Chemico-biological interactions最新文献_第2页

The effects of Co-exposure of tobacco smoke with Dibenzo[a,l]pyrene diol epoxide on molecular targets and immune cells in the mouse oral cavity. 烟草烟雾与二苯并[a， 1]芘二醇环氧化物共暴露对小鼠口腔分子靶点和免疫细胞的影响

IF 5.4

Chemico-biological interactions Pub Date : 2025-10-22 Epub Date: 2025-08-05 DOI: 10.1016/j.cbi.2025.111694

Todd D Schell, Zachary T Bitzer, Kun-Ming Chen, Cesar Aliaga, Yuan-Wan Sun, Dhimant Desai, Matthew Lanza, Jiafen Hu, Neil Christensen, Karam El-Bayoumy

{"title":"The effects of Co-exposure of tobacco smoke with Dibenzo[a,l]pyrene diol epoxide on molecular targets and immune cells in the mouse oral cavity.","authors":"Todd D Schell, Zachary T Bitzer, Kun-Ming Chen, Cesar Aliaga, Yuan-Wan Sun, Dhimant Desai, Matthew Lanza, Jiafen Hu, Neil Christensen, Karam El-Bayoumy","doi":"10.1016/j.cbi.2025.111694","DOIUrl":"10.1016/j.cbi.2025.111694","url":null,"abstract":"Tobacco smoking (TS) is an established etiological factor in the development of head and neck squamous cell carcinoma (HNSCC). We previously developed a mouse model using a select tobacco carcinogen, dibenzo[a,l]pyrene (DB[a,l]P, and its ultimate carcinogenic metabolite diol-epoxide (DB[a,l]PDE) to induce oral squamous cell carcinoma (OSCC) in mice; the molecular characteristics and histological changes observed in the mouse oral cavity mimic those found in human HNSCC. In the present study, using our mouse model, we examined for the first time the co-carcinogenic effects of TS with DB[a,l]PDE on DNA damage, histology, molecular targets, and immune cell regulation. We observed a non-significant increase of the levels of DB[a,l]PDE-DNA adduct in the oral cavity of mice exposed to TS as compared to those exposed to compressed air. Histologically, we observed significant increases in epithelial hyperplasia and epithelial single cell necrosis in TS treated mice. TS significantly enhanced protein expression of NF-κB and Ki67 while the enhancement of COX-2 did not reach significance but p53 expression was significantly decreased. We analyzed immune cell regulation in both spleen and tongue (target organ). No significant changes were observed in the spleen; however, in the tongue, we observed a significantly reduced frequency of CD3+T cells that included reductions of both CD4 and CD8 T cells and a corresponding increase was observed for multiple myeloid cell populations. While preliminary, our results offer the foundation for future research using this mouse model to explore the impact of co-carcinogens/tumor promotors other than TS on critical factors involved in the development of HNSCC.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111694"},"PeriodicalIF":5.4,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12392687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144777259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to testicular damage and impaired spermatogenesis in Wilson disease. 铜暴露会通过 TLR4/NF-κB 信号通路诱发炎症和 PAN 细胞凋亡，导致威尔逊氏病患者的睾丸损伤和精子发生障碍。

Chemico-biological interactions Pub Date : 2024-06-01 Epub Date: 2024-05-17 DOI: 10.1016/j.cbi.2024.111060

Dan Zhao, Limin Wu, Xinru Fang, Luyao Wang, Qianzhuo Liu, Pengyu Jiang, Zhihui Ji, Nian Zhang, Miaozhu Yin, Hui Han

{"title":"Copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to testicular damage and impaired spermatogenesis in Wilson disease.","authors":"Dan Zhao, Limin Wu, Xinru Fang, Luyao Wang, Qianzhuo Liu, Pengyu Jiang, Zhihui Ji, Nian Zhang, Miaozhu Yin, Hui Han","doi":"10.1016/j.cbi.2024.111060","DOIUrl":"10.1016/j.cbi.2024.111060","url":null,"abstract":"Copper is a toxic heavy metal that causes various damage when it accumulates in the body beyond the physiological threshold. Wilson disease (WD) is an inherited disorder characterized by impaired copper metabolism. Reproductive damage in male patients with WD is gradually attracting attention. However, the underlying mechanisms of copper toxicity are unclear. In this study, we investigated the role of inflammation and PANoptosis in testicular damage and impaired spermatogenesis caused by copper deposition using the WD model toxic milk (TX) mice. Copper chelator-penicillamine and toll-like receptor 4 (TLR4) inhibitor-eritoran were used to intervene in TX mice in our animal experiment methods. Testis samples were collected from mice for further analysis. The results showed that the morphology and ultrastructure of the testis and epididymis in TX mice were damaged, and the sperm counts decreased significantly. The TLR4/nuclear factor kappa-B (NF-κB) signaling pathway was activated by copper deposition, which led to the upregulation of serum and testicular inflammatory factors in TX mice. Meanwhile, pyroptosis, apoptosis, and necroptosis were significant in the testis of TX mice. Both chelated copper or inhibited TLR4 expression markedly suppressed the TLR4/NF-κB signaling pathway, thereby reducing the expression of inflammatory factors. PANoptosis in the testis of TX mice was also reversed. Our study indicated that pathological copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to toxic testicular damage and impaired spermatogenesis in WD.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111060"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961149","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}

引用次数: 0

Elucidating the Molecular Mechanisms of Pterostilbene Against Cervical Cancer Through an Integrated Bioinformatics and Network Pharmacology Approach 通过综合生物信息学和网络药理学方法阐明紫檀芪抗宫颈癌的分子机制

Chemico-biological interactions Pub Date : 2024-05-01 DOI: 10.1016/j.cbi.2024.111058

Xiang Li, Dequan Yu, Qiming Wang, Yating Chen, Hanbing Jiang

引用次数: 0

Assessment of anti-hyperglycemic and anti-hyperlipidemic effects of thiazolidine-2,4-dione derivatives in HFD-STZ diabetic animal model 评估噻唑烷-2,4-二酮衍生物在 HFD-STZ 糖尿病动物模型中的降血糖和降血脂作用

Chemico-biological interactions Pub Date : 2024-02-01 DOI: 10.1016/j.cbi.2024.110902

S. Fettach, Fatima Zahra Thari, Khalid Karrouchi, Laila Benbacer, Learn-Han Lee, Abdelhakim Bouyahya, Y. Cherrah, Hassan Sefrioui, Khalid Bougrin, M. El Abbes Faouzi

引用次数: 0

Loss of VRK1 alters the nuclear phosphoproteome in the DNA damage response to doxorubicin VRK1缺失会改变DNA损伤对多柔比星反应的核磷酸蛋白组

Chemico-biological interactions Pub Date : 2024-02-01 DOI: 10.1016/j.cbi.2024.110908

Elena Navarro-Carrasco, Aurora Campos-Díaz, Eva Monte-Serrano, F. Rolfs, Richard de Goeij-de Haas, T. Pham, S. Piersma, Connie R. Jimenez, Pedro A. Lazo

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Neurotoxicity of Pyrethroids in exacerbating neurodegenerative diseases: From animals' models to humans’ studies 拟除虫菊酯在加剧神经退行性疾病方面的神经毒性：从动物模型到人体研究

Chemico-biological interactions Pub Date : 2024-02-01 DOI: 10.1016/j.cbi.2024.110911

Rafael Arsuffi-Marcon, Lizandra Gomes Souza, Artur Santos-Miranda, J. Joviano-Santos

引用次数: 0