{"title":"Targeting the SP1/ACSL4 axis attenuates ferroptosis in trastuzumab-induced cardiotoxicity.","authors":"Qiyuan Hu, Bincheng Zhong, Yajie Zheng, Henghua Zhou","doi":"10.1080/01480545.2025.2586862","DOIUrl":"10.1080/01480545.2025.2586862","url":null,"abstract":"<p><p>Trastuzumab, a mainstay in treating HER2-positive breast, gastric, and lung cancers, inhibits tumor growth by inducing cell cycle arrest, apoptosis, and anti-angiogenesis. However, its clinical use is limited by cardiotoxicity. This study demonstrates that trastuzumab-induced myocardial injury is mechanistically linked to ferroptosis. Trastuzumab dysregulates key ferroptosis-related proteins (increasing ACSL4 (Acyl-CoA Synthetase Long Chain Family Member 4) and decreasing SLC7A11 (Solute Carrier Family 7 Member 11) expression), elevating lipid peroxidation levels. Crucially, we screen out the transcription factor SP1 (Sp1 transcription factor) from the public database, regulator of ACSL4. Silencing SP1 significantly attenuates trastuzumab-triggered myocardial ferroptosis. Collectively, our findings establish ferroptosis as the primary pathway underlying trastuzumab-associated cardiotoxicity and propose SP1 inhibition as a promising therapeutic strategy to mitigate this adverse effect.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":"49 5","pages":"1104-1113"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Junyi Du, Jia Du, Linlin Qiu, Qingwei Zhou, Meiqing Jin, Jianjun Chen, Weihong Wu
{"title":"The vector effect of microplastics and nanoplastics: co-transport and ecological risks of chemical pollutants and antibiotic resistance genes in the soil-water continuum.","authors":"Junyi Du, Jia Du, Linlin Qiu, Qingwei Zhou, Meiqing Jin, Jianjun Chen, Weihong Wu","doi":"10.1080/01480545.2026.2717208","DOIUrl":"https://doi.org/10.1080/01480545.2026.2717208","url":null,"abstract":"<p><p>Microplastics (MPs) and nanoplastics (NPs) act as dynamic environmental vectors across the soil-water continuum, allowing them to enter organisms through direct ingestion, leading to potential tissue accumulation. Under specific exposure conditions, these vectors can undergo trophic transfer through food chains, contributing to combined toxicological risks. This paper reviews how the adsorption and co-transport behaviors of chemical pollutants by MPs and NPs are collectively regulated by the intrinsic physicochemical properties of the material and environmental weathering processes. The formation of the \"plastisphere\" on the surface of these particles provides a physical substrate that selectively enriches microbial communities and mobile genetic elements (MGEs). Under specific combined chemical stresses, this localized enrichment can act as a precursor to facilitate the horizontal gene transfer (HGT) of antibiotic resistance genes (ARGs), although the actual occurrence of HGT remains highly context-dependent. Additionally, MPs and NPs exacerbate their ecotoxicological impacts by operating via an \"adsorption-ingestion-release\" pathway within host gastrointestinal tracts, significantly influencing the dynamic bioavailability and combined toxicity (e.g., synergistic, antagonistic, or additive) of co-existing pollutants across multiple trophic levels. Given the numerous unresolved scientific challenges-such as the lack of standardized quantification methodologies for complex soil matrices and the poorly understood biomagnification of composite pollutant mixtures-there is a pressing need to promote further research through AI-driven coupled kinetic models and a comprehensive \"One Health\" risk assessment paradigm.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-26"},"PeriodicalIF":2.2,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ana Paula Ávila, Bianca Mello Cerato, Flavio Gomes Figueira Camacho, Luiz Henrique Garcia Pereira, Wagner Antonio Chiba De Castro, Aline Theodoro Toci, Marcela Boroski
{"title":"Integrated assessment of pesticides, inorganic ions, and health risks in drinking water from Missal, a rural agricultural municipality in Southern Brazil.","authors":"Ana Paula Ávila, Bianca Mello Cerato, Flavio Gomes Figueira Camacho, Luiz Henrique Garcia Pereira, Wagner Antonio Chiba De Castro, Aline Theodoro Toci, Marcela Boroski","doi":"10.1080/01480545.2026.2714874","DOIUrl":"https://doi.org/10.1080/01480545.2026.2714874","url":null,"abstract":"<p><p>Missal is a small municipality in Paraná, southern Brazil, with an economy predominantly based on soybean and corn cultivation. This study evaluated the occurrence of pesticides and inorganic ions in nine groundwater-derived drinking water sources and one surface water reference site. A total of 120 water samples were collected monthly over one year and analyzed using chromatographic methods. Results were evaluated according to Brazilian drinking water regulations and compared with international guidelines. Paraquat and parathion, both banned in Brazil, were detected at concentrations of 4.50-93.21 µg L<sup>-1</sup> and up to 71.02 µg L<sup>-1</sup>, respectively. Glyphosate and AMPA were found in 53% and 77% of samples, respectively, while 2,4-D and parathion were present in all samples. Temporal analysis indicated seasonal variation, with significantly higher concentrations during periods of increased precipitation (p < 0.05), with total pesticide concentrations reaching up to 400 µg L<sup>-1</sup>. These patterns suggest temporal influence associated with agricultural application and rainfall-driven transport. Cytotoxicity and genotoxicity were assessed using the <i>Allium cepa</i> assay, revealing increased mitotic index and chromosomal aberrations at six sampling points. A Hazard Index (HI) greater than 1 was observed at seven points, mainly due to nitrate and parathion, suggesting potential non-carcinogenic health risks. These findings suggest that combined exposure to pesticides and inorganic ions may contribute to non-carcinogenic risk, supporting the relevance of continuous and integrative monitoring.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-15"},"PeriodicalIF":2.2,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Banu Orta Yilmaz, Iremnur Sarialioglu, Gokce Elmaci, Yasemin Aydin
{"title":"Antioxidant efficacy of N-acetylcysteine against acrylamide-induced toxicity in Leydig cells by modulating p53/Bax/Caspase-3 pathway.","authors":"Banu Orta Yilmaz, Iremnur Sarialioglu, Gokce Elmaci, Yasemin Aydin","doi":"10.1080/01480545.2026.2718396","DOIUrl":"https://doi.org/10.1080/01480545.2026.2718396","url":null,"abstract":"<p><p>Acrylamide (Acr) is a widely encountered environmental and dietary toxicant known to induce oxidative stress and disrupt male reproductive function. Leydig cells, due to their high metabolic activity and mitochondrial dependence, are particularly vulnerable to redox imbalance. N-acetylcysteine (Nac), a thiol-containing antioxidant and glutathione precursor, has been extensively studied for its cytoprotective properties. However, its modulatory effects on Acr-induced toxicity in Leydig cells and its pharmacodynamic interaction profile remain incompletely characterized. In this study, TM3 Leydig cells were exposed to Acr in the presence or absence of Nac. Cell viability was assessed by MTT assay, and chemical interaction profiles were evaluated using ZIP, Bliss, and Chou-Talalay combination index analyses. Oxidative stress parameters, including intracellular reactive oxygen species (ROS), lipid peroxidation, antioxidant enzyme activities (SOD, CAT, GPx), and glutathione levels, were measured. Apoptotic responses were analyzed through double fluorescence staining, RT-qPCR of apoptosis-related genes (<i>Bax</i>, <i>Bcl2</i>, <i>Casp3</i>, <i>Trp53</i>), and Western blot analysis of CASP3 protein expression. Acr exposure significantly reduced cell viability, increased ROS and lipid peroxidation levels, suppressed antioxidant defenses, and activated the mitochondrial apoptotic pathway. Nac treatment markedly improved cell viability, restored antioxidant capacity, reduced oxidative stress markers, and suppressed p53/Bax/Casp3-mediated apoptotic signaling. Combination analyses revealed an antagonistic interaction profile, indicating that Nac biologically limits Acr-induced cytotoxicity. Collectively, these findings demonstrate that Nac exerts protective effects in Leydig cells by modulating redox homeostasis and mitochondrial apoptosis, suggesting its potential as a protective regulator against Acr-induced reproductive toxicity.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-12"},"PeriodicalIF":2.2,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohammad Shokrzadeh, Parham Motamedi, Neshat Mirbozorg, Shaghayegh Aghajanshakeri, Yasaman Kolki
{"title":"The effects of epicatechin on oxidative stress and genotoxicity induced by cypermethrin in PC-12 cell line.","authors":"Mohammad Shokrzadeh, Parham Motamedi, Neshat Mirbozorg, Shaghayegh Aghajanshakeri, Yasaman Kolki","doi":"10.1080/01480545.2026.2700295","DOIUrl":"https://doi.org/10.1080/01480545.2026.2700295","url":null,"abstract":"<p><p>This study investigated the protective effects of epicatechin against cypermethrin-induced oxidative stress and genotoxicity in PC-12 cells. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay following exposure to cypermethrin (1-300 μM). The IC<sub>50</sub> concentration was determined and subsequently used to induce toxicity. PC-12 cells were treated with epicatechin (50, 100, 150, and 200 μM) in the presence of cypermethrin. Intracellular reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and DNA damage were evaluated using 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) assay, biochemical assays, and alkaline comet assay, respectively. Cypermethrin induced concentration-dependent cytotoxicity, reducing cell viability from 107.5% at 1 μM to 40.29% at 300 μM, with an IC<sub>50</sub> value of 238.5 ± 6.9 μM. Cypermethrin significantly increased ROS production (83.55%), depleted intracellular GSH (93.00 ± 1.73 to 50.33 ± 1.53 nmol/mg protein), and elevated MDA levels (22.67 ± 2.52 to 81.00 ± 2.00 nmol/mg protein) compared with the control group (<i>p</i> < 0.05). Epicatechin treatment dose-dependently attenuated oxidative stress, restoring GSH levels to 74.67 ± 1.53 nmol/mg protein, reducing MDA levels to 51.00 ± 2.65 nmol/mg protein, and decreasing ROS production to 53.43% at 200 μM. Comet assay analysis demonstrated that cypermethrin significantly increased tail length, percentage DNA in tail, and tail moment, whereas epicatechin (200 μM) markedly reduced all genotoxicity parameters and comet tail formation. Epicatechin protects PC-12 cells from cypermethrin-induced oxidative and genotoxic injury by enhancing antioxidant defenses, limiting lipid peroxidation, and reducing DNA damage. Further <i>in vivo</i> studies are required to confirm its neuroprotective potential and define optimal dosing.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-8"},"PeriodicalIF":2.2,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ameliorative effects of forskolin and pinitol on ethyl methanesulfonate-induced genotoxicity in somatic and germline cells of <i>Drosophila melanogaster</i>.","authors":"Tamara M Mladenović, Sanja Lj Matić","doi":"10.1080/01480545.2026.2711641","DOIUrl":"https://doi.org/10.1080/01480545.2026.2711641","url":null,"abstract":"<p><p>Forskolin and pinitol are bioactive dietary compounds studied for several pharmacological properties. Considering their widespread therapeutic application and the limited information available regarding their genotoxic and/or antigenotoxic properties, the present study investigated whether commercially available forskolin and pinitol can induce DNA damage and/or protect DNA against damage induced by ethyl methanesulfonate (EMS). The sex-linked recessive lethal (SLRL) test in germline and the alkaline comet assay in somatic cells were performed in <i>Drosophila melanogaster</i> to assess <i>in vivo</i> genotoxicity and DNA-protective effects against EMS-induced DNA damage. The SLRL assay demonstrated that neither forskolin nor pinitol induced genotoxic effects in <i>D. melanogaster</i> males. Both compounds significantly reduced EMS-induced sex-linked recessive lethal mutations, indicating a marked DNA-protective effect in germline cells. In the comet assay, no significant increase in DNA damage was observed following forskolin treatment, whereas pinitol induced moderate increases in the total comet score only at the highest concentration compared with the negative control, with values statistically significantly lower than those of the positive control. The greatest DNA-protective effect against EMS was observed following co-treatment with 0.5 mg/mL of forskolin or pinitol, resulting in percentage reductions of 94.2% and 80.5%, respectively. The findings suggest that forskolin and pinitol possess protective effects against EMS-induced DNA damage. Their DNA-protective capacity at non-genotoxic concentrations indicates potential chemopreventive properties and supports further investigation of their biological effects. These findings support further investigation into the molecular mechanisms underlying their protective effects and their potential application in the prevention and management of diseases associated with genomic instability.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-8"},"PeriodicalIF":2.2,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Phthalate exposure and human reproductive health: an epidemiological review.","authors":"Binyu Sun, Hongbeichen Shi, Xin Liu, Mengxi Zeng, Zhangchi Yuan, Yuyang Xiao","doi":"10.1080/01480545.2026.2711644","DOIUrl":"https://doi.org/10.1080/01480545.2026.2711644","url":null,"abstract":"<p><p>Plastics are ubiquitous in the environment and are widely used in food packaging, medicine, agriculture, construction and other sectors. However, the plasticizers they contain pose a substantial threat to environmental safety and human health. Phthalates represent the most important class of plasticizers and are classified as endocrine-disrupting chemicals (EDCs), capable of causing adverse effects even at very low exposure levels. Extensive in vitro and in vivo studies have demonstrated that phthalates and their metabolites exhibit reproductive toxicity, leading to reduced sperm motility and count, hormonal dysregulation, ovarian failure, preterm birth and other detrimental outcomes. This review synthesizes current evidence on the association between phthalate exposure and various reproductive system disorders. Epidemiological studies show that phthalate exposure is linked to impaired sperm quality, prostate disease and erectile dysfunction in males, suggesting a contributing role in the pathogenesis of infertility. However, the association with shortened anogenital distance remains unclear. In females, phthalate exposure has been associated with endometriosis, polycystic ovary syndrome, premature ovarian failure, infertility and miscarriage, although the epidemiological evidence is inconsistent. In conclusion, paying attention to the reproductive health risks posed by phthalate exposure is of critical importance, particularly for vulnerable groups including women of childbearing age, pregnant women, and children.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-18"},"PeriodicalIF":2.2,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Okan Sancer, Pınar Aslan Koşar, Uğur Şahin, Vehbi Atahan Toğay
{"title":"HIF-1α-associated transcriptional responses to chemical hypoxia in breast and liver cancer cells.","authors":"Okan Sancer, Pınar Aslan Koşar, Uğur Şahin, Vehbi Atahan Toğay","doi":"10.1080/01480545.2026.2711646","DOIUrl":"https://doi.org/10.1080/01480545.2026.2711646","url":null,"abstract":"<p><p>Hypoxia is a defining feature of the tumor microenvironment and a key driver of malignant progression through transcriptional reprogramming of metabolic, angiogenic, and survival pathways. In this study, hypoxia-induced molecular responses were investigated in human hepatocellular carcinoma (HepG2) and breast adenocarcinoma (MCF-7) cells using cobalt(II) chloride (CoCl2) as a hypoxia mimetic. Cell viability profiling was performed to determine the optimal experimental concentration, followed by quantitative PCR analysis of hypoxia-related genes and miRNA-gene interaction network analysis. Cell viability profiling identified 100 µM CoCl2 as the optimal condition for downstream analyses. Quantitative PCR revealed robust induction of HIF-1α in both cell lines, indicating activation of hypoxic signaling. However, downstream responses differed markedly between cell types. MCF-7 cells exhibited significant upregulation of SLC2A1 and increased VEGFA and NFKB1 expression, consistent with activation of glycolytic and pro-angiogenic pathways. In contrast, HepG2 cells showed limited downstream transcriptional engagement despite elevated HIF1A expression. Furthermore, miRNA-gene interaction analysis revealed a dense regulatory network in MCF-7 cells, whereas HepG2 cells displayed a more restricted, VEGFA-centered miRNA profile. These findings demonstrate that chemical hypoxia induces cell-type-specific transcriptional and post-transcriptional responses in breast and liver cancer cells. The results suggest that miRNA-mediated regulation may contribute to differential tumor adaptation to hypoxic stress and highlight the importance of cellular context in hypoxia-associated signaling pathways.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-11"},"PeriodicalIF":2.2,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Curcumin protects SH-SY5Y cells against glutamate-induced excitotoxicity by maintaining genomic integrity and antioxidant balance.","authors":"Burak Tan, Seza Nur Suluhan, Oğuzhan Yaylalı, Melike Sedef Güneş, Nurcan Dursun","doi":"10.1080/01480545.2026.2712041","DOIUrl":"https://doi.org/10.1080/01480545.2026.2712041","url":null,"abstract":"<p><p>Glutamate-induced excitotoxicity, characterized by oxidative stress and genomic instability, is a hallmark of neurodegenerative disorders. This study investigated the protective effects of curcumin against glutamate-induced excitotoxicity in SH-SY5Y cells, focusing on oxidative balance and DNA integrity. SH-SY5Y cells were exposed to 40 mM L-glutamate to induce excitotoxicity. Cells were concurrently treated with curcumin (2.5-15 µM). Cell viability was assessed via XTT assay. Oxidative status was evaluated by measuring Total Antioxidant Status (TAS) and Total Oxidant Status (TOS). Genomic integrity was analyzed using the Comet assay (Tail DNA%). Exposure to 40 mM glutamate caused ∼50% cell death, significantly increased TOS levels, and induced extensive DNA damage (increased Tail DNA%). Co-treatment with 10 and 15 µM curcumin significantly restored cell viability in a dose-dependent manner. Notably, 10 µM curcumin ameliorated glutamate-induced TAS depletion and significantly reduced DNA fragmentation, restoring genomic stability to near-baseline levels. Curcumin alone exhibited no pro-oxidant or genotoxic effects. Curcumin exerts a significant cytoprotective effect against glutamate excitotoxicity in SH-SY5Y cells. This protection is primarily mediated through the restoration of the cellular antioxidant pool and the preservation of genomic integrity, suggesting curcumin as a promising therapeutic agent for mitigating excitotoxic neuronal damage.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-10"},"PeriodicalIF":2.2,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Toxicity study of a novel composite dust suppressant in C57BL/6 mice.","authors":"Hao Ding, Rongxia Yu, Zhian Huang, Junchuan Zhang, Xiangrui Meng, Longsheng Huang, Songyu Chen, Jinlu Chang, Yinghua Zhang, Asim Farooq, Jinhui Li, Yingjie Gao","doi":"10.1080/01480545.2026.2711648","DOIUrl":"https://doi.org/10.1080/01480545.2026.2711648","url":null,"abstract":"<p><p>Construction dust is a major source of air pollution and easily causes intractable respiratory diseases such as pneumoconiosis. Dust suppressants are effective for dust control, yet most existing studies only focus on dust suppression performance, lacking systematic toxicological assessments, especially data on extrapulmonary multi-organ toxicity. In this study, SPF male C57BL/6 mice were used to establish three subchronic inhalation exposure groups: dust alone, dust suppressant alone, and co-exposure of dust and suppressant. Indicators including body weight, organ coefficients, blood routine, serum cytokines, and liver, kidney, and heart pathological lesions were detected to investigate the extrapulmonary multi-organ toxicity of an eco-friendly composite dust suppressant. The suppressant had little effect on mouse body weight. At appropriate concentrations (4-20 mg/m<sup>3</sup>), it inhibited dust-induced inflammatory responses and alleviated liver and kidney injuries. When the concentration reached 100 mg/m<sup>3</sup>, the suppressant interacted with dust to increase DNA oxidative damage markers, indicating potential genotoxic risks. This study fills the gap in extrapulmonary toxicological research of dust suppressants, provides references for toxicology evaluation and experimental basis for determining safe application concentrations on construction sites.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-14"},"PeriodicalIF":2.2,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}