Toxicology最新文献

{"title":"Mechanistic insights into deoxynivalenol-induced cytotoxicity in an SH-SY5Y 3D spheroid model.","authors":"Martina Sánchez, Veronica Zingales, Josefa Tolosa, María-José Ruiz","doi":"10.1016/j.tox.2026.154563","DOIUrl":"10.1016/j.tox.2026.154563","url":null,"abstract":"<p><p>Deoxynivalenol (DON) is a trichothecene mycotoxin frequently detected in cereal-derived foods and animal feed. Exposure to DON has been associated with a variety of toxic effects, including neurotoxicity. Three-dimensional (3D) cell culture systems have emerged as more physiologically relevant models than conventional two-dimensional (2D) cultures, as they better reproduce cellular organization, including cell-cell and cell-matrix interactions, and more accurately reflect in vivo conditions. In this context, the present study aimed to investigate the cytotoxic effects of DON and its underlying mechanisms using a 3D spheroid model derived from the human neuroblastoma cell line SH-SY5Y. Spheroids were exposed to different concentrations of DON and cell viability was assessed using the MTT assay, yielding an IC₅₀ value > 64 µM. No significant changes were detected in total intracellular reactive oxygen species (ROS) levels. However, a significant increase in mitochondrial superoxide production was observed at 16 µM, together with alterations in mitochondrial membrane potential between 2 and 16 µM. In addition, DON treatment altered cell cycle progression and increased the proportion of early apoptotic cells at 16 µM, as determined by Annexin V/propidium iodide staining. Protein analysis further revealed increase expression of Bax and Bcl-2 at 16 µM, resulting in a Bax/Bcl-2 ratio close to unity, along with elevated levels of cleaved caspase-3. Overall, these results demonstrate that DON induces cytotoxic effects in SH-SY5Y spheroids, accompanied by mitochondrial alterations, increased mitochondrial superoxide production, and apoptotic cell death. These findings contribute to the understanding of DON-induced alterations in neuronal cells and highlight the potential of SH-SY5Y spheroids as a biologically relevant human in vitro model for mechanistic studies of mycotoxin toxicity.</p>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":" ","pages":"154563"},"PeriodicalIF":5.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148698033","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":"Co-exposure to fluoride and arsenic induces endoplasmic reticulum stress in C2C12 myoblasts and MC3T3 preosteoblasts.","authors":"Deepika Bhat K, Joel Rimson Pinto, Apoorva H Nagendra, Bipasha Bose, Sudheer Shenoy P","doi":"10.1016/j.tox.2026.154566","DOIUrl":"10.1016/j.tox.2026.154566","url":null,"abstract":"<p><p>Environmental exposure to fluoride and arsenic is a major public health concern in many regions worldwide. Although both toxicants are known to impair skeletal development, the cellular mechanisms underlying their combined effects on skeletal muscle and bone cells remain poorly understood. This study investigated the impact of sodium fluoride (NaF) and arsenic trioxide (As₂O₃) co-exposure, for the first time, in C2C12 myoblasts (at 0.14 mM NaF + 2.4 µM As₂O₃) and MC3T3 preosteoblasts (at 0.64 mM NaF + 13 µM As₂O₃). Co-exposure significantly reduced cell proliferation and decreased the expression of the lineage specific transcription factors such as MYOD and RUNX2 in C2C12 and MC3T3 cells, respectively. Both individual and combined treatments increased ROS production, with co-exposure producing the highest oxidative stress. Further, fluoride and arsenic co-exposure exerted its effects by inducing endoplasmic reticulum stress in both cell types which was witnessed by the activation of the unfolded protein response (UPR) pathways. Specifically, in C2C12 myoblasts, co-exposure predominantly activated the PERK-Atf4-Chop pathway while suppressing IRE1α-Xbp1 expression, indicating unresolved ER stress. In contrast, MC3T3 preosteoblasts activated both PERK-Atf4-Chop and IRE1α-Xbp1 pathways, suggesting engagement of adaptive ER stress mechanisms. Collectively, these findings demonstrate that fluoride and arsenic co-exposure disrupts cellular homeostasis by inducing ER stress in both myoblasts and preosteoblasts. The differences in activation of different UPR pathways suggests C2C12 myoblasts to be more susceptible to fluoride and arsenic co-exposure compared to MC3T3 preosteoblasts.</p>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":" ","pages":"154566"},"PeriodicalIF":5.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707763","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":"Perfluorooctanoic acid alters mitochondrial bioenergetics and redox status in isolated mouse liver mitochondria.","authors":"Dongshin Yang, Jaeyeong Shin, Joo Young Huh, Sooim Shin","doi":"10.1016/j.tox.2026.154615","DOIUrl":"https://doi.org/10.1016/j.tox.2026.154615","url":null,"abstract":"<p><p>Perfluorooctanoic acid (PFOA) is a persistent environmental pollutant linked to metabolic diseases, wherein mitochondrial dysfunction plays a critical role. This study investigated the direct effects of PFOA on isolated liver mitochondria from male and female mice exposed to 50-1,000μM PFOA for 10min. We assessed mitochondrial respiratory complex (CI-CIV) activities, ATP production, oxidative stress markers, and mitochondrial membrane potential (MMP). PFOA selectively altered CII and CIV activities, while CI and CIII remained largely unaffected. Notably, CIV activity increased at higher concentrations, while ATP production decreased at 1mM and MMP showed a decreasing trend at 500μM and 1mM, consistent with impaired mitochondrial energy coupling. Furthermore, ROS/RNS levels showed an increasing trend with increasing PFOA concentrations. Male- and female-derived mitochondria showed different response patterns across several endpoints. GSH levels showed no consistent concentration-dependent pattern, SOD activity showed no statistically significant changes, and cytochrome c levels showed no statistically significant changes under the present experimental conditions. These findings suggest that PFOA directly alters mitochondrial bioenergetic and redox-related processes, consistent with impaired energy coupling and altered redox status.</p>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":" ","pages":"154615"},"PeriodicalIF":5.2,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149196753","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":"Persistent organic pollutants: Neurotoxic mechanisms and insights from organoid models","authors":"Ziyu Ji ,&nbsp;Liqun Chen,&nbsp;Dong Ming","doi":"10.1016/j.tox.2026.154408","DOIUrl":"10.1016/j.tox.2026.154408","url":null,"abstract":"<div><div>Persistent Organic Pollutants (POPs) pose significant global environmental health risks due to their persistence, bioaccumulation, and long-range transport. Exposure to POPs has been linked to a range of neurological disorders, including cognitive impairment, neurodevelopmental abnormalities, and neurodegenerative diseases. This review examines the neurotoxic effects of various POP categories, such as flame retardants, pesticides, plasticizers, and preservatives, and explores the underlying molecular mechanisms. It also highlights the potential of brain organoids as a more physiologically relevant experimental platform. Although organoid models offer improved translational value, their capacity to fully replicate the complexity of the human nervous system remains limited, necessitating further technical refinement and interdisciplinary collaboration. The integration of organoid technology into environmental toxicology is anticipated to enhance the accuracy and efficiency of neurotoxicity assessment, thereby supporting the development of robust health risk evaluation frameworks and informing evidence-based environmental policy.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154408"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146039966","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":"PFOS promotes Alzheimer’s disease through aggravating the cell apoptosis and AKT/GSK3β/NF-κB/NLRP3 pathway mediated inflammation","authors":"Ming Li ,&nbsp;Xianhao Ping ,&nbsp;Huixin Song ,&nbsp;Jin Sun ,&nbsp;Qian Yang ,&nbsp;Li-Na Gao","doi":"10.1016/j.tox.2026.154423","DOIUrl":"10.1016/j.tox.2026.154423","url":null,"abstract":"<div><div>Perfluorooctane sulfonate (PFOS) and its alternatives are widely utilized in industrial and commercial applications. Nevertheless, their environmental persistence and widespread detection in diverse matrices in recent years have raised significant public health concerns. Studies reported that exposure to PFOS in cerebrospinal fluid will increase the risk of cognitive decline in humans. However, the underlying toxicological mechanism is still unclear. The aim of this study was to elucidate the possible toxic targets and potential molecular mechanisms of Alzheimer's disease (AD) induced by PFOS exposure through network toxicology, molecular docking and <em>in vitro</em> verification. Firstly, the results of network toxicology suggested that the mechanisms of PFOS-induced AD were mainly associated with the PI3K-AKT, neurodegeneration, apoptosis and NOD-like receptor signaling pathways. Subsequently, molecular docking simulations confirmed a strong binding interaction between PFOS and the key targets including SRC, ESR1, CASP3, BCL2, ERBB2, and TNF. Finally, we used HT22 and SH-SY5Y cell lines to validate the toxic effects of PFOS and found that PFOS aggravated neuronal cell apoptosis and AKT/GSK3β/NF-κB/NLRP3 pathway mediated inflammatory damages. Briefly, these findings indicated that PFOS exposure could affect the proliferation of neural cells by activating apoptosis and inflammatory related signaling pathways, thus promoting the occurrence and development of AD. This study provides a theoretical basis for understanding the molecular mechanisms involved in PFOS-induced neurotoxicity.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154423"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146143556","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":"Cigarette smoke exposure disrupts the blood–testis barrier and negatively impacts reproductive capacity in mice","authors":"Yuan Zhong ,&nbsp;Xueyu Wei ,&nbsp;Zimangul Yasin ,&nbsp;Yunfei Huang ,&nbsp;Lijuan He","doi":"10.1016/j.tox.2026.154407","DOIUrl":"10.1016/j.tox.2026.154407","url":null,"abstract":"<div><div>Maintaining normal testicular structure and function is closely related to the blood–testis barrier (BTB). Meanwhile, cigarette smoke extract (CSE) affects testicular function. However, whether CSE mediates BTB damage and the underlying mechanism(s) are unclear. This study investigates the effects of CSE on the BTB in mice by focusing on changes in hormone levels. CSE was prepared and administered intranasally at different concentrations to 6–8-week-old male Balb/c mice for five weeks. After cigarette smoke components successfully entered and accumulated in the mice, the seminiferous tubules of the testes were atrophied, spermatogenic cell arrangement became disordered, sperm quality declined, and spermatogenesis was impaired. Furthermore, CSE exposure disrupted the hypothalamic–pituitary–gonadal axis. CSE also damaged the ultrastructure of the BTB, leading to impaired integrity and increased permeability. The associated disruption of BTB function was caused by inhibiting key proteins, including occludin, Zonula occludens-1(ZO-1), N-cadherin, β-catenin, and connexin-43, correlated with hormonal changes. Collectively, these findings suggest that cigarette smoke exposure disrupts BTB structure and function by altering hormone levels and suppressing the expression of BTB-related proteins, affecting spermatogenesis and male reproductive capacity.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154407"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146041350","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":"Nanoplastics induce SH-SY5Y cell damage through oxidative stress and disruption of amino acid metabolism","authors":"Tianyi Ma ,&nbsp;Yuyang Liu ,&nbsp;Jingran Sun ,&nbsp;Yanjun Fang ,&nbsp;Yonghui Wang ,&nbsp;Xiaoli Li ,&nbsp;Nan Su ,&nbsp;Mingzhu Liu ,&nbsp;Zunquan Zhao ,&nbsp;Jin Wu ,&nbsp;Jialei Bai","doi":"10.1016/j.tox.2026.154419","DOIUrl":"10.1016/j.tox.2026.154419","url":null,"abstract":"<div><div>With the pervasive environmental distribution of plastics, their fragmentation into nanoplastics (NPs) has raised growing concerns regarding potential biological toxicity, particularly in neuronal cells. This study investigated the toxic effects and underlying mechanisms of NPs on SH-SY5Y cells. Five types of NPs were first systematically characterized using scanning electron microscopy (SEM), hydrodynamic diameter measurement, and Zeta potential analysis. Cell internalisation of fluorescently labelled NPs was observed using confocal microscopy. Cell viability was assessed across different NP concentrations to determine the optimal exposure dose. In vitro exposure to the five types of nanoplastics (PE-NPs, PET-NPs, PMMA-NPs, PP-NPs, and PS-NPs) resulted in differential reductions in SH-SY5Y cell viability. Notably, the PE-NPs and PP-NPs treatment groups exhibited a more significant decrease in cell viability, whereas the PET-NPs and PMMA-NPs treatment groups showed a relatively mild reduction in cell viability. Oxidative stress indicators (ROS, MMP, LDH, MDA, GSH, and SOD) were measured, and apoptosis was evaluated by TUNEL and EdU assays. Transcriptome sequencing was performed on PE- and PP-exposed cells, followed by GO/KEGG enrichment analyses; differentially expressed genes were validated via RT-qPCR, Western blotting, and amino acid content detection. Characterisation results showed that NPs were uniformly spherical particles (∼200 nm) with high aqueous stability (zeta potential: –30 to –20 mV) and could be internalized by SH-SY5Y cells. NPs reduced cell viability in a concentration-dependent manner, with 400 μg/mL selected for subsequent experiments. NP exposure increased reactive oxygen species (ROS) levels, impaired mitochondrial function, induced apoptosis, and disrupted cell proliferation in SH-SY5Y cells. Transcriptomic and validation results revealed that NPs disrupted amino acid and one-carbon unit metabolism. Collectively, NPs induce SH-SY5Y cell damage through oxidative stress, apoptosis, and amino acid metabolism disorder. These findings provide insights into NP-induced neuronal toxicity, laying the groundwork for further studies on the health risks of NPs and the development of targeted protective strategies.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154419"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100725","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-nanoplastics in the central nervous system: Evidence, mechanisms and perspectives","authors":"Zhexun Pei ,&nbsp;Hang Zhong ,&nbsp;Xiaoqing Li ,&nbsp;Shaowei Guo ,&nbsp;Tingting Wang","doi":"10.1016/j.tox.2026.154424","DOIUrl":"10.1016/j.tox.2026.154424","url":null,"abstract":"<div><div>Environmental exposure to micro-nanoplastics (MNPs) has emerged as a significant concern for neurological health. This review synthesizes evidence that MNPs translocate the blood-brain barrier (BBB) and induce neurotoxicity through mechanisms including oxidative stress, neuroinflammation, mitochondrial dysfunction, and neurotransmitter disruption. In rodent models, these disturbances lead to pathological and behavioral deficits relevant to neurodegeneration, neurodevelopmental disorders, and psychiatric conditions. Critically, we evaluate emerging clinical studies confirming the presence of MNPs within human central nervous system tissues and fluids. Our review then provides a critical appraisal of these human studies, highlighting their methodological limitations and inconsistent application of quality assurance/quality control (QA/QC) protocols, which currently constrain robust exposure assessment and causal inference. While clinical correlations exist between MNP levels and markers of BBB integrity, cognitive function, and stroke severity, establishing causality requires standardized detection methods and rigorous QA/QC integrated with longitudinal cohort studies. Generating such reliable evidence is paramount for informing public health strategies aimed at mitigating plastic exposure.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154424"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150646","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":"Physiologically relevant 3D CRISPR screening enhances mechanistic insight into chemical toxicity compared to 2D screening","authors":"Chanhee Kim ,&nbsp;Zhaohan Zhu ,&nbsp;Abderrahmane Tagmount ,&nbsp;W. Brad Barbazuk ,&nbsp;Rhonda Bacher ,&nbsp;Christopher D. Vulpe","doi":"10.1016/j.tox.2026.154422","DOIUrl":"10.1016/j.tox.2026.154422","url":null,"abstract":"<div><div>CRISPR-based approaches can complement other genomics-based toxicology studies by enabling causal interrogation of gene function modulating chemical-induced toxicity. Moreover, CRISPR screens enable scalable and systematic identification of functional pathways involved in cellular response to chemical exposure. Cell-based functional toxicogenomics approaches using CRISPR provide a potential powerful tool for the development of mechanism-driven new approach methodologies (NAMs) for toxicodynamic and toxicokinetic hazard screening to enable more effective risk assessment. To improve the physiological relevance of <em>in vitro</em> functional toxicogenomics, we developed a three-dimensional (3D) CRISPR screening platform using HepG2/C3A spheroids cultured in a continuously rotating bioreactor (ClinoStar). We evaluated the potential utility of a 3D CRISPR screen as compared to conventional 2D screen using a custom CRISPR sgRNA library representing common loss-of-function genetic variants in the human population and exposure to the well characterized DNA damaging toxicant, doxorubicin. The 3D platform identified more genes and pathways in which variants have previously been associated with doxorubicin toxicity in clinical studies than the 2D system. These results support the utility of 3D CRISPR screening to identify physiologically relevant genetic determinants underlying chemical toxicity.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154422"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146126522","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":"Arsenite sensitizes to ferroptosis by disrupting selenium metabolism and reducing GPx4 expression","authors":"Hayato Takashima ,&nbsp;Reiko Makino ,&nbsp;Hiroki Taguchi ,&nbsp;Junya Ito ,&nbsp;Eikan Mishima ,&nbsp;Yoshika Takenaka ,&nbsp;Yasutoshi Akiyama ,&nbsp;Daigo Sumi ,&nbsp;Marcus Conrad ,&nbsp;Yoshihisa Tomikoka ,&nbsp;Takashi Toyama ,&nbsp;Yoshiro Saito","doi":"10.1016/j.tox.2026.154409","DOIUrl":"10.1016/j.tox.2026.154409","url":null,"abstract":"<div><div>Arsenic (As), an environmental toxicant commonly found in groundwater, exerts its toxic effects primarily through oxidative stress. Selenium (Se) plays a crucial role in counteracting oxidative stress by promoting the synthesis of Se-containing antioxidant enzymes, such as glutathione peroxidases (GPx). To elucidate the impact of As on cellular Se metabolism, we investigated the effects of inorganic arsenic on cultured cells (HT-1080, Jurkat, and SH-SY5Y). Our findings indicate that As(III) disrupts Se metabolism and inhibits Se-induced GPx expression. By comparing different Se sources (selenoprotein P, selenocysteine, and selenite), we determined that As(III) primarily interferes with Se metabolism downstream of selenite, an inorganic form of Se. Notably, exposure to As(III) reduced Se incorporation into RNA, suggesting inhibition of Sec-tRNA^Sec synthesis, a critical step in selenoprotein biosynthesis. Additionally, As(III) increased cellular susceptibility to ferroptosis, a form of oxidative stress-driven lipid peroxidation-mediated cell death primarily regulated by GPx4. Supporting this, genetic deletion of PRDX6, a recently identified regulator of cellular Se metabolism, further suppressed selenoprotein expression and exacerbated As(III)-induced ferroptosis. These findings provide new insights into the toxicological mechanisms of As compounds, highlighting their role in disrupting Se metabolism and potentially mitigating the side effects associated with arsenic-based anticancer therapies.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154409"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146067188","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}