Chemico-Biological Interactions最新文献

{"title":"Review on the role of autophagy in the toxicity of nanoparticles and the signaling pathways involved","authors":"Na Liu,&nbsp;Bo Zhang,&nbsp;Nengming Lin","doi":"10.1016/j.cbi.2024.111356","DOIUrl":"10.1016/j.cbi.2024.111356","url":null,"abstract":"<div><div>As the development of nanotechnology, the application of nanoproducts and the advancement of nanomedicine, the contact of nanoparticles (NPs) with human body is becoming increasingly prevalent. This escalation elevates the risk of NPs exposure for workers, consumers, researchers, and both aquatic and terrestrial organisms throughout the production, usage, and disposal stages. Consequently, evaluating nanotoxicity remains critically important, though standardized assessment criteria are still lacking. The diverse and complex properties of NPs further complicate the understanding of their toxicological mechanisms. Autophagy, a fundamental cellular process, exhibits dual functions—both pro-survival and pro-death. This review offers an updated perspective on the dual roles of autophagy in nanotoxicity and examines the factors influencing autophagic responses. However, no definitive framework exists for predicting NPs-induced autophagy. Beyond the conventional autophagy pathways, the review highlights specific transcription factors activated by NPs and explores metabolic reprogramming. Particular attention is given to NPs-induced selective autophagy, including mitophagy, ER-phagy, ferritinophagy, lysophagy, and lipophagy. Additionally, the review investigates autophagy's involvement in NPs-mediated biological processes such as ferroptosis, inflammation, macrophage polarization, epithelial-mesenchymal transition, tumor cell proliferation and drug resistance, as well as liver and kidney injury, neurotoxicity, and other diseases. In summary, this review presents a novel update on selective autophagy-mediated nanotoxicity and elucidates the broader interactions of autophagy in NPs-induced biological processes. Collectively, these insights offer valuable strategies for mitigating nanotoxicity through autophagy modulation and advancing the development of NPs in biomedical applications.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"406 ","pages":"Article 111356"},"PeriodicalIF":4.7,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142866687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antigen B from Echinococcus granulosus regulates macrophage phagocytosis by controlling TLR4 endocytosis in immune thrombocytopenia","authors":"Yunfei Zhang,&nbsp;Yingbin Yue,&nbsp;Yongfeng Cheng,&nbsp;Hongjie Jiao,&nbsp;Mei Yan","doi":"10.1016/j.cbi.2024.111350","DOIUrl":"10.1016/j.cbi.2024.111350","url":null,"abstract":"<div><div>Immune thrombocytopenia (ITP) is characterized by a reduction in platelet counts, stemming from an autoimmune-mediated process where platelets are excessively cleared by macrophages. This enhanced phagocytosis is a cardinal pathogenic mechanism in ITP. Antigen B (AgB), a principal component of the Echinococcus granulosus cyst fluid, plays a pivotal role in safeguarding the parasite from host immune defenses by modulating macrophage activation. In this study, we explored the potential of AgB to regulate macrophage activation in the context of ITP. Our observations indicated a diminished presence of M1 macrophages and a reduced phagocytic capacity in patients infected with E. granulosus sensu stricto. We isolated AgB from E. granulosus cyst fluid (EgCF) and discovered that it could suppress the polarization of M1 macrophages and weaken their phagocytic activity via Fcγ receptors, consequently alleviating thrombocytopenia in an ITP mouse model. At the molecular level, AgB was found to suppress the activation of nuclear factor kappa B (NF-κB) and interferon regulatory factor 3 (IRF3) by impeding their nuclear translocation, leading to a reduction in the generation of inflammatory cytokines. Furthermore, AgB was shown to inhibit Toll-like receptor 4 (TLR4) endocytosis and the recycling of CD14. In aggregate, our findings uncover a novel immunomodulatory mechanism of AgB, which suppresses macrophage phagocytosis by regulating TLR4 endocytosis and the subsequent activation of NF-κB and IRF3 signaling pathways. These insights shed new light on the molecular intricacies of E. granulosus-induced immune evasion and suggest that AgB may serve as a promising therapeutic agent for ITP.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"406 ","pages":"Article 111350"},"PeriodicalIF":4.7,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Timosaponin B II as a novel KEAP1-NRF2 inhibitor to alleviate alcoholic liver disease:Receptor structure-based virtual screening and biological evaluation","authors":"Junjie Wang ,&nbsp;Baoyi Chen ,&nbsp;Chaofan Cheng ,&nbsp;Qingqing Wang ,&nbsp;Lili Yang ,&nbsp;Zeng Li ,&nbsp;Xiongwen lv","doi":"10.1016/j.cbi.2025.111390","DOIUrl":"10.1016/j.cbi.2025.111390","url":null,"abstract":"<div><div>Oxidative stress induced by excess ethanol is an important factor in the progression of alcoholic liver disease (ALD). In recent years, inhibiting Kelch-like ECH-associated protein 1 (KEAP1) to activate the antioxidant regulator Nuclear factor erythroid 2-related factor 2 (NRF2) has been considered an effective strategy for treating oxidative stress-related diseases, but its application in ALD remains insufficiently explored. This study aims to discover high-affinity inhibitors targeting the KEAP1 receptor. We conducted virtual screening of a compound library based on a structure-based pharmacophore model, ultimately identifying the candidate compound Timosaponin B II (TBII). Subsequently, we established ALD models in AML-12 cells and C57BL/6 mice, and evaluated the therapeutic effects and mechanisms of TBII on ALD using methods including Immunofluorescence, Western blotting, RT-qPCR, Biochemical assays, and histological staining. Results indicate that TBII significantly improved ethanol-induced liver injury, inhibited the elevation of serum Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), Total Cholesterol (T-CHO), and Triglycerides (TG) levels, and reduced lipid droplet accumulation in liver tissues. Furthermore, TBII treatment enhanced the antioxidant capacity of AML-12 cells and mouse liver, increasing Glutathione (GSH) and Superoxide Dismutase (SOD) levels while reducing Malondialdehyde (MDA) and Reactive Oxygen Species (ROS) levels. Mechanistic studies indicated that TBII inhibited the ethanol-induced increase in KEAP1 and reversed the ethanol-induced changes in NRF2 and its downstream targets. In conclusion, this study suggests that TBII may become a potential therapeutic agent for ALD by modulating the KEAP1-NRF2 pathway to alleviate oxidative stress and lipid metabolism abnormalities.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"408 ","pages":"Article 111390"},"PeriodicalIF":4.7,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In memoriam of Professor Eugenio Vilanova","authors":"Jorge Estévez ,&nbsp;Carmen Estevan ,&nbsp;Miguel A. Sogorb","doi":"10.1016/j.cbi.2025.111395","DOIUrl":"10.1016/j.cbi.2025.111395","url":null,"abstract":"","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"408 ","pages":"Article 111395"},"PeriodicalIF":4.7,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Airborne particulate matter inhalation bioaccessibility: A review of methodological aspects","authors":"Marlene Soares ,&nbsp;Helena Oliveira ,&nbsp;Célia Alves","doi":"10.1016/j.cbi.2025.111403","DOIUrl":"10.1016/j.cbi.2025.111403","url":null,"abstract":"<div><div>Research has consistently linked exposure to particulate matter (PM) with adverse health outcomes, including cardiovascular and pulmonary morbidity and mortality. Understanding the mechanisms by which PM leads to these effects on human health is crucial for developing effective mitigation strategies. One aspect of PM research that has gained increasing attention in the past few years is the bioaccessibility of inhaled PM-bound pollutants that have potential to cause adverse health effects. To assess the bioaccessibility of PM-bound pollutants, such as polycyclic aromatic hydrocarbons, phthalate esters, organophosphorus flame retardants and metal(loid)s, simulated lung fluids (SLF) are used as a tool to mimic the conditions in the human respiratory system. In addition to different SLF, various extraction methodologies and experimental conditions (e.g., incubation period, solid to liquid ratio, and pH) have been employed to extract the bioaccessible part of these pollutants, though there is not yet a standardised procedure to do so. This review aims to critically evaluate existing inhalation bioaccessibility methodologies and explore their connection with PM characteristics. More research is needed, and a standardised procedure should be implemented to allow the comparation of data between studies. Better <em>in vitro-in vivo</em> relationships need to be established to enhance the feasibility of <em>in vitro</em> bioaccessibility assays as surrogates in human health exposure assessments. Long-term effects of bioaccessible pollutants and any potential synergetic effects between multiple contaminants should also be explored to assess health repercussions more thoroughly.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"408 ","pages":"Article 111403"},"PeriodicalIF":4.7,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prostate cancer-selective anticancer action of an oxindole derivative via HO-1-mediated disruption of metabolic reprogramming","authors":"Kalpana Ghimire,&nbsp;Bhuwan Prasad Awasthi,&nbsp;Kiran Yadav,&nbsp;Jiwoo Lee,&nbsp;Hyunjin Kim,&nbsp;Byeong-Seon Jeong,&nbsp;Jung-Ae Kim","doi":"10.1016/j.cbi.2025.111393","DOIUrl":"10.1016/j.cbi.2025.111393","url":null,"abstract":"<div><div>Prostate cancer, the second leading cause of cancer-related mortality in men, exhibits distinct metabolic reprogramming involving zinc and citrate metabolism. This study investigated whether targeting this unique metabolic profile could offer an effective therapeutic approach. A series of novel oxindole derivatives were synthesized and evaluated for their inhibitory effects on transcription factors (TFs) and antiproliferative activity across various cancer cell lines. Among these, compound <strong>3D</strong> showed the strongest inhibition of master TFs (HIF-1α, c-Myc, and SP-1) and demonstrated selective antiproliferative activity in prostate cancer cells. In PC-3 and LNCaP cells, compound <strong>3D</strong> suppressed aerobic glycolysis by downregulating lactate-modulating genes (LDHA, MCT1/4, and CAIX) and the zinc influx transporter (ZIP1), without affecting the zinc efflux transporter (ZnT4). Notably, <strong>3D</strong> selectively increased heme oxygenase-1 (HO-1) levels in prostate cancer cells, as shown by the proteome profiler oncogene array assay and confirmed by Western blotting. This response was reversed by ZnCl₂ treatment. The decreases in LDHA, mitochondrial mass (measured by FACS), and cell proliferation induced by compound <strong>3D</strong> were blocked by HO-1-IN-1, an HO-1 inhibitor, and ZnCl₂. Furthermore, <strong>3D</strong> induced a more pronounced reduction in the oxygen consumption rate (OCR) than in the extracellular acidification rate (EACR), indicating a strong effect on oxidative metabolism. <strong>3D</strong> exhibited dose-dependent antitumour efficacy in vivo comparable to that of docetaxel. These findings reveal that the oxindole derivative <strong>3D</strong> substantially lowers intracellular zinc levels, yielding potent antitumour effects in prostate cancer through HO-1 upregulation, which impairs mitochondrial function more significantly than aerobic glycolysis.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"408 ","pages":"Article 111393"},"PeriodicalIF":4.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of cuproptosis in gliomas pathogenesis with targeting options","authors":"Mariam Markouli ,&nbsp;Panagiotis Skouras ,&nbsp;Christina Piperi","doi":"10.1016/j.cbi.2025.111394","DOIUrl":"10.1016/j.cbi.2025.111394","url":null,"abstract":"<div><div>Gliomas constitute the most prevalent primary central nervous system tumors, often characterized by complex metabolic profile, genomic instability, and aggressiveness, leading to frequent relapse and high mortality rates. Traditional treatments are commonly ineffective because of gliomas increased heterogeneity, invasive characteristics and resistance to chemotherapy. Among several pathways affecting cellular homeostasis, cuproptosis has recently emerged as a novel type of programmed cell death, triggered by accumulation of copper ions. Although the precise molecular mechanisms of cuproptosis are not fully elucidated, there is evidence that copper ions can target mitochondrial lipoylated proteins, disrupting the tricarboxylic acid cycle and electron transport chain, thus leading to deregulated mitochondrial metabolism, protein aggregation and cell death. Of importance, altered expression of copper transporters and abnormally high intracellular copper levels have been observed in several cancer types, including gliomas, contributing to tumor growth and metastasis. Furthermore, a range of prognostic models incorporating cuproptosis-related genes and lncRNAs have been proposed and are currently under clinical validation. Drugs modulating cuproptosis or interfering with copper-binding proteins are under development, causing metabolic failure and cell death, thus offering potential new avenues for glioma diagnosis and therapy. In this article, we explore the role of copper metabolism in gliomas and the potential synergistic effects of cuproptosis-based treatments with current therapies, in effective targeting of tumor progression and chemoresistance.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"408 ","pages":"Article 111394"},"PeriodicalIF":4.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3-Nitropropionic acid exposure inhibits embryo development by disrupting mitochondrial function and inducing oxidative stress","authors":"Xu Zhou ,&nbsp;Hongzhen Ruan ,&nbsp;Liuliu Dong ,&nbsp;Yaru Yu ,&nbsp;Yan Sun ,&nbsp;Huifen Xiang ,&nbsp;Yunxia Cao ,&nbsp;Zhiming Ding","doi":"10.1016/j.cbi.2025.111389","DOIUrl":"10.1016/j.cbi.2025.111389","url":null,"abstract":"<div><div>3-Nitropropionic acid (3-NP) is a naturally occurring mycotoxin produced by various fungi and plants. Despite reports on its toxicity, the potential impact of 3-NP exposure on reproductive health remains elusive. To this end, we conducted an <em>in vitro</em> study to investigate the toxic effects of 3-NP on the developmental processes of mouse embryos. Our results suggested that exposure to 50 μM 3-NP resulted in significant pre-implantation developmental arrest , with most embryos arrested at the 2-cell stage, indicating disruption of normal development. Further analysis indicated that 3-NP exposure altered embryonic gene expression, disrupted zygotic genome activation and maternal gene degradation, and inhibited maternal-zygote transition. Moreover, it impaired mitochondrial dysfunction, causing dysfunctional cellular energy metabolism and elevated intracellular oxidative stress, culminating in increased DNA damage. Additionally, 3-NP exposure caused aberrant epigenetic modifications, particularly the upregulation of histone methylation levels, including elevated H3K27me3 and H3K9me3, which are strongly related to gene expression silencing. In summary, this study elucidates the <em>in vitro</em> toxic effects of 3-NP on mouse embryo development and highlights its potential adverse effects on female reproductive health.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"408 ","pages":"Article 111389"},"PeriodicalIF":4.7,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluconazole induces cardiovascular toxicity in zebrafish by promoting oxidative stress, apoptosis, and disruption of key developmental genes","authors":"Hanzhi Wu ,&nbsp;Gang Zhao ,&nbsp;Wubing Feng ,&nbsp;Chenjian Yang ,&nbsp;Yu Jiang","doi":"10.1016/j.cbi.2025.111391","DOIUrl":"10.1016/j.cbi.2025.111391","url":null,"abstract":"<div><div>This study systematically evaluated the toxic effects of fluconazole on the cardiovascular development of zebrafish. Zebrafish embryos were treated with different concentrations of fluconazole (200, 400, and 800 μg/ml) to observe its impact on heart development, reactive oxygen species (ROS) generation, apoptosis, and hemoglobin production. The results showed that as the concentration of fluconazole increased, significant changes in zebrafish heart structure were observed, along with a notable reduction in heart rate. Pericardial edema and cardiac morphological abnormalities were particularly prominent in the high-dose group. In addition, fluconazole treatment significantly increased ROS levels and induced apoptosis in cardiac cells. Enzyme-linked immunosorbent assay (ELISA) results showed that fluconazole treatment significantly increased the malondialdehyde (MDA) content and reduced superoxide dismutase (SOD) and catalase (CAT) activity, suggesting that oxidative stress and cell death may play a key role in its cardiotoxicity. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis revealed that fluconazole treatment significantly affected the expression of several key genes related to heart development and function, particularly cardiac myosin light chain 2 (<em>cmlc2</em>), ventricular myosin heavy chain (<em>vmhc</em>), and myosin heavy chain 6 (<em>myh6</em>), whose expression changes were closely associated with alterations in heart morphology and function. Transcriptomic analysis showed that several signaling pathways related to cardiac development, apoptosis, and metabolism were affected. In summary, this study reveals the multifaceted cardiotoxic mechanisms of fluconazole in zebrafish and provides new insights into drug safety assessment.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"408 ","pages":"Article 111391"},"PeriodicalIF":4.7,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isobolographic interactions of cannabidiol and AM 1172 with cisplatin in human neuroblastoma and glioblastoma cell lines: An in vitro study","authors":"Katarzyna Załuska-Ogryzek ,&nbsp;Paula Wróblewska-Łuczka ,&nbsp;Agnieszka Góralczyk ,&nbsp;Jarogniew J. Łuszczki","doi":"10.1016/j.cbi.2025.111392","DOIUrl":"10.1016/j.cbi.2025.111392","url":null,"abstract":"<div><div>Glioblastoma is the most aggressive brain cancer in humans with very poor prognosis and high mortality rate. Despite advances in treatment, glioblastoma almost always recurs and new therapeutic methods are urgently needed. This study aimed at assessing the cytotoxic and antiproliferative effects of AM 1172 and cannabidiol (two cannabinoid receptor ligands) <em>in vitro</em>, when used alone and in combination with cisplatin (a standard cytotoxic drug), in various human neuroblastoma (CHP-134, KELLY), human glioblastoma (U-87MG and T98G) and rat glioblastoma (C6) cell lines. Our experiments showed that AM 1172 and cannabidiol inhibited cell proliferation with IC₅₀ values in the range of 2.29–17.21 μM (for AM 1172) and 11.61–20.35 μM (for cannabidiol), respectively. The selectivity index for AM 1172 ranged from 0.61 to 4.60 and that for cannabidiol ranged from 1.45 to 2.55 in the studied glioblastoma and neuroblastoma cell lines. With isobolographic analysis, it was found that AM 1172 combined with cisplatin exerted a synergistic interaction in the CHP-134 cell line (p &lt; 0.01). In contrast, AM 1172 when combined with cisplatin produced an antagonistic interaction in the C6 cell line (p &lt; 0.01). The remaining combinations of AM 1172 with cisplatin in the U-87MG, KELLY and T98G cell lines were additive. In case of cannabidiol, its combination with cisplatin produced an antagonistic interaction in the T98G cell line (p &lt; 0.0001), whereas the combinations of cannabidiol with cisplatin in the CHP-134, U-87MG, KELLY, and C6 cell lines were additive in nature. The synergistic and additive interactions for the combination of AM 1172 and cannabidiol with cisplatin seem to be a promising direction in glioblastoma therapy. Unfortunately, the combinations producing antagonistic interactions (AM 1172+cisplatin in C6, and cannabidiol + cisplatin in T98G cell lines) should be avoided due to the antagonistic antiproliferative effect of two-drug mixtures.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"408 ","pages":"Article 111392"},"PeriodicalIF":4.7,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}