Toxicology最新文献_第6页

Ferroptosis contributing to spermatocyte injury induced by silica nanoparticles via BRCA1/GPX4 signaling 二氧化硅纳米颗粒通过BRCA1/GPX4信号通路诱导精母细胞损伤

IF 4.8 3区医学

Toxicology Pub Date : 2025-07-07 DOI: 10.1016/j.tox.2025.154231

Jianhui Liu , Enjie Zhang , Shaofei Su , Shuanghua Xie , Ruixia Liu , Lihua Ren , Chenghong Yin

{"title":"Ferroptosis contributing to spermatocyte injury induced by silica nanoparticles via BRCA1/GPX4 signaling","authors":"Jianhui Liu , Enjie Zhang , Shaofei Su , Shuanghua Xie , Ruixia Liu , Lihua Ren , Chenghong Yin","doi":"10.1016/j.tox.2025.154231","DOIUrl":"10.1016/j.tox.2025.154231","url":null,"abstract":"<div><div>Amorphous silica nanoparticles (SiNPs) have gradually been established to pose a threat to male reproductive health, but the underlying mechanisms are not yet fully elucidated. Ferroptosis is an emerging programmed cell death mechanism associated with spermatogenic disorders. Here, we examined how ferroptosis contributes to SiNP-induced male reproductive damage and assessed the regulatory role of the BRCA1/GPX4 axis in this context. GC-2spd cells were exposure to SiNPs with concentrations of 0, 10, and 20 μg/mL and RNA sequencing of GC-2spd cells was performed. Follow-up experiments were performed to validate the enrichment analysis findings. According to the bioinformatic analysis, after exposure to SiNPs, oxidative stress, ferroptosis and cell cycle pathway were markedly enriched. SiNPs triggered iron overload and significantly decreased the expression levels of glutathione peroxidase 4 (GPX4) and glutathione (GSH) in GC-2spd cells, while upregulating malondialdehyde (MDA) and heme oxygenase-1 (HO-1). Of particular note, the ferroptosis inhibitor Ferrostatin-1 (Fer-1) and a potent iron chelator deferoxamine (DFO) attenuated SiNPs-induced lipid peroxidation, iron overload and cytotoxicity. Of mechanistic importance, we found that BRCA1 targeted GPX4 as a pivotal factor in mediating ferroptosis triggered by SiNPs. Curcumin, the specifical activator of BRCA1, treatment significantly alleviate SiNPs-stimulated down-regulation on expressions of BRCA1 and GPX4. Our findings first emphasize that BRCA1/GPX4 signal-mediated ferroptosis was a factor in SiNPs-caused spermatocyte injury, which offers novel insights for clarifying the toxicity of SiNPs and for the safe application of SiNPs-related nanoproducts in the future.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"517 ","pages":"Article 154231"},"PeriodicalIF":4.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144581281","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}

引用次数: 0

Formyl peptide receptor 2 (FPR2) mediates cisplatin-induced cochlear inflammation and hair cell apoptosis 甲酰基肽受体2 （FPR2）介导顺铂诱导耳蜗炎症和毛细胞凋亡。

IF 4.8 3区医学

Toxicology Pub Date : 2025-07-05 DOI: 10.1016/j.tox.2025.154229

Jiaojiao Hou , Rui Liang , Yuhan Lin , Daiyao Liu , Jiamei Li , Yifan Liu , Tao Xu , Shuangyue Liu , Aimei Wang

{"title":"Formyl peptide receptor 2 (FPR2) mediates cisplatin-induced cochlear inflammation and hair cell apoptosis","authors":"Jiaojiao Hou , Rui Liang , Yuhan Lin , Daiyao Liu , Jiamei Li , Yifan Liu , Tao Xu , Shuangyue Liu , Aimei Wang","doi":"10.1016/j.tox.2025.154229","DOIUrl":"10.1016/j.tox.2025.154229","url":null,"abstract":"<div><div>Despite its efficacy in cancer treatment, cisplatin is significantly limited by its debilitating ototoxicity and the poorly understood mechanisms underlying this adverse effect. This study investigates the role of formyl peptide receptor 2 (FPR2), a G protein-coupled receptor, in cisplatin-induced hearing loss. We demonstrate a significant upregulation of FPR2 in the cochlea of mice after cisplatin exposure, accompanied by profound hearing loss. Blocking FPR2 with either genetic (knockdown) or pharmacological (antagonist Boc-2, 50 µg/kg) strategies mitigates cisplatin-induced hearing impairment. Our in vivo experiments indicate that intraperitoneal injection of Boc-2 substantially alleviated the increase in auditory brainstem response (ABR) thresholds induced by cisplatin in mice. Mechanistically, FPR2 directly activates ERK1/2 and NF-κB signaling pathways, triggering a pro-inflammatory cytokine storm and subsequent hair cell apoptosis in the cochlea. Furthermore, FPR2 inhibition substantially attenuates cisplatin-induced inflammatory factor release and hair cell death. These findings identify FPR2 as a novel mediator of cisplatin-induced ototoxicity, suggesting its potential as a therapeutic target for preventing hearing loss in cancer patients.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"517 ","pages":"Article 154229"},"PeriodicalIF":4.8,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144576332","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}

引用次数: 0

Retraction notice to “Arsenic-induced mitochondrial instability leading to programmed cell death in the exposed individuals" [Toxicology 246 (2008) 101–111] 对“砷诱导的线粒体不稳定导致暴露个体的程序性细胞死亡”的撤回通知[毒理学246(2008)101-111]。

IF 4.6 3区医学

Toxicology Pub Date : 2025-07-01 DOI: 10.1016/j.tox.2025.154228

Nilanjana Banerjee , Mayukh Banerjee , Sudipto Ganguly , Santu Bandyopadhyay , Jayanta K. Das , Apurba Bandyopadhay , Mitali Chatterjee , Ashok K. Giri

引用次数: 0

miR-144-3p suppression mediates Nrf2 activation induced by developmental arsenic exposure in mice miR-144-3p抑制介导发育性砷暴露小鼠诱导的Nrf2激活。

IF 4.8 3区医学

Toxicology Pub Date : 2025-06-30 DOI: 10.1016/j.tox.2025.154227

Ruirui Wu , Xin Chen , Yongqin Xia , Mengqi Cui , Sihang Hou , Yuxin Hu , Huihui Wang , Jingbo Pi , Yuanyuan Xu

{"title":"miR-144-3p suppression mediates Nrf2 activation induced by developmental arsenic exposure in mice","authors":"Ruirui Wu , Xin Chen , Yongqin Xia , Mengqi Cui , Sihang Hou , Yuxin Hu , Huihui Wang , Jingbo Pi , Yuanyuan Xu","doi":"10.1016/j.tox.2025.154227","DOIUrl":"10.1016/j.tox.2025.154227","url":null,"abstract":"<div><div>Developmental arsenic exposure enhances the risk for hepatic diseases in later life, which has been found to be related to Nrf2 activation. Epigenetic alterations are suggested to contribute to Nrf2 activation but the potential mechanism is to be elucidated. This study reveals that developmental exposure to 0.5 ppm arsenic induced a 1.5-fold increase in hepatic Nrf2 activity in weaned pups, as indicated by over-expression of Nrf2 and its downstream genes. Blood GSH/GSSG ratio showed a 4.4-fold increase in pups after 0.5 ppm arsenic exposure. <em>Nrf2</em> deficiency attenuated arsenic-induced GSH/GSSG ratio elevation. DNA methylation at the global level and Nrf2 promoter region was not significantly altered in the liver of pups exposed to arsenic during the developmental stage. The levels of miR-144-3p and miR-27a-3p in the liver of pups were significantly decreased to 40 % and 70 % of control by 0.5 ppm arsenic exposure, respectively. The levels of miR-101a-3p and miR-155-5p in the liver of pups were significantly increased to 2.2 and 1.8-fold of control by 0.5 ppm arsenic exposure, respectively. Notably, transfection with a miR-144-3p inhibitor significantly increased mRNA levels of <em>Nrf2</em> (2.2-fold) and its target genes <em>Gsr</em> (1.8-fold), <em>Gclc</em> (1.5-fold), and <em>Gclm</em> (2.0-fold) in primary mouse hepatocytes. Taken together, our data suggest that developmental arsenic exposure induced activation of Nrf2 via miR-144-3p suppression.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"517 ","pages":"Article 154227"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144555028","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}

引用次数: 0

Deficiency of aldehyde dehydrogenase 2 sensitizes cells to glutamate-induced cytotoxicity via elevation of GluN1 expression 醛脱氢酶2缺乏通过升高GluN1表达使细胞对谷氨酸诱导的细胞毒性敏感。

IF 4.8 3区医学

Toxicology Pub Date : 2025-06-29 DOI: 10.1016/j.tox.2025.154226

Jing Zhang, Yan Zhao

{"title":"Deficiency of aldehyde dehydrogenase 2 sensitizes cells to glutamate-induced cytotoxicity via elevation of GluN1 expression","authors":"Jing Zhang, Yan Zhao","doi":"10.1016/j.tox.2025.154226","DOIUrl":"10.1016/j.tox.2025.154226","url":null,"abstract":"<div><div>Glutamate is the principal excitatory neurotransmitter in the central nervous system. It is essential for neurotransmission and synaptic plasticity; however, excessive glutamate leads to neuronal toxicity, which is considered as a key mechanism contributing to neurodegeneration. Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme in ethanol metabolism, which converts the toxic alcohol metabolite acetaldehyde to acetate; meanwhile, ALDH2 is also important for the detoxification of other reactive aldehydes such as lipid peroxidation product 4-hydroxy-2-nonenal. ALDH2 deficiency has been associated with the acceleration of neurodegeneration and cognitive impairment accompanied by increased brain oxidative damages. However, there is a lack of reports on how ALDH2 deficiency affects glutamate-induced cytotoxicity. In the present study, it was found that ALDH2-deficient N2a cells exhibited heightened susceptibility to glutamate, displaying aggravated oxidative stress, mitochondrial dysfunction, and calcium imbalance in response to glutamate. ALDH2 deficiency led to reduced antioxidant capacity and elevated intracellular calcium concentration at basal state, thus predisposing the cells to a higher sensitivity to glutamate. Further analyses showed that ALDH2 deficiency elevated the expression of GluN1 subunit of N-methyl-D-aspartate receptors (NMDARs), which are major ionic glutamate receptors allowing the passage of calcium. Consistently, treatment with the NMDAR channel blocker MK-801 (100 μM) or knockdown of GluN1 reduced the susceptibility of <em>Aldh2</em><sup>-/-</sup> cells to glutamate, suggesting that the elevation of GluN1 was a key determinant for the increased sensitivity of ALDH2-deficient cells to glutamate-induced cytotoxicity. The results demonstrated that ALDH2 plays a critical protective role in glutamate-induced neuronal cytotoxicity, while blocking the overactivation of NMDARs might be beneficial for preventing glutamate-induced neuronal toxicity in individuals with defective ALDH2.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"517 ","pages":"Article 154226"},"PeriodicalIF":4.8,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144544977","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}

引用次数: 0

Cadmium-mediated autophagy increases ferroptosis of ovarian granulosa cells 镉介导的自噬增加卵巢颗粒细胞的铁下垂

IF 4.8 3区医学

Toxicology Pub Date : 2025-06-24 DOI: 10.1016/j.tox.2025.154224

Lu Yang , Yanling Xu , Yixiao Gao , Xiaoyan Wan , Na Chen

{"title":"Cadmium-mediated autophagy increases ferroptosis of ovarian granulosa cells","authors":"Lu Yang , Yanling Xu , Yixiao Gao , Xiaoyan Wan , Na Chen","doi":"10.1016/j.tox.2025.154224","DOIUrl":"10.1016/j.tox.2025.154224","url":null,"abstract":"<div><div>Cadmium (Cd) is a pervasive environmental toxicant that poses significant threats to female reproductive health. Accumulating evidence has linked Cd exposure to ovarian dysfunction and infertility. As critical somatic components of ovarian follicles, granulosa cells (GCs) regulate folliculogenesis and oocyte maturation, and their dysfunction is implicated in various reproductive disorders including premature ovarian insufficiency (POI) and polycystic ovary syndrome (PCOS). However, the precise mechanisms underlying Cd-induced GC injury are not yet fully understood. Here, we demonstrate that Cd exposure triggers GC death via ferroptosis, an iron-dependent form of regulated cell death characterized by uncontrolled lipid peroxidation. Mechanistically, Cd induces mitochondrial dysfunction and glutathione peroxidase 4 (GPX4) downregulation, leading to reactive oxygen species (ROS) accumulation and subsequent oxidative damage. Intriguingly, we identified autophagy activation as a key regulator of Cd-triggered ferroptosis, evidenced by increased LC3-II conversion and autophagic flux. Importantly, the protective effect of chloroquine (Cq) against Cd-induced cell death provides compelling evidence for the essential role of autophagic activation in mediating Cd-triggered ferroptosis. Our findings not only elucidate a novel molecular pathway connecting Cd exposure to female infertility but also provide preclinical evidence for targeting the autophagy-ferroptosis axis in reproductive toxicology.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"517 ","pages":"Article 154224"},"PeriodicalIF":4.8,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144501691","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}

引用次数: 0

The Cost Outcome Pathway framework: Integrating socio-economic impacts to Adverse Outcome Pathways for supporting policy makers 成本结果路径框架：将社会经济影响与不利结果路径相结合，以支持政策制定者

IF 4.8 3区医学

Toxicology Pub Date : 2025-06-24 DOI: 10.1016/j.tox.2025.154225

Thibaut Coustillet , Angela Bearth , Xavier Coumoul , Anne-Sophie Villégier , Michèle Bisson , Ellen Fritsche , Jean-Marc Brignon , Florence Zeman , Karine Audouze

{"title":"The Cost Outcome Pathway framework: Integrating socio-economic impacts to Adverse Outcome Pathways for supporting policy makers","authors":"Thibaut Coustillet , Angela Bearth , Xavier Coumoul , Anne-Sophie Villégier , Michèle Bisson , Ellen Fritsche , Jean-Marc Brignon , Florence Zeman , Karine Audouze","doi":"10.1016/j.tox.2025.154225","DOIUrl":"10.1016/j.tox.2025.154225","url":null,"abstract":"<div><div>The Adverse Outcome Pathway (AOP) concept leverages existing data to formalize and disseminate knowledge and is a well-accepted concept in chemical risk assessment. However, it does not handle the socio-economic impact that environmentally-induced diseases may generate, which might be highly relevant for risk management and prioritization. Here, we propose to connect the AOP framework by bridging an Adverse Outcome (AO) to Cost Outcomes (CO) creating so-called Cost Outcome Pathways (COPs) for including the socio-economic costs of exposure to chemicals into the AOP framework. Exposures to certain classes of chemicals have been linked to loss of intellectual quotient (IQ) points in children. This may lead to healthcare costs and reduced working productivity and contribute to increasing the substantial socio-economic burden worldwide. As an <em>in silico</em> case study, a new COP related to neurodevelopmental toxicity was designed, with a connection between the AO ‘decreased, IQ’ and an umbrella CO ‘increased, socio-economic burden’. This framework can support policymaking in the public health sector and might also hold great potential for other environmental exposure-related diseases such as cancer, obesity or neurodegeneration, which are diseases known to have detrimental socio-economic impacts.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"517 ","pages":"Article 154225"},"PeriodicalIF":4.8,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144490107","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}

引用次数: 0

Transcriptomic dose response assessment of PFAS chemicals 3:3 fluorotelomer carboxylic acid, 7:3 fluorotelomer alcohol, and perfluorohexanesulfonamide PFAS化学物质3:3氟端粒羧酸、7:3氟端粒醇和全氟己胺的转录组剂量反应评估。

IF 4.8 3区医学

Toxicology Pub Date : 2025-06-20 DOI: 10.1016/j.tox.2025.154223

Esra Mutlu, Leah Wehmas, Alison H. Harrill, Michael Devito, Russell S. Thomas, Michael F. Hughes, Denise Macmillan, Amanda Brennan, Jackson Bounds, Chelsea A. Weitekamp, Logan J. Everett

{"title":"Transcriptomic dose response assessment of PFAS chemicals 3:3 fluorotelomer carboxylic acid, 7:3 fluorotelomer alcohol, and perfluorohexanesulfonamide","authors":"Esra Mutlu, Leah Wehmas, Alison H. Harrill, Michael Devito, Russell S. Thomas, Michael F. Hughes, Denise Macmillan, Amanda Brennan, Jackson Bounds, Chelsea A. Weitekamp, Logan J. Everett","doi":"10.1016/j.tox.2025.154223","DOIUrl":"10.1016/j.tox.2025.154223","url":null,"abstract":"<div><div>Per- and polyfluoroalkyl substances (PFAS) are a diverse class of anthropogenic chemicals, and their widespread use in manufacturing and commerce has led to introduction of these chemicals into the environment. Owing to the lack of traditional toxicology data on the majority of PFAS, novel testing methods that provide supporting information to inform human health impacts in a relatively short time frame will be increasingly important. The US Environmental Protection Agency’s (EPA) Transcriptomic Assessment Process (ETAP) was recently implemented by the Agency as an efficient and cost-effective method to begin assessing potential human health impacts of chemicals that lack traditional toxicity testing data. The method involves short-term oral dosing in male and female adult rats over a five-day interval, followed by transcriptomic dose-response assessment in twelve tissues to determine a point of departure. The ETAP point of departure identifies the dose at which there are no coordinated transcriptional changes that would indicate a potential toxicity of concern. However, this approach does not explore any specific association with hazard or mechanism. Reported here are ETAP results for three PFAS chemicals: 3:3 fluorotelomer carboxylic acid (3:3 FTCA), 7:3 fluorotelomer alcohol (7:3 FTOH), and perfluorohexanesulfonamide (PFHxSA). The transcriptomic points of departure associated with the tested chemicals, as assessed via ETAP and allometrically scaled to human equivalent doses, were 0.00235 (3:3 FTCA), 0.0152 (7:3 FTOH), and 0.00358 (PFHxSA) mg/kg-day.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"517 ","pages":"Article 154223"},"PeriodicalIF":4.8,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144369245","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}

引用次数: 0

Assessing the impact of in vitro xenobiotic metabolism on estrogenic chemical bioactivity in high-throughput profiling assays 在高通量谱分析中评估体外外源代谢对雌激素化学生物活性的影响。

IF 4.8 3区医学

Toxicology Pub Date : 2025-06-19 DOI: 10.1016/j.tox.2025.154215

Amanda Jurgelewicz , Kristen Breaux , Clinton M. Willis , Felix R. Harris , Gabrielle Byrd , Joshua Witten , Derik E. Haggard , Chad Deisenroth , Joshua A. Harrill

{"title":"Assessing the impact of in vitro xenobiotic metabolism on estrogenic chemical bioactivity in high-throughput profiling assays","authors":"Amanda Jurgelewicz , Kristen Breaux , Clinton M. Willis , Felix R. Harris , Gabrielle Byrd , Joshua Witten , Derik E. Haggard , Chad Deisenroth , Joshua A. Harrill","doi":"10.1016/j.tox.2025.154215","DOIUrl":"10.1016/j.tox.2025.154215","url":null,"abstract":"<div><div>High-throughput profiling assays such as high-throughput phenotypic profiling (HTPP) with Cell Painting and high-throughput transcriptomics (HTTr) are new approach methods that have been used to characterize the bioactivity and potential hazards of chemicals. To enhance the ability to identify potential <em>in vivo</em> hazards during chemical screening, we previously coupled both assays to an <em>in vitro</em> metabolism platform, Alginate Immobilization of Metabolic Enzymes (AIME). In this study, we used the AIME platform to expand upon our previous results for three estrogenic reference chemicals by screening an additional 40 chemicals anticipated to have varied activity and/or shifts in activity with metabolism in an estrogen receptor transactivation assay (ERTA) in VM7Luc4E2 breast carcinoma cells. The results demonstrated that HTTr could detect estrogen receptor (ER) activation and identify chemicals with metabolism-induced shifts in estrogenicity via ER gene signature enrichment analysis. Additionally, HTPP could detect cases where metabolism impacted chemical cytotoxicity and cases where metabolites generated by AIME produced distinct bioactivity profiles compared to their respective parent compounds. Notably, our findings highlighted examples of chemicals that had very different phenotypic and gene expression profiles between metabolic conditions that would not be observed in traditional chemical screening in most immortalized cell line models. Incorporation of metabolism using the AIME platform into high-throughput profiling assays could help inform next generation risk assessment by providing more comprehensive hazard characterizations.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"517 ","pages":"Article 154215"},"PeriodicalIF":4.8,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340423","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}

引用次数: 0

Effects of miR-200b-3p and miR-424–5p regulating notch signaling pathway on atherosclerosis induced by PM2.5 in vitro miR-200b-3p和miR-424-5p调控Notch信号通路在体外pm2.5诱导动脉粥样硬化中的作用

IF 4.8 3区医学

Toxicology Pub Date : 2025-06-17 DOI: 10.1016/j.tox.2025.154216

Tianyang Zhao, Xu Li, Zhili Ge, Jingjing Shi, Tianyou Wang, Jiaxin Zhang, Xinyu Zhang, Huibin Jiang, Liting Zhou, Lin Ye

引用次数: 0