and 10 mg/kg, p.o. respectively once daily from day 1 to day 14. Various behavioral tests like OFT, rotarod, hanging wire, narrow beam walk, MWM, and Y-maze were performed. On day-15, the animals were euthanised by cervical dislocation and brain sample were isolated for biochemical and histopathological analysis. Administration of 3-NP showed a significant decrease in motor coordination and cognitive function. Furthermore, 3-NP altered the activity of acetylcholinesterase, anti-oxidant enzymes, Nrf-2, NF-κB, BDNF, CREB levels, and histological features. However, treatment with SGZ showed ameliorative effects in the 3-NP induced neurotoxicity <em>via</em> PPAR α/γ pathway by reducing motor dysfunction, memory impairment, cholinesterase levels, oxidative stress, neuroinflammation. It also enhanced the levels of Nrf-2, BDNF, and CREB expression and improved histological features. In conclusion, treatment with Saroglitazar attenuated Huntington’s disease-like symptoms in rats which are induced by 3-NP via activation of PPAR α/γ pathway.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 131-146"},"PeriodicalIF":3.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142327835","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":"Welding techniques and manganese concentrations in blood and brain: Results from the WELDFUMES study","authors":"Per Thunberg ,&nbsp;Gunilla Wastensson ,&nbsp;Göran Lidén ,&nbsp;Mary Adjeiwaah ,&nbsp;Jens Tellman ,&nbsp;Bernt Bergström ,&nbsp;Louise Fornander ,&nbsp;Peter Lundberg","doi":"10.1016/j.neuro.2024.09.005","DOIUrl":"10.1016/j.neuro.2024.09.005","url":null,"abstract":"<div><div>This study used whole-brain mapping to investigate the effect of different welding processes on manganese (Mn) accumulation in the brain. Exposure measurements were performed at the welders’ workplaces about 3 weeks before a magnetic resonance imaging (MRI) examination. The welders were categorized into three main groups based on welding method, and the T1-relaxation rate (R1) was measured using quantitative MRI (qMRI). Welders using shielded metal arc welding (SMAW) were found to have lower accumulations of total Mn in clusters encompassing white matter, thalamus, putamen, pallidum, and substantia nigra compared with welders using inert gas tungsten arc welding (GTAW) or continuous consumable electrode arc welding (CCEAW). A positive correlation was found between Mn in red blood cells (Mn-RBC) and R1 in a region encompassing pre-and post-central gyri. The results of this study show that the accumulation of free, bound, or compartmentalized Mn ions in the brain differed depending on the welding method used. These differences were predominately located in the basal ganglia but were also found in regions encompassing white matter. The level of Mn-RBC was correlated to the deposition of Mn in the left primary somatosensory and motor cortex and may therefore be linked to neurological and neurobehavioral symptoms.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 121-130"},"PeriodicalIF":3.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322171","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":"Corrigendum to: “The protective effect of rutin against the cisplatin-induced cochlear damage in vitro” [Neurotoxicology vol. 90 (2022) 102–111]","authors":"Shimei Zheng ,&nbsp;Chang Liu ,&nbsp;Dongmei Tang ,&nbsp;Zhiwei Zheng ,&nbsp;Renchun Yan ,&nbsp;Cheng Wu ,&nbsp;Na Zuo ,&nbsp;Jun Ma ,&nbsp;Yingzi He ,&nbsp;Shaofeng Liu","doi":"10.1016/j.neuro.2024.09.002","DOIUrl":"10.1016/j.neuro.2024.09.002","url":null,"abstract":"","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 94-95"},"PeriodicalIF":3.4,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0161813X24001153/pdfft?md5=b8be765367cac4d2acb9c647dad530e3&pid=1-s2.0-S0161813X24001153-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142239816","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":"Unraveling the effects of prenatal anesthesia on neurodevelopment: A review of current evidence and future directions","authors":"Qiu-Xia Xiao ,&nbsp;Min-Jian Geng ,&nbsp;Qiu-Lin Wang ,&nbsp;Chang-Le Fang ,&nbsp;Jing-Han Zhang ,&nbsp;Qi Liu ,&nbsp;Liu-Lin Xiong","doi":"10.1016/j.neuro.2024.09.003","DOIUrl":"10.1016/j.neuro.2024.09.003","url":null,"abstract":"<div><p>Human brain development is a complex, multi-stage, and sensitive process, especially during the fetal stage. Animal studies over the last two decades have highlighted the potential risks of anesthetics to the developing brain, impacting its structure and function. This has raised concerns regarding the safety of anesthesia during pregnancy and its influence on fetal brain development, garnering significant attention from the anesthesiology community. Although preclinical studies predominantly indicate the neurotoxic effects of prenatal anesthesia, these findings cannot be directly extrapolated to humans due to interspecies variations. Clinical research, constrained by ethical and technical hurdles in accessing human prenatal brain tissues, often yields conflicting results compared to preclinical data. The emergence of brain organoids as a cutting-edge research tool shows promise in modeling human brain development. When integrated with single-cell sequencing, these organoids offer insights into potential neurotoxic mechanisms triggered by prenatal anesthesia. Despite several retrospective and cohort studies exploring the clinical impact of anesthesia on brain development, many findings remain inconclusive. As such, this review synthesizes preclinical and clinical evidence on the effects of prenatal anesthesia on fetal brain development and suggests areas for future research advancement.</p></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 96-110"},"PeriodicalIF":3.4,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142239815","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-specific effects on elements of the social brain neural network in Wistar rats from perinatal exposure to FireMaster 550 or its components","authors":"Stacy Schkoda ,&nbsp;Brian Horman ,&nbsp;Shannah Witchey ,&nbsp;Genevieve St. Armour ,&nbsp;Mason Nelson ,&nbsp;Emily Gaeta ,&nbsp;Madeline Scott ,&nbsp;Heather B. Patisaul","doi":"10.1016/j.neuro.2024.09.001","DOIUrl":"10.1016/j.neuro.2024.09.001","url":null,"abstract":"<div><p>Developmental exposure to chemical flame retardants (FRs) has been linked to a variety of neurodevelopmental disorders and abnormal socioemotional behaviors in human and laboratory animal studies. We have previously shown in Wistar rats that gestational and lactational exposure to the FR mixture Firemaster 550 (FM 550) or its brominated or organophosphate ester (OPFR) components (at 2000 µg, 1000 µg, and 1000 µg oral to the dam respectively (absolute and not by bodyweight)) results in increased anxiety-like behaviors in females and decreased sociality in both sexes. Using their siblings, this study characterized sex and chemical specific targets of disruption in brain regions underlying each behavioral phenotype. Offspring were exposed across gestation and lactation then prepared for either immunohistochemistry or autoradiography at postnatal day 90 to quantify expression of serotonin, estrogen receptor α (ERα), and oxytocin receptor (OTR) in multiple brain regions. No effect of exposure was found in males for any biological target. In females, serotonin innervation was increased in the medial amygdala of FM 550 exposed animals while ERα expression in the bed nucleus of the stria terminalis (BNST) was reduced by FM 550 and OPFR. Evidence of disrupted OTR was observed in males, particularly the BNST but considered an exploratory finding given the small sample size. These results begin to shed light on the mechanisms by which developmental FR exposure alters socioemotional behaviors of relevance to neurodevelopmental disorders.</p></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 111-120"},"PeriodicalIF":3.4,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142146062","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":"Neurobehavioral toxicity of Cold plasma activated water following oral gavage in mice","authors":"Ghada Abd El-Reda ,&nbsp;Usama T. Mahmoud ,&nbsp;Fatma Abo Zakaib Ali ,&nbsp;Fatma M. Abdel-Maksoud ,&nbsp;Manal A.M. Mahmoud ,&nbsp;F.M. El-Hossary","doi":"10.1016/j.neuro.2024.08.007","DOIUrl":"10.1016/j.neuro.2024.08.007","url":null,"abstract":"<div><p>Cold plasma-activated water (PAW) is a novel technology that was recently used in biomedical research; Despite its potential, PAW's safety remains inadequately assessed. The study explores the impact of PAW on behavioral responses and brain tissue histopathology in mice. Ten-week-old female albino mice were divided into three groups each containing 10 mice (5 replicates, 2 mice/cage) and received either distilled water (DW), or distilled water exposed to cold atmospheric plasma (CAP) for 3 min (PAW-3), or 15 min (PAW-15) by oral gavage in a dose of 200 μL/mice (3 times/week) for four weeks. PAW exhibited altered physicochemical properties compared to DW. Mice exposed to PAW demonstrated reduced burrowing activity, marble burying ability, and novel object recognition compared to controls, indicating potential neurobehavioral alterations. PAW-treated groups displayed notable histological lesions in brain tissues, including nerve cell necrosis, vascular congestion, and Purkinje cell degeneration, confirming neurotoxic effects. Positive reactions for NF-κB and iNOS in brain tissues of PAW-treated mice corroborated the histopathological findings, suggesting neuroinflammation and oxidative stress. The study highlights the need for further investigation into PAW's safety profile and optimal treatment protocols to mitigate potential neurobehavioral toxicity in biomedical research.</p></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 45-57"},"PeriodicalIF":3.4,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109994","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":"Cerium oxide nanoparticles (nanoceria) pretreatment attenuates cell death in the hippocampus and cognitive dysfunction due to repeated isoflurane anesthesia in newborn rats","authors":"Ezgi Kargı-Gemici ,&nbsp;Aslıhan Şengelen ,&nbsp;Yunus Aksüt ,&nbsp;Onat Akyol ,&nbsp;Selma Şengiz-Erhan ,&nbsp;Mehmet Bay ,&nbsp;Evren Önay-Uçar ,&nbsp;Ayşin Selcan ,&nbsp;Serdar Demirgan","doi":"10.1016/j.neuro.2024.08.005","DOIUrl":"10.1016/j.neuro.2024.08.005","url":null,"abstract":"<div><p>General anesthetics exposure, particularly prolonged or repeated exposure, is a crucial cause of neurological injuries. Notably, isoflurane (ISO), used in pediatric anesthesia practice, is toxic to the developing brain. The relatively weak antioxidant system at early ages needs antioxidant support to protect the brain against anesthesia. Cerium oxide nanoparticles (CeO₂-NPs, nanoceria) are nano-antioxidants and stand out due to their unique surface chemistry, high stability, and biocompatibility. Although CeO₂-NPs have been shown to exhibit neuroprotective and cognitive function-facilitating effects, there are no reports on their protective effects against anesthesia-induced neurotoxicity and cognitive impairments. Herein, Wistar albino rat pups were exposed to ISO (1.5 %, 3-h) at postnatal day (P)7+P9+P11, and the protective properties of CeO₂-NP pretreatment (0.5 mg/kg, intraperitoneal route) were investigated for the first time. The control group at P7+9+11 received 50 % O₂ (3-h) instead of ISO. Exposure to nanoceria one-hour before ISO protected hippocampal neurons of the developing rat brain against apoptosis [determined by hematoxylin-eosin (HE) staining, immunohistochemistry (IHC) analysis with caspase-3, and immunoblotting with Bax/Bcl2, cleaved caspase-3 and PARP1] oxidative stress, and inflammation [determined by immunoblotting with 4-hydroxynonenal (4HNE), nuclear factor kappa-B (NF-κB), and tumor necrosis factor-alpha (TNF-α)]. CeO₂-NP pretreatment also reduced ISO-induced learning (at P28–32) and memory (at P33) deficits evaluated by Morris Water Maze. However, memory deficits and thigmotactic behaviors were detected in the agent-control group; elimination of these harmful effects will be possible with dose studies, thus providing evidence supporting safer use. Overall, our findings support pretreatment with nanoceria application as a simple strategy that might be used for pediatric anesthesia practice to protect infants and children from ISO-induced cell death and learning and memory deficits.</p></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 82-93"},"PeriodicalIF":3.4,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109996","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":"BBPT attenuated 6-OHDA-induced toxicity by modulating oxidative stress, apoptotic, and inflammatory proteins in primary neurons and rat models of Parkinson's disease","authors":"Jyoti Mishra,&nbsp;Vaishali Walecha,&nbsp;Tuithung Sophronea,&nbsp;Ankit Singh,&nbsp;Saurabh Agrawal,&nbsp;Pratibha Mehta Luthra","doi":"10.1016/j.neuro.2024.08.008","DOIUrl":"10.1016/j.neuro.2024.08.008","url":null,"abstract":"<div><p>Parkinson’s disease (PD) results from the degeneration of dopaminergic neurons in substantia nigra pars compacta (SNpc). Adenosine A_2AR acting through the striato-pallidal pathway has emerged as a non-dopaminergic target in the therapy of PD. In the present work, the anti-parkinsonian potential of (4<em>E</em>)-4-(4-bromobenzylideneamino)-3-phenyl-2,3-dihydro-2-thioxo- thiazole-5-carbonitrile (BBPT) was explored. BBPT exhibited significant antioxidant activity in situ. In the MTT assay, the BBPT treatment showed insignificant toxicity to the primary midbrain neuronal (PMDN) cells. 6-OHDA induced PMDN cells, 3 h post-treated with BBPT showed 80–85 % survival of the cells and restoration of dopamine and TNF-α levels. The acute and sub-acute toxicity test for BBPT was performed with Sprague Dawley (SD) rats. In toxicity assay, any significant physical, hematological, or biochemical changes in the rats were not observed. To evaluate the effect of BBPT in vivo, a 6-OHDA-induced unilaterally lesioned SD rat model of PD was established. We observed that the BBPT treatment improved the behavioral symptoms in 6-OHDA-induced unilaterally lesioned rats. The proteins of 6-OHDA-induced BBPT-treated rats were isolated from the brain tissue to assess the antioxidant effect (GSH, catalase, SOD, lipid-peroxidation, nitrite), dopamine levels, and the restoration in the apoptosis and inflammation. Our results demonstrated that BBPT increased the anti-oxidant enzyme levels, restored the caspase-3/Bcl-2 levels to arrest apoptosis, and attenuated the TNF-α/IL-6 levels, thus restoring the neuronal damage in unilaterally lesioned 6-OHDA-induced SD rats. Precisely, the findings suggested that BBPT possessed significant anti-parkinsonian activity and has the potential to prevent dopaminergic neurodegeneration.</p></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 67-81"},"PeriodicalIF":3.4,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109995","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":"Coenzyme Q10 ameliorates cyclophosphamide-induced chemobrain by repressing neuronal apoptosis and preserving hippocampal neurogenesis: Mechanistic roles of Wnt/ β-catenin signaling pathway","authors":"Zeina Hussein ,&nbsp;Haidy E. Michel ,&nbsp;Reem N. El-Naga ,&nbsp;Ebtehal El-Demerdash ,&nbsp;Eman M. Mantawy","doi":"10.1016/j.neuro.2024.08.003","DOIUrl":"10.1016/j.neuro.2024.08.003","url":null,"abstract":"<div><p>Deterioration in the neurocognitive function of cancer patients referred to as “Chemobrain” is a devastating obstacle associated with cyclophosphamide (CYP). CYP is an alkylating agent, clinically utilized as an efficient anticancer and immunosuppressant. Coenzyme Q10 (CoQ10) is a worthwhile micronutrient with diverse biological activities embracing antioxidant, anti-apoptotic, and neuroprotective effects. The current experiment was designed for investigating the neuroprotective capability of CoQ10 versus CYP-elicited chemobrain in rats besides elucidating the causal molecular mechanisms. Male Sprague Dawley rats received CoQ10 (10 mg/kg, orally, once daily, for 10 days) and/or a single dose of CYP (200 mg/kg i.p. on day 7). CoQ10 counteracted CYP-induced cognitive and motor dysfunction as demonstrated by the findings of neurobehavioral tests (passive avoidance, Y maze, locomotion, and rotarod tests). Histopathological analysis further affirmed the neuroprotective abilities of CoQ10. CoQ10 effectually diminished CYP-provoked oxidative injury by restoring the antioxidant activity of catalase (CAT) enzyme while reducing malondialdehyde (MDA) levels. Besides, CoQ10 efficiently repressed CYP-induced neuronal apoptosis by downregulating the expression of Bax and caspase-3 while upregulating the Bcl-2 expression. Moreover, CoQ10 hampered CYP-provoked upregulation in acetylcholinesterase (AChE) activity. Furthermore, CoQ10 considerably augmented hippocampal neurogenesis by elevating the expressions of brain-derived neurotrophic factor (BDNF) and Ki-67. These promising neuroprotective effects can be credited to upregulating Wnt/β-catenin pathway as evidenced by the elevated expressions of Wnt-3a, β-catenin, and Phoshpo-glycogen synthase kinase-3 β (p-GSK-3β). Collectively, these findings proved the neuroprotective capabilities of CoQ10 against CYP-induced chemobrain through combating oxidative injury, repressing intrinsic apoptosis, boosting neurogenesis, and eventually upregulating the Wnt/β-catenin pathway.</p></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 21-33"},"PeriodicalIF":3.4,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142095640","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":"Early postnatal and concurrent exposure to metals and neurobehavioral outcomes at 5 years: Associations with individual environmental exposures and mixtures","authors":"Sui-Ling Liao ,&nbsp;Shen-Hao Lai ,&nbsp;Yuan-Ting Hsu ,&nbsp;Li-Chen Chen ,&nbsp;Ming-Han Tsai ,&nbsp;Man-Chin Hua ,&nbsp;Tsung-Chieh Yao ,&nbsp;Kuan-Wen Su ,&nbsp;Kuo-Wei Yeh ,&nbsp;Chih-Yung Chiu ,&nbsp;Shau-Ku Huang ,&nbsp;Jing-Long Huang","doi":"10.1016/j.neuro.2024.08.006","DOIUrl":"10.1016/j.neuro.2024.08.006","url":null,"abstract":"<div><h3>Background</h3><p>Little is known about the effect of postnatal exposure to heavy metals on children’s behavior problems. This study aimed to investigate the association between metal exposure during different stages of postnatal life and neurobehavioral outcomes in preschool children.</p></div><div><h3>Methods</h3><p>Urinary concentrations of six metals (arsenic, cadmium, chromium, lead, manganese, and vanadium) were measured using inductively coupled plasma mass spectrometry in 220 participants at two time points: before 1 year and at 5 years of age. Mothers completed the Child Behavior Checklist when the children were 5 years old. Multivariable linear and logistic regression analyses were used to evaluate the association between metal concentrations and behavioral outcomes. We employed Bayesian kernel machine regression (BKMR) to assess possible joint effects and potential interactions between metal mixtures and behavioral outcomes.</p></div><div><h3>Results</h3><p>Concentrations of urinary arsenic (As) in infants were associated with higher scores for anxious/shy behavior problems (β ranging from 0.03 to 0.23). Further analyses showed that As exposure increased the odds of scores falling into the borderline or clinical range on anxious/depressed, affective, and pervasive developmental problems (ORs: 2.45–3.40). Stratification by sex indicated significance in girls but not in boys. BKMR analysis showed that, among the metal mixtures, As displayed a major effect on behavior scores. Concentrations of urinary cadmium in infants were also associated with higher behavioral scores but did not increase the risk of clinical problems. A cross-sectional survey in 5-year-olds did not show a significant association between concurrent metal exposure and behavioral outcome.</p></div><div><h3>Conclusion</h3><p>Our results showed that exposure to As and Cd during infancy was associated with emotional problems in children. The effect of arsenic exposure was more pronounced among female infants. We suggest reducing exposure to toxic metals during early postnatal life to prevent behavioral problems in children.\"</p></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 58-66"},"PeriodicalIF":3.4,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110001","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}