Current Research in Toxicology最新文献

{"title":"Systematic evaluation of the evidence base on ethyl tert-butyl ether and tert-butyl alcohol for carcinogenic potential in humans; lack of concern based on animal cancer studies and mechanistic data","authors":"Brianna N. Rivera ,&nbsp;Isabel A. Lea ,&nbsp;Seneca Fitch ,&nbsp;Neepa Choksi ,&nbsp;Allison Franzen ,&nbsp;James Bus ,&nbsp;Erik Rushton ,&nbsp;Susan J. Borghoff","doi":"10.1016/j.crtox.2025.100270","DOIUrl":"10.1016/j.crtox.2025.100270","url":null,"abstract":"<div><div>Ethyl <em>tert</em>-butyl ether (ETBE), a fuel additive, and <em>tert</em>-butyl alcohol (TBA), a solvent and metabolite of ETBE and methyl <em>tert</em>-butyl ether (MTBE), may be encountered via inhalation, oral, or dermal exposure. This assessment evaluated the human carcinogenic hazard of ETBE and TBA by systematically reviewing available human, animal, and mechanistic data. No epidemiological studies were identified, and two standard cancer bioassays were available for each compound. Tumor responses were limited to low incidences at high exposure levels: liver tumors in male F344 rats, kidney tumors in male F344 rats, and thyroid tumors in female B6C3F1 mice exposed to ETBE or TBA, respectively. Mechanistic evidence was organized within the framework of the key characteristics of carcinogens (KCC) and established rodent non-genotoxic modes of action (MoAs) for the overall evaluation. Aside from supportive evidence for KCC2 (is genotoxic) and KCC10 (alters cell proliferation, death, or nutrient supply), mechanistic data across KCCs were sparse and inconsistent. Both substances lacked genotoxic activity with available data supporting non-genotoxic MoAs that are not relevant to humans. Overall, the evidence indicates little concern for a carcinogenic hazard of ETBE or TBA in humans.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100270"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low-dose arsenic exposure disrupts rat uterine physiology independent of generation of oxidative stress","authors":"Aniruddha Chatterjee ,&nbsp;Urmi Chatterji","doi":"10.1016/j.crtox.2026.100289","DOIUrl":"10.1016/j.crtox.2026.100289","url":null,"abstract":"<div><div>Arsenic is known to adversely affect the female reproductive physiology, specifically at environmentally-relevant or accidentally-high doses, mostly by generation of high amounts of reactive oxygen species (ROS). However, the exact molecular events at very low doses of arsenic exposure, leading to uterine dysfunctions haven’t yet been ascertained. This study aims to evaluate the effect and mechanism of action of oral exposure to 0.4 ppm arsenic for 28 days in adult female albino rats. Alterations in the uterine histomorphology, levels of serum estradiol, expression of the estrogen receptor and cell cycle regulating genes were analyzed. The levels of glutathione, catalase and SOD were also evaluated biochemically. The results indicated that rats exposed to 0.4 ppm sodium arsenate showed reduced circulating levels of estradiol, along with degeneration of epithelial cells of uterine lumen and endometrial glands. Concomitantly, downregulation of the estrogen receptor alpha (ERα), cell cycle regulating proteins (cyclin D1, CDK4), PI3K and Akt were also observed. However, no significant change was observed in the levels of the cellular antioxidant components. The findings thereby indicate that arsenic, at very low concentrations, leads to debilitating effects in the rat physiology by modulating estradiol production, estrogen receptor expression and uterine cell proliferation, without involving redox imbalance, eventually leading to reproductive failures.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100289"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bridging the Gap: How environmental exposures compromise male fertility and clinical Outlook","authors":"Hongxia Chen ,&nbsp;Shenglong He ,&nbsp;Zhuoran Zhu ,&nbsp;Xia Wang ,&nbsp;Zhongji Meng","doi":"10.1016/j.crtox.2026.100286","DOIUrl":"10.1016/j.crtox.2026.100286","url":null,"abstract":"<div><div>The growing prevalence of male infertility has become a significant clinical and public health issue, with environmental exposures increasingly recognized as a major modifiable risk factor. This review synthesizes current evidence within the framework of the “male reproductive exposome”, linking lifelong exposure to environmental toxicants—ranging from endocrine-disrupting chemicals to emerging contaminants—to clinically relevant outcomes such as impaired semen parameters, altered reproductive hormone profiles, and an increased risk of testicular dysfunction. We critically evaluate the concept of life-course vulnerability, highlighting how exposures during critical developmental windows—including prenatal, peripubertal, and adult stages—may program distinct pathological trajectories that manifest as reproductive disorders in later life. In addition to classical mechanisms of endocrine disruption, we emphasize oxidative stress and, particularly, epigenetic reprogramming of the germline as key biological pathways contributing to both immediate fertility impairments and potential transgenerational health effects. Furthermore, we discuss the translational importance of these insights, focusing on the development of mechanism-informed biomarker panels for early detection and risk stratification, as well as addressing the persistent challenge of assessing toxicity from complex chemical mixtures. Finally, we underscore the necessity of integrating epidemiological research, mechanistic toxicology, and clinical practice to advance preventive and clinical strategies. This integration requires overcoming methodological challenges in mixture exposure assessment, accelerating biomarker discovery for personalized risk prediction, and formulating evidence-based public health interventions. In a word, this review advocates for a proactive, science-driven approach to mitigate environmental threats to male reproductive health and protect the well-being of future generations.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100286"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147384963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-mediated changes contributing to benzo[a]pyrene toxicity in a 3D respiratory model for asthma","authors":"Reese M. Valdez ,&nbsp;Yvonne Chang ,&nbsp;Jamie M. Pennington ,&nbsp;Susan C. Tilton","doi":"10.1016/j.crtox.2026.100283","DOIUrl":"10.1016/j.crtox.2026.100283","url":null,"abstract":"<div><div>There is increased emphasis on understanding how non-chemical stressors that contribute to inflammation in the lung may influence adverse health outcomes after chemical exposures. Prior studies in an <em>in vitro</em> respiratory model of type 2 asthmatic inflammation found cells from the asthmatic phenotype respond uniquely to benzo[a]pyrene (BAP) treatment compared to normal cells across multiple endpoints related to mucus production, goblet cell hyperplasia, mucociliary dysfunction and airway remodeling. To further understand how cellular response to BAP is regulated in a model of inflammation-based disease, this study examines changes in miRNA and mRNA regulation following BAP exposure in primary human bronchial epithelial cells (HBECs) cultured at the air–liquid interface with normal and interlukin-13 (IL-13) induced asthmatic phenotypes. Primary 3D HBECs differentiated in the presence and absence of 10 ng/mL IL-13 were treated on day 25 with 158 µM BAP for 48 h. Differentially expressed (q &lt; 0.01) miRNA and mRNA were analyzed to predict miRNA target interactions and assess the functional consequences of miRNAs in each phenotype. While BAP-treated HBEC with the IL-13 asthmatic phenotype had a similar number of differentially expressed miRNA (93 up- and 100 down-regulated) compared to BAP-treated normal HBEC (93 up- and 94 down-regulated), IL-13 HBEC treated with BAP were shown to have unique enrichment of miRNA targets involved in up-regulation of cell cycle processes and down-regulation of processes related to NOTCH, WNT, and Hedgehog signaling. These data are the first to provide insight into the role of miRNAs as regulators of chemical toxicity in a respiratory model of inflammation-based disease.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100283"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of autophagy in microwave radiation induced toxicity in iPSC-derived cardiomyocytes","authors":"Chenjing Zhang ,&nbsp;Zhanming Liu ,&nbsp;Yingxin Wang ,&nbsp;Weilin Deng ,&nbsp;Hailong Wang ,&nbsp;Jing Zhang ,&nbsp;Qilong Feng","doi":"10.1016/j.crtox.2026.100288","DOIUrl":"10.1016/j.crtox.2026.100288","url":null,"abstract":"<div><div>This study aims to explore the impact of microwave radiation on the electrophysiological functions of human-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) and to focus on the critical role and underlying mechanism of autophagy in this process. The iPSC-CMs were irradiated with S-band microwaves at a power of 30 mw/cm². Through techniques such as immunofluorescence, Western blotting, electrophysiological recording, scanning electron microscopy, and transcriptomic analysis, the changes in electrophysiological indicators, ultrastructure, and autophagy levels of iPSC-CMs after microwave radiation were systematically evaluated. Further intervention with Acadesine (AICAR) was conducted to verify the role of autophagy in radiation-induced damage. After microwave radiation, iPSC-CMs exhibited significant electrophysiological dysfunction. Ultrastructural observations revealed aggravated mitochondrial damage after radiation, manifested as vacuolization, loss of cristae, and increased mitochondrial autophagy, accompanied by decreased ATP content and mitochondrial membrane potential. At the molecular level, transcriptomic analysis suggested that autophagy-related genes such as ULK1 were key regulatory nodes. After radiation, the expression of autophagy marker LC3II/I was upregulated while p62 expression was downregulated, indicating activation of the autophagic flux. Inhibition of autophagy with AICAR significantly improved the radiation-induced electrophysiological disorders. Microwave radiation can cause severe electrophysiological dysfunction in iPSC-CMs, and the mechanism is closely related to the abnormally elevated autophagy level induced by radiation. Inhibiting autophagy can effectively alleviate the electrophysiological damage caused by radiation, suggesting that targeting the autophagy pathway may be a potential strategy for protecting against the cardiotoxic effects of microwave radiation.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100288"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147448996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An integration of physiological, morphological and biochemical assessments in studying guinea pig models of ototoxicity and otoprotection−a systematic review","authors":"Yi-Ho Young ,&nbsp;Po-Hsuan Wu ,&nbsp;Shing-Hwa Liu","doi":"10.1016/j.crtox.2026.100292","DOIUrl":"10.1016/j.crtox.2026.100292","url":null,"abstract":"<div><h3>Purpose</h3><div>This systematic review aims to explore the development and utilization of a comprehensive test battery comprising physiological, morphological, and biochemical assessments in guinea pig models to study mechanisms of ototoxicity and otoprotection.</div></div><div><h3>Methods</h3><div>This review was developed from peer-reviewed articles almost exclusively dealing with guinea pigs published in those journals listed on Journal Citation Reports.</div></div><div><h3>Results</h3><div>Initially, 560 articles were retrieved from 1994 to 2024. Following the guidelines (PRISMA 2020 statement) for reporting reviews, 54 relevant papers were ultimately selected.</div></div><div><h3>Conclusion</h3><div>Using animal models of ototoxicity and otoprotection, particularly the guinea pig can provide valuable insights into the mechanisms underlying ototoxicity and otoprotection in humans. This approach offers a detailed framework for elucidating ototoxic mechanisms and exploring therapeutic strategies for otoprotection, while also encouraging researchers to pursue basic research in this field.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100292"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147600270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A framework for the safety evaluation of peptides in cosmetics","authors":"Donald L. Bjerke ,&nbsp;Jin Li ,&nbsp;Yuan Gao ,&nbsp;Ping Hu ,&nbsp;Karl Lintner ,&nbsp;Tomohiro Hakozaki","doi":"10.1016/j.crtox.2026.100291","DOIUrl":"10.1016/j.crtox.2026.100291","url":null,"abstract":"<div><div>As the cosmetic industry replaces traditional animal safety studies with next generation risk assessment approaches, the approach to safety substantiation for peptides used in cosmetic products must also evolve. While the need to provide assurances of safety for local and systemic toxicity endpoints remains the same, adoption of bioinformatic tools developed in the food, agricultural biotechnology, and drug development industries may add to the weight of evidence for the safety substantiation of peptides in cosmetics. Here we review the historical development and safety evaluation of peptides utilized in the cosmetic industry and provide a new safety evaluation framework that incorporates six bioinformatic tools. To test the framework, a variety of peptides (palmitoyl hexapeptide-12, caffeoyl hexapeptide-9, palmitoyl pentapeptide-4, amanitin alpha, conotoxin ArlB, bradykinin, and enkephaline) are evaluated with NCBI BLASTp, ToxinPred3.0, Peptipedia, BIOPEP-UWM, AllerCatPro 2.0, and IEDB bioinformatic tools. The results correctly identified safety concerns (toxins) for amanitin and conotoxin peptides and the biological actions of bradykinin and enkephaline, while palmitoyl hexapeptide-12, caffeoyl hexapeptide-9, and palmitoyl pentapeptide-4 demonstrated sequence homology with extracellular matrix proteins in the skin (collagen, elastin, fibronectin) without the safety concerns of the other peptides. The incorporation of bioinformatic tools into the safety framework provides an additional means to screen for toxins and allergens as well as insights into potential biological activities when sequence homology with existing proteins and peptides occurs. Further testing of the framework by the cosmetic industry is needed to lend support and reveal opportunities for refinements that advance the safety substantiation of peptides.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100291"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147600269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective role of calcitriol in PM2.5-induced apoptosis and inflammation in bronchial epithelial cells in vitro via vitamin D receptor-mediated Nrf2 signaling","authors":"Mutita Pluempreecha ,&nbsp;Anyamanee Chatsirisupachai ,&nbsp;Tanyapohn Soingam ,&nbsp;Tasanee Onkoksoong ,&nbsp;Tongchai Payungwong ,&nbsp;Siwanon Jirawatnotai ,&nbsp;Uraiwan Panich","doi":"10.1016/j.crtox.2026.100296","DOIUrl":"10.1016/j.crtox.2026.100296","url":null,"abstract":"<div><div>PM2.5 contributes to lung injury by inducing oxidative stress, inflammatory responses, and apoptosis. Calcitriol exerts a protective role against lung injury by regulating the vitamin D receptor (VDR) and Nrf2 signaling pathways, mitigating PM2.5-induced oxidative stress and inflammation. In this study, we investigated the protective effects of calcitriol against PM2.5-induced apoptosis, oxidative damage, and inflammation in human bronchial epithelial BEAS-2B cells, with a specific focus on the crosstalk between VDR and Nrf2 signaling. BEAS-2B cells were pre-treated with calcitriol (1, 10, 100 nM) for 24 h before PM2.5 exposure (100 µg/mL). Apoptosis, DNA damage, and inflammation were assessed by flow cytometry, ELISA, qRT-PCR, and Western blot analysis. Chromatin immunoprecipitation (ChIP) was performed to evaluate VDR–antioxidant response element (ARE) binding. Calcitriol suppressed apoptotic signaling by reducing p53 phosphorylation and downregulating the mRNA expression of <em>p53</em> and <em>caspase-3</em>, while also mitigating oxidative DNA damage, as indicated by decreased levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG) in BEAS-2B cells. Additionally, calcitriol suppressed inflammatory responses by downregulating NF-κB activity and the mRNA expression of <em>NF-κB p65</em> and its downstream pro-inflammatory genes, including <em>IκB-α</em>, <em>TNF-α</em>, and <em>IL-6</em>. Moreover, calcitriol treatment increased VDR protein expression and enhanced Nrf2 activity. ChIP assays demonstrated that calcitriol enhanced VDR binding to AREs, thereby promoting the transcription of key Nrf2-regulated cytoprotective genes, including heme oxygenase-1 (<em>HO-1</em>) and NADPH quinone dehydrogenase 1 (<em>NQO1</em>). These findings provide mechanistic insight into the pharmacological effects of calcitriol, underscoring its potential to alleviate PM2.5-induced cellular injury through VDR-mediated activation of Nrf2 redox signaling.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100296"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147850085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of serotonin and ergot alkaloids on tissue partitioning and contractile response of bovine blood vessels","authors":"Eriton E.L. Valente ,&nbsp;David L. Harmon ,&nbsp;John May ,&nbsp;Huihua Ji ,&nbsp;Ronald J. Trotta ,&nbsp;James L. Klotz","doi":"10.1016/j.crtox.2025.100272","DOIUrl":"10.1016/j.crtox.2025.100272","url":null,"abstract":"<div><div>Ergot alkaloids can bind serotonin (5-HT) receptors interfering with many physiological functions. However, the mechanism has not been completely established. The objective was to evaluate whether the association of 5-HT and the ergot alkaloid, ergovaline, in a 24-h pre-incubation can affect vascular tissue partitioning and contractile responses. Cross-sections of saphenous veins from five steers were used. In the tissue partitioning experiment, the treatments were the combination of three levels of ergovaline (2.01 × 10⁻⁸ M, 2.01 × 10⁻⁷ M and 2.01 × 10⁻⁶ M) with three levels of 5-HT and a control (5 × 10⁻⁸ M, 5 × 10⁻⁷ M, 5 × 10⁻⁶ M and 0 M). After 24-h exposure to the treatments, the blood vessels were washed. Afterward, the tissues were analyzed for ergovaline and 5-HT concentrations. For the contractility experiment, a parallel set of blood vessels was evaluated in the myograph after 24-h pre-incubation with the respective treatments: 1) no additional compound; 2) tall fescue seed extract (2.01 × 10⁻⁷ M of ergovaline); 3) serotonin (5 × 10⁻⁷ M)<em>;</em> or 4) ERV plus 5-HT. The tissue ergovaline increased (P &lt; 0.001) about 27.5-fold when the concentration in the media increased 100-fold (2.01 × 10⁻⁸ M to 2.01 × 10⁻⁶ M). However, the presence of 5-HT did not affect (P = 0.368) tissue ergovaline partitioning. When 5-HT was not added, ergovaline reduced (P &lt; 0.05) the 5-HT concentration in the blood vessel. Pre-incubation with ergovaline reduced contractile response by about 95 % (P &lt; 0.05) and 5-HT did not change its effect. Ergot alkaloid partitioning is associated with reduced tissue 5-HT levels and blood vessel contractility.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100272"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145735325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The NLRP3 inhibitor, MCC950, attenuates environmental pollutant PM2.5-induced acute lung injury by inhibiting alveolar macrophage pyroptosis","authors":"Zhuoxiao Han ,&nbsp;Ying Han ,&nbsp;Ranran Li ,&nbsp;Kexin Fan ,&nbsp;Xiao Zhang ,&nbsp;Tengfei Sun ,&nbsp;Yue Li ,&nbsp;Hua Qiao","doi":"10.1016/j.crtox.2026.100282","DOIUrl":"10.1016/j.crtox.2026.100282","url":null,"abstract":"<div><div>PM_2.5 is a key environmental pollutant that induces inflammatory lung injury.</div><div>Effective prevention and treatment for PM₂.₅-induced lung damage remain lacking.</div><div>This study investigated MCC950′s protective role in PM₂.₅-exposed mice and macrophages.</div><div>PM₂.₅ triggers NLRP3/Caspase-1-mediated pyroptosis, amplifying pulmonary inflammation.</div><div>MCC950 attenuates injury by inhibiting pyroptosis, suggesting therapeutic potential.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100282"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147303424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}