Toxicology最新文献

{"title":"Deoxynivalenol and male reproductive toxicity: Unraveling the hidden risks","authors":"Ana Laura Paulino Leite Gomes ,&nbsp;Glaura Scantamburlo Alves Fernandes ,&nbsp;Ana Paula Frederico Rodrigues Loureiro Bracarense","doi":"10.1016/j.tox.2025.154191","DOIUrl":"10.1016/j.tox.2025.154191","url":null,"abstract":"<div><div>Deoxynivalenol (DON) is a highly prevalent mycotoxin known for its deleterious effects on the gastrointestinal and immune systems. Recent studies have also demonstrated its potential to impair reproductive function. This review compiles current evidence on the impact of DON on male reproductive organs, with particular emphasis on its hormonal suppressive effects, disruption of the germinal epithelium, and compromise of the blood–testis barrier. This review also highlights the impact of DON on less-explored reproductive organs, such as the epididymis, prostate, and seminal vesicles. These effects are primarily mediated by increased oxidative stress, inflammation, and apoptosis. Collectively, these alterations result in reduced sperm quality and quantity, thereby impairing male fertility. In addition, we examine studies evaluating the consequences of parental DON exposure on offspring development, which reveal adverse effects across multiple developmental stages. The findings presented consolidate the classification of DON as a relevant toxicant to male reproductive health.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154191"},"PeriodicalIF":4.8,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094935","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 disrupt hepatic lipid metabolism via the inhibition of PPARγ: a study based on digestive system exposure","authors":"Shenya Xu ,&nbsp;Mei Li ,&nbsp;Yudan Zheng ,&nbsp;Menghuan Xu ,&nbsp;Jieyu Zhou ,&nbsp;Shizhi Wang ,&nbsp;Shuwei Li ,&nbsp;Meilin Wang","doi":"10.1016/j.tox.2025.154194","DOIUrl":"10.1016/j.tox.2025.154194","url":null,"abstract":"<div><div>Nanoplastics (NPs) are emerging environmental contaminants capable of crossing biological barriers and accumulating in organs such as the liver, raising growing concerns about their potential contribution to nonalcoholic fatty liver disease (NAFLD). Notably, bottled water has been recognised as a major daily source of NP exposure. However, the associations between NP exposure and NAFLD onset, as well as the mechanistic basis, remain unclear. To investigate this, we analysed data from the National Health and Nutrition Examination Survey (NHANES) 2013–2016 cycles, using daily bottled water intake to estimate NP exposure and the hepatic steatosis index (HSI) as an indicator of liver fat accumulation. Animal and cellular experiments were conducted to evaluate NP-induced hepatic alterations. Additionally, transcriptomic analysis of liver tissues was performed, and integration with DisGeNET and the Comparative Toxicogenomics Database (CTD) enabled bioinformatic analyses and identification of key regulatory pathways. Epidemiological results revealed a significant positive correlation between bottled water consumption and HSI. Experimental findings demonstrated that NP exposure induced liver vacuolisation, oxidative damage, metabolic disruption, and inflammation in both in vivo and in vitro models. Transcriptomic and database integration revealed that NP exposure suppressed the PPAR signalling pathway, particularly by downregulating PPARγ expression, with excessive ROS generation likely contributing to this inhibition. These results were summarised in an adverse outcome pathway (AOP) framework, illustrating how NP exposure may impair PPARγ signalling and promote hepatic lipid accumulation. In conclusion, this study provides evidence that environmental NP exposure may be a contributing factor to NAFLD development and highlights the potential public health impact of the intake of NPs from bottled water.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154194"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086852","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":"Tobacco smoking exposure-mediated ELAVL1 regulates bladder cancer cell senescence via autophagy activation","authors":"Qiuyi Pu ,&nbsp;Fang Gao ,&nbsp;Yanping Xiao ,&nbsp;Jiajin Wu ,&nbsp;Chao Wang ,&nbsp;Xiaoxiao Mo ,&nbsp;Zhengdong Zhang ,&nbsp;Rui Zheng ,&nbsp;Dongmei Wu","doi":"10.1016/j.tox.2025.154193","DOIUrl":"10.1016/j.tox.2025.154193","url":null,"abstract":"<div><div>Tobacco smoking is a well-established risk factor for bladder cancer, which shows connection to cell senescence in various diseases. However, the regulatory mechanisms linking tobacco smoking exposure to senescence regulation in bladder cancer remain incompletely characterized. In this investigation, we demonstrated that the smoking carcinogen 4-aminobiphenyl (4-ABP) inhibited cell senescence while enhancing proliferative, invasive, and migratory capacities of bladder cancer cells, as evidenced by SA-β-gal staining, western blot and cell malignant phenotype experiments. We further identified 275 cell senescence-related genes specific to bladder cancer based on CellAge database, the Nanjing bladder cancer dataset and public database. Through genome-wide association studies in 580 bladder cancer cases and 1101 controls, we pinpointed that rs12978895 G&gt;A in <em>ELAVL1</em> was significantly correlated with decreased bladder cancer risk (odds ratio = 0.79, 95 % confidence interval = 0.68–0.92) and interacted with smoking (<em>P</em> = 0.043). In genetic regulation, both experimental and population study showed that the A allele of rs12978895 significantly reduced <em>ELAVL1</em> expression, while elevated <em>ELAVL1</em> levels were observed in tumor tissues. Notably, exposed to smoking carcinogen 4-ABP resulted in a markedly increased expression of <em>ELAVL1</em>, which inhibited senescence of bladder cancer cells. Mechanistically, 4-ABP upregulated <em>ELAVL1</em> suppressed cell senescence through autophagy activation, thus promoting bladder cancer progression. This study elucidated the genetic susceptibility and biological function of <em>ELAVL1</em> in tobacco smoking exposure cell models, shedding light on the etiology of bladder cancer.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154193"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085814","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":"1-nitropyrene triggers trophoblast dysfunction via EMPs-mediated ferroptosis through Glutathione peroxidase 4","authors":"Shuping Yu ,&nbsp;Kai Wang ,&nbsp;Yan Kang ,&nbsp;Yaming Mu ,&nbsp;Zhenya Fang ,&nbsp;Meihua Zhang ,&nbsp;Shuxian Li","doi":"10.1016/j.tox.2025.154190","DOIUrl":"10.1016/j.tox.2025.154190","url":null,"abstract":"<div><div>1-Nitropyrene (1-NP), a prevalent environmental pollutant, poses significant risks to vascular and placental health. This study demonstrates that 1-NP induces vascular endothelial dysfunction by dose-dependently reducing human umbilical vein endothelial cell (HUVEC) viability, inhibiting proliferation, promoting apoptosis, and impairing tube formation. Notably, endothelial microparticles (EMPs) isolated from 1-NP-treated HUVECs (N-EMPs) exhibited distinct biological effects compared to control EMPs (C-EMPs). N-EMPs suppressed trophoblast viability, proliferation, invasion, and migration, correlating with N-cadherin downregulation and E-cadherin upregulation. Mechanistically, ferroptosis emerged as the primary driver of N-EMPs-induced trophoblast dysfunction, evidenced by reactive oxygen species (ROS) accumulation, glutathione depletion, elevated malondialdehyde and Fe²⁺ levels, and mitochondrial oxidative stress. Crucially, glutathione peroxidase 4 (GPX4) was identified as a central regulator, with its expression significantly downregulated by N-EMPs. Overexpression of GPX4 reversed ferroptosis markers (restoring GSH/SOD, reducing MDA/Fe²⁺) and rescued trophoblast viability, migration, and invasiveness. These findings establish a previously unrecognized pathogenic cascade wherein 1-NP triggers endothelial injury, releasing cytotoxic EMPs that propagate ferroptosis-dependent trophoblast dysfunction via GPX4 suppression. The central role of EMPs as mediators of environmental pollutant toxicity highlights their potential as biomarkers and therapeutic targets for mitigating placental developmental disorders caused by 1-NP exposure.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154190"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086850","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":"Key role of extracellular vesicles in the induction of necroptosis and apoptosis by a mixture of polycyclic aromatic hydrocarbons in the context of a steatohepatitis-like state","authors":"Florian Barathon ,&nbsp;Paul-Henri Graindorge ,&nbsp;Maelle Bescher ,&nbsp;Isabelle Gallais ,&nbsp;Agnès Burel ,&nbsp;Isabelle Morel ,&nbsp;Henri Schroeder ,&nbsp;Nathalie Grova ,&nbsp;Dominique Lagadic-Gossmann ,&nbsp;Odile Sergent","doi":"10.1016/j.tox.2025.154184","DOIUrl":"10.1016/j.tox.2025.154184","url":null,"abstract":"<div><div>A positive association between human exposure to environmental pollutants and progression from benign hepatic steatosis to advanced chronic liver diseases has been documented. Among chemicals found in air pollution, polycyclic aromatic hydrocarbons (PAHs) are of particular concern, due to their omnipresence in the environment. Ingestion of contaminated food is the primary route of exposure. Previous studies on the ability of PAHs to induce the pathological progression of liver steatosis have been limited to the analysis of individual PAHs. The aim of this study was therefore to examine the effects of a mixture of PAHs whose composition closely recapitulates that of contaminated food. The PAH mixture elicited both a steatohepatitis-like state in steatotic WIF-B9 hepatocytes (100 nM for 72 hours) and the progression of steatohepatitis in rats fed a lipid-enriched diet (0.8 mg/kg for 90 days). The PAH mixture induced transient necroptosis at 5 hours followed by a gradual increase in cellular apoptosis. PAH metabolism-dependent necroptosis appeared to be responsible for the development of the secondary apoptosis. Hepatocyte exposure induced a necroptosis-dependent release of extracellular vesicles (EVs), that appeared to be protective against necroptosis; however, those necroptotic EVs triggered apoptosis in recipient hepatocytes. Blocking of ASGR EV receptors with asialofetuin inhibited the interaction of EVs with hepatocytes and hence apoptosis. In conclusion, EV release seems to be crucial to avoid necroptosis, but inhibition of EV uptake can protect against apoptosis.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154184"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086851","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 ''β-Estradiol antagonizes the inhibitory effects of caffeine in BMMSCs via the ERβ-mediated cAMP-dependent PKA pathway'' [Toxicology 394 (2018) 1–10]","authors":"Chaowei Wang,&nbsp;Yi Zhou,&nbsp;Xiaoxu Guan,&nbsp;Mengfei Yu,&nbsp;Huiming Wang","doi":"10.1016/j.tox.2025.154183","DOIUrl":"10.1016/j.tox.2025.154183","url":null,"abstract":"","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154183"},"PeriodicalIF":4.8,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144080490","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":"Antimony induces mitochondria-dependent and ER stress-triggered apoptosis via the oxidative stress-activated JNK signaling pathway in pancreatic islet β-cells","authors":"Ken-An Lin ,&nbsp;Chin-Chuan Su ,&nbsp;Shing-Hwa Liu ,&nbsp;Kuan-I. Lee ,&nbsp;Kai-Min Fang ,&nbsp;Chih-Hsin Tang ,&nbsp;Chun-Ying Kuo ,&nbsp;Kai-Chih Chang ,&nbsp;Jun-An Ke ,&nbsp;Chun-Fa Huang ,&nbsp;Ya-Wen Chen ,&nbsp;Ching-Yao Yang","doi":"10.1016/j.tox.2025.154188","DOIUrl":"10.1016/j.tox.2025.154188","url":null,"abstract":"<div><div>Antimony (Sb), a silvery-white metal, is a heavy metal of particular prevalence that has the ability to result in adverse effects in humans through environmental exposure resulting from natural processes and human activities. Epidemiological studies have suggested that Sb has an association with the potential for diabetes mellitus (DM) development. However, the mechanisms by which Sb exerts toxicological effects on pancreatic islet β-cells are still not clear. In this investigation, Sb exposure significantly inhibited rat pancreatic islet β-cell-derived RIN-m5F cell viability and insulin secretion, while inducing mitochondria-dependent apoptotic signals, inclusive of increased apoptotic cell populations, caspase-3 activity, the expression of PARP and caspase-3/-7/-9, and mitochondrial dysfunction. RIN-m5F cells exposure to Sb also led to the triggering of endoplasmic reticulum (ER) stress via the induction of a number of vital molecules, including CHOP, XBP-1s, and caspase-12. In Sb-exposed RIN-m5F cells, 4-PBA pretreatment (an inhibitor of ER stress) significantly suppressed protein expression related to ER stress and events of an apoptotic nature. Furthermore, exposure to Sb resulted in the significant activation of AMPKα, ERK1/2, and JNK signaling, as well as reactive oxygen species (ROS) generation. Pretreatment with SP600125 (an inhibitor of JNK) and antioxidant NAC, but not PD98059 (an inhibitor of ERK) or compound C (an inhibitor of AMPK), effectively abrogated the cytotoxicity, ER stress responses, mitochondrial dysfunction, apoptotic events, insulin secretion inhibition, and JNK activation in Sb-exposed rat pancreatic islet β-cells. However, SP600125 did not prevent ROS generation, which was inhibited by the antioxidant NAC. Collectively, the results demonstrate exposure to Sb to exert β-cell cytotoxicity through oxidative stress-activated JNK signaling downstream-regulated mitochondria-dependent and ER stress-triggered cell apoptotic pathways, eventually resulting in the death of rat pancreatic islet β-cells.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154188"},"PeriodicalIF":4.8,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143943186","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":"Insights into the molecular mechanisms underlying phthalates-induced nephrotoxicity","authors":"Mohammed Nazish Quasmi ,&nbsp;Jiten Singh ,&nbsp;Dinesh Kumar ,&nbsp;Dinesh Dhingra ,&nbsp;Ashok Jangra","doi":"10.1016/j.tox.2025.154187","DOIUrl":"10.1016/j.tox.2025.154187","url":null,"abstract":"<div><div>Phthalates are the most common environmental toxicants<!--> <!-->that are added to plastics to improve their elasticity and extensibility. Different products such as baby toys, personal<!--> <!-->care products, packaging materials and pharmaceutical products contain various phthalates like Di-(2-ethylhexyl) phthalate (DEHP), Dibutyl phthalate (DBP), etc. During processing, transportation and preparation, these phthalates can leach out into food and<!--> <!-->drinks. Despite their commercial advantages, phthalates have shown multi-organ toxicity, including nephrotoxicity. Phthalates exposure can lead to morphological as well as functional alterations in renal tissues. Intoxication to these phthalates can increase the risk of nephrotoxicity through various signaling pathways, including ferroptosis, oxidative stress, inflammatory, mitochondrial and DNA damage-associated pathways. This review aims to outline recent <em>in-vivo</em> and epidemiological studies to deepen the knowledge on underlying molecular mechanisms of nephrotoxicity caused by different phthalates. Moreover, various pharmacological interventions have also been discussed in this review, which serve as the scientific basis for the prevention and treatment of the Phthalates-induced kidney damage.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154187"},"PeriodicalIF":4.8,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144080492","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":"Enantiospecific hepatotoxicity of usnic acid in vitro, and the attempt to modify the toxic effect","authors":"Agnieszka Galanty ,&nbsp;Paweł Paśko ,&nbsp;Paulina Koczurkiewicz-Adamczyk ,&nbsp;Gabriela Siedlarczyk ,&nbsp;Elżbieta Pękala ,&nbsp;Irma Podolak","doi":"10.1016/j.tox.2025.154189","DOIUrl":"10.1016/j.tox.2025.154189","url":null,"abstract":"<div><div>Usnic acid, a chiral secondary lichen metabolite, is known for its diverse biological activities, yet concerns about its hepatotoxicity limit its therapeutic potential. Notably, the enantiospecific effects of its two forms, (+)- and (−)-usnic acid, remain underexplored. This study aimed to compare the hepatotoxic potential of the enantiomers of usnic acid in wide range of concentration to HepG2 cells, by evaluating their impact on cell viability, membrane integrity, and mitochondrial function. Additionally, we investigated whether hepatotoxicity could be mitigated by co-treatment with known hepatoprotectants: silybin, squalene, and N-acetylcysteine. Our results demonstrated for the first time that (−)-usnic acid exhibited significantly greater hepatotoxicity than its (+)-enantiomer, particularly after 24–48 h of exposure (IC₅₀: 16.0 vs. 28.2 µg/mL at 48 h). This enantiospecific toxicity was confirmed by LDH leakage and mitochondrial membrane depolarization, with more pronounced effect induced by (−)-usnic acid. Co-treatment with hepatoprotectants partially alleviated toxicity at 48 h, with squalene and N-acetylcysteine showing better protective effects than silybin. However, the protective effects diminished after 72 h. These findings underscore the importance of enantiospecific analysis in natural compound safety assessments and suggest that the hepatotoxicity of usnic acid is influenced by more than just mitochondrial uncoupling. Further in vivo studies and mechanistic analyses are necessary to evaluate the clinical potential of usnic acid and to identify strategies for safe therapeutic use.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154189"},"PeriodicalIF":4.8,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143943187","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":"Differential susceptibility of Leydig and Sertoli cells to bisphenol A","authors":"Do-Yeal Ryu ,&nbsp;Won-Ki Pang ,&nbsp;Md Saidur Rahman ,&nbsp;Yoo-Jin Park ,&nbsp;Myung-Geol Pang","doi":"10.1016/j.tox.2025.154182","DOIUrl":"10.1016/j.tox.2025.154182","url":null,"abstract":"<div><div>Bisphenol A (BPA) is an endocrine-disrupting chemical that is increasingly becoming a vital factor in public health due to its ubiquity and toxicity. BPA is associated with male infertility via the disrupted function of Leydig and Sertoli cells. Despite extensive research, the current understanding of the specific pathological concentrations and the mechanisms following BPA exposure still remain questionable. Therefore, we investigated the susceptibilities and underlying mechanisms in Leydig and Sertoli cells following treatment with various BPA doses (0.0001–100 µM in a 10-fold serial dilution). Our results showed that the lowest BPA levels (10⁻⁴ μM) decreased mitochondrial membrane potential and ATP levels. In contrast, ROS levels were increased at high BPA levels regardless of exposure time (24 or 48 h) in both cell types. Mitochondrial-mediated apoptosis was identified along with increased ROS levels and abnormal mitochondrial dynamics, but both cell types showed different susceptibility to BPA toxicity. Subsequently, BPA had detrimental impacts on the mRNA expression levels of steroidogenic enzymes and testosterone synthesis in Leydig cells and reduced anchoring junction proteins in Sertoli cells. Consequently, our results demonstrated that both cells were affected via estrogen receptor alpha. However, protein kinase A was oppositely expressed following BPA exposure in each cell type. Therefore, it is plausible to suggest that each cell has distinct sensitivities and mechanisms in response to BPA.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"516 ","pages":"Article 154182"},"PeriodicalIF":4.8,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143937282","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}