Toxicology最新文献

{"title":"Synergistic effects of lead and copper co-exposure on promoting oxidative stress and apoptosis in the neuronal cells","authors":"Di Wu ,&nbsp;Desheng Wang ,&nbsp;Shuang-Shuang Tan ,&nbsp;Yu-Qi Li ,&nbsp;Su-Li Hong ,&nbsp;Tao Wang ,&nbsp;Gang Zheng","doi":"10.1016/j.tox.2025.154103","DOIUrl":"10.1016/j.tox.2025.154103","url":null,"abstract":"<div><div>Exposure to lead (Pb) or copper (Cu) is common and has been associated with increased risk of neurodegenerative disease. However, combined neurotoxic effects of co-exposure to these elements remain unclear. This study aimed to determine the toxic effects of Pb and Cu co-exposure on HT22 cells. In this study, Pb and Cu co-exposure exhibited enhanced toxicity, including increased reactive oxygen species (ROS) and Malondialdehyde (MDA) levels, Superoxide Dismutase 1 (SOD1) activity, lower cell viability and higher apoptotic rates, compared to single-element exposure. Pb and Cu co-exposure also resulted in significantly increased cellular labile Cu level by altering the protein levels of Cu transporters, including Copper Transporter-1 (CTR1), ATPase Copper Transporting-α(ATP7A) and ATPase Copper Transporting-β (ATP7B). Treating with antioxidants or Cu chelator to the co-exposed cells blocked the reduction cell viability and elevation of apoptotic rates. This study suggests that Pb and Cu co-exposure can result in a synergistic toxicity in neuronal cells by inducing oxidative stress and apoptosis. The cellular Cu accumulation may play an important role in inducing these synergistic effects, and both antioxidation and Cu chelation may be promising control measures to alleviate the neurotoxicity of Pb and Cu co-exposure.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154103"},"PeriodicalIF":4.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143511163","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":"Copper oxide nanoparticles disrupt lysosomal function and promote foam cell formation in RAW264.7 macrophages","authors":"Yilin Luo ,&nbsp;Kun Zhang ,&nbsp;Lejiao Mao ,&nbsp;Meiling Tan ,&nbsp;Xiaomei Dong ,&nbsp;Na Li ,&nbsp;Yuexing Zhou ,&nbsp;Chengzhi Chen ,&nbsp;Zhen Zou ,&nbsp;Jun Zhang","doi":"10.1016/j.tox.2025.154101","DOIUrl":"10.1016/j.tox.2025.154101","url":null,"abstract":"<div><div>Macrophage-derived foam cells are crucial in the development of atherosclerosis, a multifaceted and progressive disorder characterized by lipid and fibrous accumulation in major arteries. Copper oxide nanoparticles (CuONPs) have found widespread applications but their potential role in atherosclerosis remains understudied. In this study, we investigated the impact of CuONPs on foam cell formation in RAW264.7 macrophages. Our results showed that CuONPs, at concentrations as low as 10 μg/ml, significantly exacerbated foam cell formation induced by oxidized low-density lipoprotein (ox-LDL). Exposure to CuONPs stimulated LDL release and elevated the expression of NLRP3 inflammasome components, including NLRP3, Caspase-1, and IL-1β. Transmission electron microscopy (TEM) revealed accumulation of CuONPs within macrophage lysosomes, leading to disrupted lysosomal function. CuONPs-treated cells exhibited autophagosome accumulation due to impaired lysosomal degradation, as confirmed by Western blot analysis showing abnormal expression of LAMP-1 and LAMP-2 proteins. Flow cytometry analysis further demonstrated decreased lysosomal acidity in CuONPs-exposed cells. Our findings reveal a novel mechanism whereby CuONPs activate the inflammasome, disrupt lysosomal function, and hinder cholesterol efflux, thereby exacerbating the formation of macrophage-derived foam cells. These results highlight the potential risks of CuONPs exposure and provide important insights into the role of environmental particulate matter in the development of atherosclerosis.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154101"},"PeriodicalIF":4.8,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477038","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":"6PPD induces apoptosis and autophagy in SH-SY5Y cells via ROS-mediated PI3K/AKT/mTOR pathway: In vitro and in silico approaches","authors":"Ziwei Wang,&nbsp;Shutao Wang,&nbsp;Yingying Liu,&nbsp;Xingyu Wang,&nbsp;Wanlun Li,&nbsp;Hong Qi,&nbsp;Hou You","doi":"10.1016/j.tox.2025.154091","DOIUrl":"10.1016/j.tox.2025.154091","url":null,"abstract":"<div><div>N-(1,3-dimethylbutyl)-N’-phenyl-p-phenylenediamine (6PPD), an extensively employed antioxidant in rubber materials, is considered as an emerging contaminant. 6PPD was proven to have potential neurotoxicity, which poses risks to human health. However, the research on its neurotoxicity is still limited. This work explored the neurotoxicity of 6PPD to SH-SY5Y cells and in-depth mechanisms with a combination of <em>in vitro</em> and <em>in silico</em> approaches. Our results indicated that 6PPD could reduce cell viability and cause oxidative damage by increasing reactive oxygen species (ROS) accumulation and altering the levels of glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA). 6PPD induced neuronal apoptosis of mitochondrial pathway and autophagy dysfunction, as characterized by the increased expressions of Cleaved caspase-3, Bax/Bcl-2, Beclin-1, LC3-II/I, and P62. 6PPD downregulated the expression of PI3K, p-AKT, and p-mTOR, while the PI3K inhibitor suppressed PI3K/AKT/mTOR pathway and promoted both apoptosis and autophagy, indicating that PI3K/AKT/mTOR pathway was involved in 6PPD-induced apoptosis and autophagy. The inhibition of this pathway was attributed to ROS accumulation in SH-SY5Y cells. Molecular docking analysis further revealed that 6PPD exhibits strong binding affinity to PI3K, AKT, and mTOR protein molecules, which could effectively interfere with downstream signaling pathways. These findings enrich the understanding of 6PPD-induced neurotoxicity and contribute to the evaluation of ecological risks associated with 6PPD.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154091"},"PeriodicalIF":4.8,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143473076","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":"NNMT is involved in deoxynivalenol-induced hepatocyte toxicity via promoting ferroptosis","authors":"Weiling Huang ,&nbsp;Chenchen Song ,&nbsp;Yu Hua ,&nbsp;Aimei Liu","doi":"10.1016/j.tox.2025.154084","DOIUrl":"10.1016/j.tox.2025.154084","url":null,"abstract":"<div><div>Deoxynivalenol (DON) is a common contamination mycotoxin that which exerts significant hepatotoxicity, posing a serious threat to human and animal health. Ferroptosis has been linked to the development of hepatotoxicity induced by DON. However, the mechanism by which DON promotes ferroptosis in hepatocytes is not well understood. Although studies have shown that DON upregulates the expression of nicotinamide N-Methyltransferase (NNMT), its role in DON hepatotoxicity has not been elucidated. In this study, we found that DON inhibited SLC7A11/GPX4 and increased cytosolic free Fe^2 + and lipid ROS, thereby inducing ferroptosis of HepG2 cells. Overexpression of NNMT markedly downregulated the expression of SLC7A11, GPX4, GCLC, and NQO1, exacerbated the DON-induced increase in free Fe²⁺ and lipid ROS, thus promoting ferroptosis. Silencing or inhibition of NNMT produced opposite effects and abolished the DON-induced ferroptosis. Further application of SLC7A11 and GPX4 inhibitor treatments confirmed that following DON exposure, NNMT triggered ferroptosis by inhibiting SLC7A11 and GPX4, to reduce cell viability and inhibit cell growth. Taken together, this study found that DON-induced NNMT may enhance ferroptosis by inhibiting the SLC7A11/GPX4 proteins in HepG2 cells. These findings provide valuable insights for controlling DON hepatotoxicity and hepatocellular carcinoma.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154084"},"PeriodicalIF":4.8,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143473081","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":"High content imaging of relative ATP levels for mitochondrial toxicity prediction in human induced pluripotent stem cell derived cardiomyocytes","authors":"John Bassett,&nbsp;Bharathi Balasubramanian,&nbsp;Holly Clouse,&nbsp;Elena Trepakova","doi":"10.1016/j.tox.2025.154088","DOIUrl":"10.1016/j.tox.2025.154088","url":null,"abstract":"<div><div>Human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) are increasingly being evaluated in assays aimed at better understanding potential cardiotoxic liability of newly developed therapeutic compounds. Disruption of mitochondria has been implicated in the mechanism of drug-induced cardiotoxicity of some compounds. Therefore, we have developed a high content imaging assay for the investigation of mitochondrial toxicity in hiPSC-CMs using ATP-Red, a fluorescent dye capable of detecting subcellular localization of relative ATP levels in living cells. We demonstrated time-dependent decreases in ATP-Red signal over 6 h treatment with known mitochondrial toxicants antimycin (0.03, 0.1 µM) or oligomycin (3, 10 µM). Concentration-dependent decreases in ATP-Red signal with antimycin (0.001–0.3 µM) and oligomycin (0.003–1 µM) were rescued by restoring glycolysis through glucose supplementation. Decreased ATP levels were also identified in a selection of clinically available drugs with reported association with mitochondrial toxicity but absent in compounds with no known association with mitochondrial dysfunction. ATP measurements using the ATP-Red imaging assay were consistent with orthogonal measurements of whole cell ATP levels in lysed hiPSC-CMs following compound treatment. Similar findings were also obtained with measurement of mitochondrial membrane potential, except amiodarone which had no change despite decreased ATP levels. The developed high throughput imaging assay, assessing subcellular ATP dynamics, could provide mechanistic insights for tested compounds.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"514 ","pages":"Article 154088"},"PeriodicalIF":4.8,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459395","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":"EFSA prohibits titanium dioxide in food- should pharmaceuticals be next?","authors":"Chandni Dand,&nbsp;Aanchal Bajaj,&nbsp;Sarika Wairkar","doi":"10.1016/j.tox.2025.154089","DOIUrl":"10.1016/j.tox.2025.154089","url":null,"abstract":"<div><div>Titanium dioxide (TiO₂) is a natural, inorganic compound widely used across various industries due to its multiple properties. Recently, the European Food Safety Authority (EFSA) raised safety concerns regarding the use of TiO₂ in foods, specifically its potential for genotoxicity, accumulation in the body, and associated health risks when used as a food additive. As a result, its use in food has been banned in the food industry in the European Union (EU) since 2022. Furthermore, the safety of TiO₂ is currently being evaluated as a pharmaceutical excipient, and its use is likely to be banned in EU by 2025. The food industry is significantly impacted by the ban, and a subsequent pharmaceutical ban can lead to issues such as the lack of a single replacement for its multiple applications, product redevelopment/revalidation and regulatory submissions. Other regulatory authorities from other countries conducted independent reviews and concluded that there is insufficient evidence to justify a ban on TiO₂ in foods, thereby allowing its continued use. Various substitutes, both natural and synthetic, are being explored, however none can fully replicate all the properties provided by TiO₂ alone. In this review, we discuss the safety concerns associated with TiO₂, which have led to its ban on food products, as well as the challenges that may arise if a similar ban is imposed on its use in pharmaceuticals.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154089"},"PeriodicalIF":4.8,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459387","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":"Polystyrene microplastics trigger colonic inflammation in rats via the TLR4/NF-κB/COX-2 pathway and modulation of intestinal microbiota","authors":"Xuemin Feng ,&nbsp;Meng Zhang ,&nbsp;Tianyang Zhao ,&nbsp;Jianwei Cui ,&nbsp;Hui Ye ,&nbsp;Chunkui Zhou ,&nbsp;Lin Ye ,&nbsp;Liting Zhou","doi":"10.1016/j.tox.2025.154090","DOIUrl":"10.1016/j.tox.2025.154090","url":null,"abstract":"<div><div>Polystyrene microplastics (PS-MPs) are common microplastics that pose significant health hazards to humans. Due to multifunctionality in the gut system, MP-associated damage and mechanisms require further exploration. This study was undertaken with the objective of elucidating the impact of PS-MP exposure on colonic inflammation in rats, and to explore its potential mechanisms. Forty-eight specific-pathogen-free Wistar male rats were administered 0, 0.5, 5, and 50 mg/kg/d of PS-MPs for 90 days, after which intestinal flora distribution, inflammatory factor levels in the colon, and <em>TLR4/NF-κB/COX-2</em> gene levels were examined. To clarify whether PS-MPs directly infiltrate intestinal epithelial cells and induce cytotoxicity, human intestinal epithelial cells (HIECs) were exposed to a range of PS-MP concentrations (0 ∼ 100 μg/mL) for 48 h, and CCK-8 assays were conducted to assess the cell survival rates. In the colon tissue of rats exposed to PS-MP, goblet cells decreased, muscular layer arrangements were disordered, and disrupted and discontinuous crypt structures appeared in colon tissue, while high numbers of inflammatory cells infiltrated the colonic mucosa and submucosa. PS-MPs could accumulate in HIECs, and cell survival rates were decreased. In the colons of rats exposed to PS-MPs, the levels of Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were found to be elevated. Additionally, the mRNA and protein levels of TLR4/MyD88 in the colons of PS-MP-exposed rats exhibited a significant increase. Furthermore, the TLR4/NF-κB/COX-2 signaling pathway in rat colons was activated after MP exposure. When the TLR4/NF-κB/COX-2 signaling pathway was inhibited, the significant increases in IL-6 and TNF-α levels caused by PS-MPs were significantly reversed. PS-MP exposure also altered intestinal flora abundance in rats. Compared with the control group, the proportion of Firmicutes, Proteobacteria and Actinobacteria in PS-MPs exposed group was increased. In contrast, the proportion of Bacteroidetes and Verrucomicrobia decreased. Taken together, our results suggest that PS-MP could exert adverse effects on the gastrointestinal health of rats. Pro-inflammatory cytokine (IL-6, IL-1β and TNF-α) levels increased, and the TLR4/NF-κB/COX-2 signaling pathway was triggered. Thus, flora changes and increased intestinal inflammation may interact with each other.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154090"},"PeriodicalIF":4.8,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143437727","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":"Emerging concerns associated with e-waste exposure","authors":"Chukwuebuka ThankGod Eze,&nbsp;David O. Carpenter","doi":"10.1016/j.tox.2025.154087","DOIUrl":"10.1016/j.tox.2025.154087","url":null,"abstract":"","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154087"},"PeriodicalIF":4.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442064","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":"Gender difference and BMDL exploration of developmental immunotoxicity induced by early-life low-dose exposure to 4-nonylphenol in Wistar rats","authors":"Jiuming Yan ,&nbsp;Xiaoya Wang ,&nbsp;Jinghua Xie ,&nbsp;Liang Wang ,&nbsp;Qijie Wei ,&nbsp;Zhenchao Jia ,&nbsp;Jinyao Chen","doi":"10.1016/j.tox.2025.154085","DOIUrl":"10.1016/j.tox.2025.154085","url":null,"abstract":"<div><h3>Background</h3><div>Nonylphenol (NP) is a widespread environmental endocrine disruptor with potential developmental immunotoxicity. The present study aimed to investigate the gender-specific developmental immunotoxic effects of early-life exposure to low doses of 4-nonylphenol (4-NP) on Wistar rats and the corresponding thresholds.</div></div><div><h3>Methods</h3><div>Pregnant rats (F0 generation) were exposed to low doses of 4-NP from gestational day 6 (GD6) to postnatal day 90 (PND90), and F1 offspring continued to be exposed until the maturation of the immune system on PND42. We assessed immune organ development, immune responses, lymphocyte subset composition, cytokine secretion, and the Th17/Treg cell balance as endpoints for developmental immunotoxicity. Benchmark Dose analysis was conducted to explore the thresholds.</div></div><div><h3>Results</h3><div>Early-life exposure to 4-NP led to significant gender-specific differences in the immune response. Female pups exhibited greater sensitivity to 4-NP, with reduced thymus and spleen weights, suppressed humoral immune function, decreased natural killer (NK) cell activity, and an imbalance in the Th17/Treg cell ratio. Male pups showed inhibition of NK cell activity but no significant changes in humoral immune function. Levels of phosphorylated STAT3, STAT5, and JAK3 proteins increased in the spleens of exposed pups of both gender. The lowest benchmark dose lower limit (BMDL) value of developmental immunotoxicity was lower in female rats (based on the thymus weight) than in male rats (based on the NK cell activity).</div></div><div><h3>Conclusion</h3><div>Early-life exposure to 4-NP has been shown to induce gender-specific developmental immunotoxicity in rats, with female pups exhibiting greater sensitivity. And developmental immunotoxicity may serve as a more sensitive indicator for the risk assessment of 4-NP. Th17/Treg balance may be interrupted through JNK/STAT pathway by 4-NP exposure, which needs to be further investigated.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154085"},"PeriodicalIF":4.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419983","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":"A network toxicology and molecular docking-based approach revealed shared hepatotoxic mechanisms and targets between the herbicide 2,4-D and its metabolite 2,4-DCP","authors":"Rafael Xavier Martins ,&nbsp;Cleyton Gomes ,&nbsp;Matheus Carvalho ,&nbsp;Juliana Alves da Costa Ribeiro Souza ,&nbsp;Terezinha Souza ,&nbsp;Davi Farias","doi":"10.1016/j.tox.2025.154086","DOIUrl":"10.1016/j.tox.2025.154086","url":null,"abstract":"<div><div>The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) and its major environmental metabolite 2,4-dichlorophenol (2,4-DCP) are pollutants associated with hepatotoxicity, whose molecular mechanisms remain poorly understood. This study investigated the molecular pathways and targets involved in 2,4-D and 2,4-DCP-induced hepatotoxicity using protein-protein interaction (PPI) network analyses and molecular docking. Target genes were identified using PharmMapper and SwissTargetPrediction, and cross-referenced with hepatotoxicity-related genes from GeneCards and OMIM databases. The PPI network, constructed via STRING and visualized in Cytoscape, revealed 12 critical hub nodes, including HSP90AA1, RXRA, EGFR, SRC, CREBBP, PIK3R1, ESR1, AKT1, RAF1, IGF1R, MDM2, and MAPK14. Gene Ontology (GO) analysis indicated processes such as apoptosis, oxidative stress, mitochondrial dysfunction, and lipid metabolism impairment, while Reactome pathway analysis highlighted disruptions in PI3K/AKT and nuclear receptors signaling. Molecular docking confirmed significant interactions of 2,4-D and 2,4-DCP with key proteins, including SRC, AKT, RXRA, MDM2, and HSP90AA1. These results suggest that 2,4-D and 2,4-DCP share similar toxic mechanisms, providing new insights into their hepatotoxicity pathways for the first time.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"513 ","pages":"Article 154086"},"PeriodicalIF":4.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426255","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}