Toxicology最新文献

{"title":"Toxicological effects of PM2.5-derived and PM2.5-relevant mixture of chlorinated paraffins on A549/THP-1 co-culture cells","authors":"Jing-Wen Huang ,&nbsp;Chu Chu ,&nbsp;Mo Yang ,&nbsp;Henri Hakkarainen ,&nbsp;Anna-Katharina Hensel ,&nbsp;Nan-Xiang Jin ,&nbsp;Marjut Roponen ,&nbsp;Ari Leskinen ,&nbsp;Mika Komppula ,&nbsp;Dong Liang ,&nbsp;Guang-Hui Dong ,&nbsp;Pasi Jalava","doi":"10.1016/j.tox.2026.154425","DOIUrl":"10.1016/j.tox.2026.154425","url":null,"abstract":"<div><div>Chlorinated paraffins (CPs) are complex mixture of chlorinated straight-chain hydrocarbons, including short-, medium-, and long-chain CPs (SCCPs, MCCPs, and LCCPs), to which humans are exposed environmentally. Although PM_2.5-bound CPs were positively associated with asthma and related symptoms, the toxicological effects of CPs on the respiratory system remain limitedly understood. CPs were extracted from PM_2.5 samples collected in three cities in southern China, representing distinct SCCPs, MCCPs, and LCCPs profiles. The A549/THP-1 co-culture cells, an <em>in vitro</em> respiratory model, were exposed to PM_2.5-derived extracts containing CPs (CP extract). The gradient was established according to the extract dosage calibrated based on its quantified SCCP content with environmentally relevant concentrations. Cell viability, oxidative stress, inflammatory factors, cell cycle distribution, and genotoxicity were assessed. CP extracts reduced cell viability, increased pro-inflammatory factors concentrations, induced cell cycle arrest and DNA damage. Furthermore, CP mixtures were prepared using standards to simulate PM_2.5-relevant compositions. But the results showed weak toxicological effects of CP mixtures, suggesting CPs play a relatively weak role or CPs exhibit toxicological effects through alternative pathways. Interesting, varying compositional ratios of SCCPs, MCCPs, and LCCPs may induce different cytotoxic effects. These findings provide <em>in vitro</em> evidence for explaining adverse effects of PM_2.5-bound CPs on A549/THP-1 cells. More research is needed to clarify the respiratory toxicological effects of CPs.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154425"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137251","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 comparative toxicological evaluation of nicotine and its analog 6-methyl nicotine in E-cigarette aerosol utilizing a 3D in vitro human respiratory model","authors":"Felix Effah ,&nbsp;Mohana Sengupta ,&nbsp;Yehao Sun ,&nbsp;Md Imam Faizan ,&nbsp;Gagandeep Kaur ,&nbsp;Rhea Raghu ,&nbsp;Atallah Elzein ,&nbsp;Tim Marczylo ,&nbsp;Robert M. Strongin ,&nbsp;Irfan Rahman","doi":"10.1016/j.tox.2026.154421","DOIUrl":"10.1016/j.tox.2026.154421","url":null,"abstract":"<div><div>Under the U.S. Tobacco Regulatory Act of 2020, all novel nicotine-containing products require a Premarket Tobacco Product Application (PMTA) and FDA authorization before they can be marketed. However, lengthy PMTA review timelines have prompted some manufacturers to replace traditional nicotine with 6-methyl-nicotine (6-MN), a non-tobacco-derived analog that delivers comparable psychoactive effects while evading existing regulatory pathways. Despite its growing market presence as a purportedly “safer” alternative, the toxico-pharmacokinetic profile of 6-MN remains poorly characterized. This study assessed the toxicity after exposure to nicotine or 6-MN-containing e-liquid aerosols using a 3D EpiAirway tissue model. RT-qPCR analyses revealed differential effects on transcripts associated with DNA damage (<em>53BP1, ATR</em>), inflammation (<em>NF-κB1</em>), and cancer (<em>MYCBP</em>). Morphological evaluation of the airway tissues exposed to either aerosol showed an increase in epithelial thickness, a decrease in E-cadherin protein levels, increased goblet cell hypertrophy, evidenced by positive PAS staining and elevated mucus (MUC5AC protein) production, and a reduction in Occludin protein (part of the tight junction complex), which is suggestive of epithelial remodeling. Exposure to PG/VG aerosols alone significantly increased the release of MIP-1α, IFN-γ, and IL-4. Conversely, spearmint-flavored aerosols containing 6-MN or nicotine decreased several pro-inflammatory cytokines, significantly reducing TNF-α, Eotaxin, MCP-1, RANTES, and G-CSF levels, potentially via NF-κB and ERK1/2 pathways. Our findings reveal differential toxicological and chemical profiles for nicotine and 6-MN aerosols; however, flavorings may confer similar cytotoxicity, as measured by LDH and metabolic activity, in 6-MN formulations as they do in those with nicotine. Thus, 6-MN is not a “safer” nicotine alternative.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"522 ","pages":"Article 154421"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146107388","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 “Titanium nanoparticles provoke ferritinophagy-mediated ferroptosis via inhibition of the Nrf2-HO-1 signaling pathway in osteocytes’’ [Toxicology 519 (January) (2026) 154324, doi:10.1016/j.tox.2025.154324]","authors":"Ruirong Zhu,&nbsp;Yun Zhang,&nbsp;Yuting Wang,&nbsp;Xinyi Bao,&nbsp;Lubing Zhang,&nbsp;Jian Fang,&nbsp;Hongjiao Mao","doi":"10.1016/j.tox.2026.154399","DOIUrl":"10.1016/j.tox.2026.154399","url":null,"abstract":"","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"521 ","pages":"Article 154399"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145967280","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":"In vitro hepatic metabolism and associated binding of enniatin B","authors":"Ludovic Le Hegarat ,&nbsp;Estelle Dubreil ,&nbsp;Nicolas Le Yondre ,&nbsp;Solenne Martin ,&nbsp;Francoise Bree ,&nbsp;Jérôme Henri","doi":"10.1016/j.tox.2025.154379","DOIUrl":"10.1016/j.tox.2025.154379","url":null,"abstract":"<div><div>Enniatin B (ENNB), a secondary metabolite produced by various Fusarium species, frequently contaminates cereals, which constitutes the main dietary source of human exposure. Critical toxicodynamic and toxicokinetic data gaps currently impede a robust and accurate risk assessment. The primary objective of this study was to characterize the <em>in vitro</em> toxicokinetic profile of ENNB. We investigated its clearance using human and mouse liver microsomes (HLM and MLM), as well as 2D and 3D HepaRG cell models. To facilitate reliable in vitro-in vivo extrapolation (IVIVE), we also determined key parameters: plasma protein binding, binding to microsomes and HepaRG cells, CYP450 inhibition, and the identification of HepaRG metabolites. Binding studies revealed a very high binding of ENNB to human plasma proteins and a high binding to inactivated human liver microsomes and HepaRG cells. The predicted <em>in vivo</em> hepatic clearance (cl_H,blood) of ENNB, calculated using the <em>in vitro</em> results from MLM, HLM, and HepaRG 2D indicated a low hepatic first pass effect. Interestingly, no observable disappearance of ENNB was found in the HepaRG 3D model. Our findings on ENNB-mediated CYP inhibition in HLM, in combination with literature results, suggest a potential for CYP3A4/5-related auto-inhibition. Finally, we successfully performed a putative identification of 13 Phase I metabolites using the human HepaRG cell line. In conclusion, the low hepatic first pass effect could imply a high oral bioavailability <em>in vivo</em> if intestinal barrier passage is significant, as predicted elsewhere. However, this could be counteracted by transport limited hepatic clearance that should be further investigated and a pre-systemic first-pass effect already demonstrated <em>in vitro.</em></div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"521 ","pages":"Article 154379"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145935170","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":"Neurotoxic potential of synthetic cannabinoids’ pyrolysis products","authors":"Filipa Pita ,&nbsp;Ricardo Jorge Dinis-Oliveira ,&nbsp;João Pedro Silva ,&nbsp;Paula Guedes de Pinho ,&nbsp;Félix Carvalho","doi":"10.1016/j.tox.2025.154374","DOIUrl":"10.1016/j.tox.2025.154374","url":null,"abstract":"<div><div>Synthetic cannabinoids (SCs) represent a prominent class of new psychoactive substances (NPS), primarily consumed via inhalation methods such as smoking or vaping. Although the direct neurotoxic effects of SCs are well established, the pyrolysis process that occurs during smoking induces structural alterations that generate novel, frequently unidentified toxicants with potentially severe neurobiological consequences. This review addresses the neurotoxicity associated with parent SC compounds and their pyrolysis products, with particular emphasis on mechanisms, including oxidative stress, mitochondrial dysfunction, excitotoxicity, and neuroinflammation. A PRISMA-guided systematic review identified only nine studies specifically investigating the neurotoxic effects of SC pyrolysis products, revealing a significant gap in the literature and underscoring the urgent need for targeted research in this domain. The review further highlights that additional constituents, such as plant materials incorporated into SC formulations, can contribute to the generation of harmful byproducts and complicate forensic interpretation. The structural heterogeneity of SCs, in conjunction with variables such as polydrug use and chronic exposure, further exacerbates their toxicological profile. Future research should prioritise the identification and characterisation of pyrolysis-derived toxicants, the advancement of analytical methodologies for their detection, and the implementation of evidence-based public health strategies aimed at risk mitigation.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"521 ","pages":"Article 154374"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145799682","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":"Evaluating the absence of allometric scaling for hepatic microsomal Phase I and Phase II xenobiotic biotransformation among mammals","authors":"Luke Ockhuijsen,&nbsp;Ad M.J. Ragas,&nbsp;A. Jan Hendriks","doi":"10.1016/j.tox.2025.154377","DOIUrl":"10.1016/j.tox.2025.154377","url":null,"abstract":"<div><div>Elucidating consistent patterns for xenobiotic biotransformation among mammals is challenging because of intrinsic species differences. At the organism level, pharmacokinetic rate constants are believed to scale allometrically to body weight with a power of ¾, akin to metabolic rate constants, but the mechanism for biotransformation scaling is unclear. Predicting xenobiotic biotransformation through a quantitative <em>in vitro</em> to <em>in vivo</em> extrapolation (QIVIVE) approach combining allometric scaling relationships related to liver physiology and <em>in vitro</em> xenobiotic biotransformation could be promising. This study explores the previously unexplored potential of allometric scaling for hepatic microsomal Michaelis-Menten parameters. Hepatic microsomal Michaelis-Menten parameters, viz., affinity (K_m), maximum velocity (V_max), and <em>in vitro</em> clearance (CL_int), were examined for the xenobiotic biotransformation enzymes Cytochrome P450 (CYP) and UDP-glucuronosyl transferase (UGT). To ensure validity, data for ≥ 4 mammals per substrate biotransformation pathway were collected through a literature search and available databases. Ordinary linear regressions per pathway for each parameter showed that only a few individual regressions scaled statistically significantly to body weight. Averaging all scaling exponents of significant regressions revealed that hepatic microsomal Michaelis-Menten parameters are independent of body weight. Although not statistically significant, the average scaling exponent for each Michaelis-Menten parameter was close to 0. Therefore, differences in enzyme abundance or liver physiology between species are likely contributors to the observed ¾ exponent for allometric scaling relationships of <em>in vivo</em> xenobiotic clearance. Characterisation of underlying mechanisms at an enzyme-substrate level might ultimately improve understanding and estimation of xenobiotic clearance for mammals in QIVIVE approaches.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"521 ","pages":"Article 154377"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bisphenol TMC exhibits greater estrogenic activity than Bisphenol A and three other structural analogues exemplified by higher estrogen receptor α-mediated gene expression and breast cancer cell proliferation","authors":"Friedrich L. Joos ,&nbsp;Rianne E. van Diest ,&nbsp;Martin Smieško ,&nbsp;Marie-Christin Jäger ,&nbsp;Manuel Kley ,&nbsp;Alex Odermatt ,&nbsp;Jamal Bouitbir","doi":"10.1016/j.tox.2025.154393","DOIUrl":"10.1016/j.tox.2025.154393","url":null,"abstract":"<div><div>Bisphenol A (BPA) and its structural analogues are widely used in plastics production, raising concern due to endocrine-disrupting properties. While many analogues share structural similarities with BPA, their endocrine-disrupting effects remain insufficiently characterized. Cyclo-di-bisphenol A diglycidyl ether (cyclo-di-BADGE), tetrabromobisphenol S (TBBPS), bisphenol SIP (BPSIP), and bisphenol TMC (BPTMC) are particularly understudied. We assessed the estrogenic activity of these four BPA analogues compared to BPA. Transactivation assays in HEK-293 cells expressing estrogen receptor alpha (ERα) revealed that BPTMC was a more potent ERα agonist than BPA, with an EC₅₀ of 87 ± 20 nM <em>versus</em> 400 ± 100 nM for BPA, while the other tested analogues showed no significant agonistic activity. <em>In silico</em> analysis attributed this higher affinity to greater hydrophobicity and a bulkier bridging group between its phenolic rings. None of the compounds inhibited 17β-hydroxysteroid dehydrogenase type 1 (17β-HSD1) activity. However, BPTMC selectively inhibited 17β-HSD2 (IC₅₀ = 4.8 ± 0.6 µM) but not BPA. Importantly, 24 h exposure of ERα-positive MCF-7 breast cancer cells to 1 µM BPTMC upregulated the expression of the ERα target genes <em>GREB1</em>, <em>TFF1</em>, and <em>PGR</em>, comparable to 10 nM E2, which was abolished by 100 nM of the ERα antagonist fulvestrant. Moreover, BPTMC stimulated MCF-7 cell proliferation at nanomolar concentrations over 72 h, and cell count analyses confirmed this effect. BPA also increased cell numbers, and both effects were reversed by fulvestrant. Collectively, we identified BPTMC as a potent ERα agonist capable of eliciting transcriptional and mitogenic responses at low concentrations, raising concerns about its endocrine-disrupting and breast cancer-promoting effects.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"521 ","pages":"Article 154393"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893092","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":"Hepatotoxicity: Mechanisms and animal-free prediction models","authors":"Julen Sanz-Serrano,&nbsp;Laura Suter-Dick","doi":"10.1016/j.tox.2026.154400","DOIUrl":"10.1016/j.tox.2026.154400","url":null,"abstract":"","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"521 ","pages":"Article 154400"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145948847","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":"Impact of PM2.5 on cardiorespiratory mortality: A study in the capitals of Brazilian amazon rainforest","authors":"Gustavo de Oliveira Silveira ,&nbsp;Rodrigo de Lima Brum ,&nbsp;Ronan Adler Tavella ,&nbsp;Alicia da Silva Bonifácio ,&nbsp;Ronabson Cardoso Fernandes ,&nbsp;Flavio Manoel Rodrigues da Silva Júnior","doi":"10.1016/j.tox.2026.154401","DOIUrl":"10.1016/j.tox.2026.154401","url":null,"abstract":"<div><div>Wildfire-related air pollution represents an escalating health threat in the Brazilian Amazon, where fine particulate matter (PM_2.5) concentrations frequently exceed safe levels (5 µg/m⁻³). This study quantified long-term PM_2.5 exposure and its impact on cardiorespiratory mortality across the seven Amazonian capitals, Belém, Boa Vista, Macapá, Manaus, Palmas, Porto Velho, and Rio Branco, between 2018 and 2023. In addition, disease-specific outcomes including chronic obstructive pulmonary disease (COPD), lung cancer (LC), and ischemic heart disease (IHD) were assessed. Daily PM_2.5 data were obtained from the CAMS reanalysis, and mortality records from the Brazilian Health Data Platform. Health impacts were estimated using the WHO <em>AirQ+</em> log-linear model. Annual mean PM_2.5 ranged from 10.47 µg.m³ (Palmas, 2020) to 49.69 µg.m³ (Porto Velho, 2021), exceeding the WHO guideline of 5 µg.m³ in all cities. Most capitals experienced over 100 days per year above the 15 µg.m³ daily guideline, and significant correlations were observed between wildfire counts and PM_2.5 in Porto Velho (r = 0.24) and Rio Branco (r = 0.21). Between 2018 and 2023, approximately 5472 (95 % CI: 4595–6711) deaths from circulatory diseases and 2621 (95 % CI: 864–4278) from respiratory diseases were attributable to PM_2.5 exposure. COPD accounted for 627 (95 % CI: 462–781) deaths, LC for 427 (95 % CI: 314–534), and IHD for 304 (95 % CI: 150–467). The highest burdens occurred in Belém, Manaus, and Porto Velho. These findings demonstrate that persistent smoke from seasonal fires has become a critical environmental health crisis in the Amazon, demanding urgent action to prevent deforestation, reduce emissions, and protect population health.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"521 ","pages":"Article 154401"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953042","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":"Toxic effects and mechanism of silver nanoparticles with different particle sizes and surface coatings in lung epithelial cells","authors":"Zige Jiang ,&nbsp;Yue Chen ,&nbsp;Xiaoyu Guo ,&nbsp;Ke Li ,&nbsp;Liqun Chen","doi":"10.1016/j.tox.2026.154398","DOIUrl":"10.1016/j.tox.2026.154398","url":null,"abstract":"<div><div>With nanotechnology's advancement and popularity, nanosafety assessment has attracted public attention, nanosafety assessment has attracted public attention. Silver nanoparticles (AgNPs) have been extensively applied in people’s work and life, but there is still limited knowledge of their potential toxicity to humans. Although many studies have shown that AgNPs causes physiological changes in the lung, the effects and molecular mechanisms of AgNPs on the lung are not fully understood at low-dose exposures and assessed with different physicochemical properties. To comprehensively compare the potential effects and molecular mechanisms of AgNPs with different particle sizes and surface modifications on A549 cells, three PVP-coated AgNPs with particle sizes of 20, 40, and 75 nm and Lipoic Acid (LA), mPEG, and BPEI-coated AgNPs with a particle size of 40 nm, which are referred to as PVP₂₀, PVP₄₀, PVP₇₅, LA₄₀, mPEG₄₀ and BPEI₄₀ were selected in this study. The methods used in this study included characterization of AgNP using transmission electron microscopy (TEM) and zeta potential, the study of cytotoxicity, oxidative stress, and subsequent damage to cell membrane integrity, apoptosis, and RNA-seq. Our findings indicated that AgNPs with different particle sizes and modifications had different toxicological effects, and the smaller size of AgNPs exerts the stronger cytotoxicity. In addition, transcriptome sequencing and qRT-PCR analyses confirmed that the mechanisms of action of these AgNPs varied, but PVP₂₀, PVP₄₀, PVP₇₅, LA₄₀, and BPEI₄₀ AgNPs could all affect A549 cells via IL-17 signaling pathway. Our research findings demonstrate the deleterious effects of different nanosilvers on lung epithelial cells and reveal related possible pathways of influence.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"521 ","pages":"Article 154398"},"PeriodicalIF":4.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145935210","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}