Journal of Biochemical and Molecular Toxicology最新文献

{"title":"SOX9, the Master Regulator of Lung Cancer, and a Therapeutic Approach.","authors":"Yongli Chen, Xiaoming Meng, Yanling Chen, Ying Jia","doi":"10.1002/jbt.70862","DOIUrl":"https://doi.org/10.1002/jbt.70862","url":null,"abstract":"<p><p>Dysregulation of transcription factors is a hallmark of lung tumorigenesis, and Sex-determining region Y-box 9 (SOX9) has emerged as a putative master regulator at the intersection of development and malignancy. Building on evidence from lung and other solid tumors, we summarize how aberrant SOX9 expression, shaped by epigenetic modification, post-translational regulation, and non-coding RNAs, drives proliferation, survival, invasion, and therapy resistance. In lung cancer, SOX9 appears to orchestrate a stem-like, plastic cell state, promoting epithelial-mesenchymal transition (EMT), metastatic dissemination, and remodeling of the tumor microenvironment (TME). These context-dependent functions position SOX9 both as an oncogenic driver and, in selected settings, as a modulator of treatment response. This review integrates current mechanistic and translational data to frame SOX9 as a clinically actionable node within key signaling circuits relevant to non-small cell and small cell lung cancer. We highlight emerging strategies that directly or indirectly target SOX9, including interference with upstream pathways, epigenetic reprogramming, and RNA-based approaches designed to modulate SOX9 expression or activity. Finally, we propose SOX9 as a dual biomarker and therapeutic handle to guide rational combination therapies aimed at overcoming drug resistance and improving patient stratification. By connecting molecular insight with unmet clinical needs, this article outlines a conceptual roadmap for SOX9-centered therapeutic approaches in lung cancer. A key novelty of this review is the integration of SOX9-centered molecular mechanisms with therapeutic resistance, biomarker potential, and emerging indirect targeting strategies in lung cancer, thereby providing a translational framework for future SOX9-guided interventions.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70862"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838354","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}

{"title":"Transcriptional Activation of SKA3 by SOX9 Promotes the Malignant Progression of Laryngeal Squamous Cell Carcinoma by Regulating AKR1C1.","authors":"Jing Peng, Zeying Pan, Yan Ruan, Chao Tang","doi":"10.1002/jbt.70874","DOIUrl":"https://doi.org/10.1002/jbt.70874","url":null,"abstract":"<p><p>Laryngeal squamous cell carcinoma (LSCC) is one of the most common types of head and neck cancer, posing a significant threat to public health. The spindle and kinetochore-associated complex subunit 3 (SKA3), a microtubule-binding subcomplex of the outer kinetochore, participates in cancer progression. However, its role in the progression of LSCC remains unclear. This study aimed to investigate the regulatory effects of SKA3 on LSCC progression and its underlying mechanism. In this study, the expression levels of SKA3 and aldo-keto reductase family 1 member C1 (AKR1C1) mRNA were assessed by quantitative real-time PCR. Protein expression was evaluated using western blotting. Cell proliferation was analyzed using the cell counting kit-8 assay, while apoptosis was assessed by flow cytometry. Cell migration and invasion were measured via Transwell assays. The levels of Fe2+ and glutathione were analyzed with colorimetric assays, while reactive oxygen species (ROS) levels were determined by flow cytometry. Chromatin immunoprecipitation and dual-luciferase reporter assays were employed to explore the interaction between SOX9 and SKA3. The impact of SKA3 silencing and AKR1C1 overexpression on tumor formation was investigated using a xenograft mouse model. The results showed that SKA3 expression was elevated in LSCC tissues and cells when compared with corresponding normal tissues and human nasopharyngeal epithelial cells. Silencing SKA3 suppressed LSCC cell proliferation, migration, and invasion, while promoting apoptosis and ferroptosis. SKA3 upregulated AKR1C1, a key ferroptosis-related gene, in TU177 and AMC-HN-8 cells. Overexpression of AKR1C1 mitigated the effects of SKA3 silencing on the malignant phenotypes of these cells. SOX9 was identified as a transcriptional activator of SKA3 in TU177 and AMC-HN-8 cells, and AKR1C1 overexpression reversed the inhibitory effect of SKA3 silencing on tumor growth in vivo. Thus, SKA3 played a pivotal role in the progression of LSCC through the SOX9/SKA3/AKR1C1 axis, suggesting that targeting SKA3 might have significant clinical implications for the treatment of LSCC.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70874"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147815538","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}

{"title":"Classifying Kidney Tumor via Adaptive SE-ResNeXt With Mutli-Novel Loss Function and Renal Mass Segmentation Using Pyramidal Attention-Based R2Unet++ Model.","authors":"Bipin Bihari Jayasingh, H Niroshini Infantia, Tejaswini Panse","doi":"10.1002/jbt.70861","DOIUrl":"https://doi.org/10.1002/jbt.70861","url":null,"abstract":"<p><p>Kidney tumors are one of the prevalent types of tumor globally and it has become a significant health concern. It is the most frequent type of urological tumor. While kidney tumors can present in various forms, the majority of the tumors are malignant. Hence, early detection is needed to reduce the mortality rates, develop preventive measures to minimize their impact and provide effective treatments. Compared to traditional, labor-intensive diagnostic process, deep learning-based automatic detection algorithms can reduce diagnosis time, lower costs and improve accuracy. In this research, a kidney cancer detection model using deep learning is introduced to speed up the diagnosis process with high efficiency. At first, the input images are taken from benchmark sites. Then, segmentation is performed on the input images using developed Pyramidal Attention-based Recurrent Residual Unet++ (PA-R2Unet++) model. The development of a tumor is identified in the early stages by this accurate segmentation procedure. Then, the segmented images are used in the classification procedure and it is accomplished via Adaptive Squeeze-And-Excitation-ResNeXt with Novel Multi-Loss Function (ASE-RX-NMLF). In addition, an Enhanced Arbitrary Value-based Flamingo Search Algorithm (EAV-FSA) is used to tune the parameters from the suggested ASE-RX-NMLF for improving the classification performance. Classifying kidney tumors based on their characteristics helps to enhance the effectiveness of therapies. The efficacy of the developed method is verified by comparing the final results of existing models.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70861"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772326","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}

{"title":"Synthesis, Characterization, and Cytotoxic Activity Properties of Some Novel Purine Derivatives.","authors":"Nurdan Akdoğan, Ayşenur Işgüzar, Senem Akkoc, Muhammed Tilahun Muhammed, Sadeq K Alhag, Laila A Al-Shuraym, Ali Dişli","doi":"10.1002/jbt.70840","DOIUrl":"https://doi.org/10.1002/jbt.70840","url":null,"abstract":"<p><p>This study reports the synthesis of nine new compounds with purine scaffolds. It thoroughly analyzes them using a variety of spectroscopic methods, including high-resolution mass spectrometry (HR-MS), proton nuclear magnetic resonance (¹H NMR), attached proton test nuclear magnetic resonance (¹³C APT NMR), and fourier-transform infrared spectroscopy (FT-IR). The in vitro cytotoxic potential of these compounds was examined using two cancer cell lines: MDA-MB-231, a model of triple-negative breast cancer, and HepG2, a model of liver carcinoma. Furthermore, compounds were tested in a normal mouse fibroblast cell line (L929). Biological screening revealed that two of the synthesized molecules, ethyl 2-(2-(2-(9H-purin-6-yl)hydrazineylidene)-3-(4-methylphenyl)-4-oxothiazolidin-5-ylidene)acetate (4b) and ethyl 2-(2-(2-(9H-purin-6-yl)hydrazineylidene)-3-(4-nitrophenyl)-4-oxothiazolidin-5-ylidene)acetate (4c) exerted cytotoxic effects with IC₅₀ values of 137.10 ± 6.46 and 130.70 ± 5.81 µM against the HepG2 cell line, respectively. At the same time, seven compounds (2b, 3a, 3b, 3c, 4a, 4b, and 4c) exhibited cytotoxic activity against MDA-MB-231 cells with IC₅₀ values of 197.40 ± 5.84, 161.90 ± 4.17, 66.33 ± 2.53, 122.10 ± 3.87, 159.80 ± 4.92, 138.10 ± 3.75, and 131.50 ± 2.46 µM, respectively. Caspase-3 activity assays were performed on the MDA-MB-231 cell line, which exhibited activity, and fluorescence imaging studies were also conducted. To elucidate potential molecular targets, in silico docking analyses were performed, indicating 15-lipoxygenase (15-LOX) as a likely enzymatic target. Among the evaluated molecules, compound 4b demonstrated superior binding affinity toward 15-LOX, even exceeding that of the co-crystallized reference inhibitor. The stability of the 4b-enzyme complex was further supported by molecular dynamics (MD) simulations, which showed an improved interaction profile compared to the original inhibitor-enzyme complex.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70840"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13103636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential of Caffeic Acid in Combating Aluminum and Beryllium Induced Oxidative Injury in Multiorgan: Insight From Hematology, Biochemistry and Histology in Rats.","authors":"Pavitra Behra, Pratima Dutta, Anurag Singh, Satendra Kumar Nirala, Monika Bhadauria","doi":"10.1002/jbt.70849","DOIUrl":"https://doi.org/10.1002/jbt.70849","url":null,"abstract":"<p><p>Metal contamination poses a significant health concern driven by industrialization, landscape modifications, and rapid urbanization. Aluminum and beryllium exposure has been associated with multiple organ dysfunction, including liver, kidney and brain. In present study investigates therapeutic effects of caffeic acid in mitigating liver, kidney and brain damage induced by combined exposure to aluminum and beryllium in female rats. Rats were assigned into five groups. Group 1 served as control. Groups 2-5 were exposed to combination of aluminum nitrate (6.5 mg/kg, i.p.) and beryllium nitrate (1 mg/kg, i.p.) daily for 4 weeks. Groups 3, 4, and 5 received oral doses of caffeic acid (10, 20, and 30 mg/kg, respectively) for 2 weeks after 2 weeks of exposure to toxicants. After 24 h of the last treatment, animals were euthanised, followed by hematology, liver kidney and brain function tests, oxidative stress and antioxidant status in studied organs. Combined exposure to metals significantly altered hematology, liver, kidney and brain function markers. Enzymatic antioxidant defenses, including reduced glutathione, catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione Sulfur transferase, and glucose-6-phosphate dehydrogenase were compromised, whereas lipid peroxidation and cholesterol levels were significantly increased. Histological observations revealed organ injury due to toxic effects of combined exposure to aluminum and beryllium. Caffeic acid treatment exhibited a dose-dependent recovery in these parameters and restored them towards control. These findings suggested that caffeic acid may perform therapeutic role by exerting direct and indirect antioxidant effects against combined exposure to aluminum and beryllium induced injury in multiple organs.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70849"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772404","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}

{"title":"Remodeling the Tumor Immune Microenvironment by Traditional Chinese Medicine: Mechanisms Focusing on TAM Polarization and CD8⁺ T Cell Exhaustion.","authors":"Yannan Geng, Yuanjun Qu, Ji Li, Xinfeng Wang, Changying Ji, Guangze Wang","doi":"10.1002/jbt.70854","DOIUrl":"https://doi.org/10.1002/jbt.70854","url":null,"abstract":"<p><p>This review focuses on two core immunosuppressive mechanisms within the tumor immune microenvironment (TIME): the polarization of tumor-associated macrophages (TAMs) towards an M2 phenotype and the functional exhaustion of CD8⁺ T cells. We systematically elucidate the multi-dimensional strategies by which Traditional Chinese Medicine (TCM) remodels the TIME. The article first dissects the interplay between TAMs and CD8⁺ T cells and their pivotal role in tumor immune escape. It then comprehensively reviews how TCM formulations and active components, through their characteristic multi-target actions, coordinately reverse TAM polarization and T cell exhaustion by modulating key signaling pathways (e.g., STAT, PI3K/Akt), reprogramming cellular metabolism (e.g., glycolysis, oxidative phosphorylation), and reshaping cytokine networks. Particular emphasis is placed on metabolic reprogramming as an upstream \"bridging\" mechanism that concurrently regulates both processes. Finally, the review explores the synergistic potential of combining TCM with immune checkpoint inhibitors and analyzes current challenges, including compositional complexity, insufficient mechanistic depth, and a paucity of high-quality clinical evidence. This work aims to provide a theoretical foundation and forward-looking perspective for developing novel TCM-based strategies in cancer immunotherapy.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70854"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772414","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}

{"title":"Investigation of Malathion-Induced Testicular Inflammation: Role of miR-24-Regulated cGAS-STING Pathway and Autophagy: The Potential Modulatory Effect of Lactobacillus acidophilus.","authors":"Mai A Abd-Elmawla, Hekmat M El Magdoub, Yara M Aboulmagd, Safaa M El-Mahdy, Nesrine Dessouky, Nora M Aborehab","doi":"10.1002/jbt.70865","DOIUrl":"https://doi.org/10.1002/jbt.70865","url":null,"abstract":"<p><p>Malathion (MAL) exerts serious reproductive toxicity in males and leads to histopathological injuries in seminiferous tubules, sperm abnormalities, and hormonal disruptions such as reduced testosterone levels. The study assessed whether Lactobacillus acidophilus (L. acidophilus) supplementation could mitigate MAL-induced testicular damage via the crosstalk of cGAS/cGAMP/STING/NF-κB signaling, which in turn modulates the inflammatory cascades IRF3/IFN-β and TNFR/TNF-α, as well as the autophagic markers such as LC3-B/p62. The study also studied the role of miRNA-24 as an upstream regulator. The study included four groups: control, MAL-intoxicated group, L. acidophilus- and scopolamine-treated group. Seminal analysis and histopathological investigations of the testes were done. cGAS, STING, TNFR, IRF3, and miR-24 were estimated using qRT-PCR. cGAMP, IFN-β, LC3-B, and p62 were estimated using ELISA, whereas NF-κB and TNF-α were estimated using immunohistochemical analysis. MAL-intoxicated group showed altered seminal fluid analysis, higher gene expression of cGAS, STING, TNFR, and IRF3, along with lower gene expression of miRNA-24 compared with the control group. Moreover, the concentrations of cGAMP and IFN-β were higher, along with lower concentrations of testosterone, LC3-B, and p62, compared with the control group. Furthermore, NF-κB and TNF-α showed marked positive cytoplasmic expression. However, the L. acidophilus-treated group reversed all the above-mentioned findings. Collectively, the present study showed that MAL-exposure induces testicular toxicity via activating the cGAS/cGAMP/STING/IRF3/NF-κB/TNF-α axis, mediated by miRNA-24. L. acidophilus treatment alleviated these adverse effects, not only by restoring sperm quality, hormonal balance, and tissue architecture but also by suppressing the inflammatory signaling cascade, reactivating autophagic flux, and upregulating protective miRNA-24.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70865"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772418","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}

{"title":"MicroRNAs as Critical Regulators of Cardiovascular Homeostasis and Disease: Diagnostic and Therapeutic Horizons.","authors":"Heba Ibrahim Abd El-Moaty, Ayman A Doghish, Sherif S Abdel Mageed, Ahmed I Abulsoud, Osama A Mohammed, Ghadir A Sayed, Shereen Saeid Elshaer, Ahmed E Elesawy, Aya Salman, Mohamed Bakr Zaki, Mahmoud A Elrebehy, Rabab S Hamad, Ahmed S Doghish","doi":"10.1002/jbt.70868","DOIUrl":"https://doi.org/10.1002/jbt.70868","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) continue to be the world's leading cause of death, driven by intricate processes such as inflammation, endothelial dysfunction, oxidative stress, and apoptosis. MicroRNAs (miRNAs), small non-coding RNAs that influence mRNA translation, have become recognized as key regulators of these harmful mechanisms in conditions like heart attack, heart failure, and atherosclerosis. Because they remain stable in the bloodstream, miRNAs hold promise as convenient, minimally invasive biomarkers for early CVD detection, assessing risk, and forecasting outcomes. On the treatment side, targeting miRNAs offers a way to correct disrupted molecular pathways with precision, though moving this approach into clinical use presents hurdles such as refining delivery methods, avoiding unintended effects, and achieving specificity for certain tissues. Current studies emphasize progress in understanding how miRNAs contribute to CVD development and their emerging potential in personalized care. Yet, translating these findings into routine practice will require overcoming technical challenges and establishing consistent standards. This evolving area holds great potential to transform cardiovascular medicine through precise diagnostics and targeted therapies, potentially addressing current shortcomings in treatment effectiveness.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70868"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772436","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}

{"title":"MiR-20b-5p Is Involved in Hydroquinone-Induced TK6 Cell Cycle Arrest and Oxidative Damage Through JNK1 Signaling Pathway and Targeting Nrf2.","authors":"Pu Guo, Xiaoyi Hu, Lingxue Yu, Lin Chen, Dewang Wang, Zeqi Ouyang, Lijun Liang, Delong Zhu, Zhuanzhuan Li, Huanwen Tang, Hao Luo","doi":"10.1002/jbt.70866","DOIUrl":"https://doi.org/10.1002/jbt.70866","url":null,"abstract":"<p><p>Hydroquinone (HQ), a metabolic byproduct of benzene, can cause oxidative damage. Oxidative stress triggers the excessive generation of reactive oxygen species (ROS), which in turn elicits diverse forms of cellular injury, including cell cycle arrest. This study sought to investigate the role and underlying regulatory mechanism of miR-20b-5p in HQ-induced cellular injury. The findings indicated that HQ increased the proportion of S-phase cells, indicating S-phase arrest. Furthermore, miR-20b-5p deletion facilitated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream proteins, while also stimulating the expression of downstream proteins associated with c-Jun N-terminal kinase 1 (JNK1). Therefore, we speculate that loss of miR-20b-5p exacerbates HQ-induced cytotoxicity and S-phase cell accumulation, potentially through the JNK1/Nrf2 signaling pathway or via direct regulation of Nrf2.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70866"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772443","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}

{"title":"Correction to \"Cardioprotective Role of 5,7,4'-Trimethoxy Flavanone Through PI3K/AKT-Nrf2 Signaling in Mice\".","authors":"","doi":"10.1002/jbt.70856","DOIUrl":"https://doi.org/10.1002/jbt.70856","url":null,"abstract":"","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 5","pages":"e70856"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772263","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}