Toxicology Research最新文献

{"title":"Catechin designates individual and co-adjuvant antiproliferative effects with docetaxel in prostate cancer cell models.","authors":"Eman E El Nahass, Safaa I Abou Eldahab, Elsayed I Salim","doi":"10.1093/toxres/tfaf057","DOIUrl":"10.1093/toxres/tfaf057","url":null,"abstract":"<p><p>The current study examined the potential therapeutic advantages of catechin, either alone or in combination with docetaxel (DTX), against PC-3 prostate cancer cells. Following the MTT assay's determination of the IC₅₀ concentrations, the cell lines were subjected to 48 h of treatment in the following protocol: untreated PC-3 control cells, docetaxel treatment, catechin (Cat) treatment, and DTX + Cat therapy at a ratio of 1:1. Treatments with DTX and Cat significantly decreased the number of viable cells in PC-3 cells in a dose-dependent manner. Additionally, the combo treatments caused the highest cytotoxicity compared with the other treatments. Also, when DTX and Cat were combined, they caused a significant synergistic effect (CI < 1) (combination index < 1). Furthermore, it was demonstrated that all treatments increased the expression of <i>BAX</i>, <i>Caspase-3</i>, and <i>P21</i> mRNA in PC-3 cells while decreasing that of <i>BCL-2</i> mRNA. The highest proportion of overexpression was observed in the combo therapy. A greater proportion of early and late apoptotic cells were caused by the combined treatment than by > DTX > Cat, according to flow cytometry. DNA damage in PC-3 cells was detected using the comet assay, and values of DNA tail, tail length, and tail moment increased considerably with increasing treatment dose. According to this study, Cat is effective against PC-3 cells when used in conjunction with DTX; by causing apoptosis, it enhances DTX's chemotherapeutic capability in cancerous cells.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf057"},"PeriodicalIF":2.2,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12021262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143951143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reproductive and developmental toxicology of nitrosamines.","authors":"Juan Liu, Wei Xu, Yi Liu, Qi Zhang","doi":"10.1093/toxres/tfaf051","DOIUrl":"10.1093/toxres/tfaf051","url":null,"abstract":"<p><p>With the development of science and technology and the acceleration of industrialization, environmental pollution is becoming more and more serious, and the global fertility rate is decreasing every year, which makes people pay more attention to reproductive health. Nitrosamines are a kind of easy to contact food pollutants, widely exist in pickled food (10.2-14.8 mg/kg) and contaminated water sources (10-150 ng/L), etc. They have been confirmed to be carcinogenic, but the reproductive and developmental toxic effects of nitrosamines have not been systematically reported. Based on relevant researches, the classification, distribution and metabolism kinetics of nitrosamines were summarized in this review. In addition, nitrosamines can inhibit testosterone synthesis (Leydig cells) and spermatogenesis (spermatogenic cells) in F0 male, and reduce ovary functions in F0 female, finally induce parental reproductive toxic effects. Meanwhile, the effects of parental (including maternal pregnancy, paternal) nitrosamine exposure on offspring development (such as cancer susceptibility) and related research deficiencies were summarized. To sum up, this paper systematically reviewed the reproductive and developmental toxic effects caused by exposure to nitrosamines, enabling people to fully understand the negative effects of nitrosamines on the body, so as to effectively avoid and reduce intake in daily life, and at the same time provide a theoretical and literature basis for guiding the healthy life and maintaining fertility.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf051"},"PeriodicalIF":2.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ellagic acid alleviates PM_2.5-induced senescence of lung epithelial cells by mediating autophagy.","authors":"Yuqi Tong, Yanping Lu, Yaqi Li, Jiaquan Ding, Chenxi Yan, Zhihui Deng, Jiekang Chen, Zhaohui Zhang","doi":"10.1093/toxres/tfaf055","DOIUrl":"10.1093/toxres/tfaf055","url":null,"abstract":"<p><p>Fine particulate matter (PM_2.5) exposure is significantly linked to lung epithelial cell senescence, and autophagy dysfunction being a key contributor to the aging process. Although the anti-aging properties of ellagic acid (EA) are well-documented, its specific protective effect on PM_2.5-induced lung epithelial cell senescence still needs to be studied in depth. To investigate the impacts of PM_2.5 on autophagy and senescence in lung epithelial cells, 16HBE and A549 cells were exposed to PM_2.5 suspension. Additionally, to explore the potential intervention effect of EA, cells were pretreated with EA before exposure to PM_2.5 suspension. Cell morphology, proliferation, senescence-related markers, senescence-associated secretory phenotype (SASP), and autophagy-related markers were then assessed. Our results showed that the proliferation of 16HBE and A549 cells were inhibited and autophagy dysfunction and senescence were induced under PM_2.5 exposure. However, pretreatment with EA can significantly improve the obstruction of autophagy flux caused by PM_2.5, thereby effectively alleviating cell senescence. This study reveals the mechanism by which PM_2.5 induces senescence in lung epithelial cells and confirms the protective role of ellagic acid in this process.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf055"},"PeriodicalIF":2.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxic endpoints or ubiquitous expression?","authors":"Rajesh Pamanji, Gisha Sivan","doi":"10.1093/toxres/tfaf052","DOIUrl":"10.1093/toxres/tfaf052","url":null,"abstract":"<p><p>This opinion article questions the underlying causes of malformations observed in early developmental stages of zebrafish exposed to a range of chemicals. The research focuses on determining whether these developmental abnormalities arise due to the inherent sensitivity of zebrafish to chemical exposure or if they are related to the ubiquitous expression of certain genes within the zebrafish genome. By analysing different studies on zebrafish embryos to various chemical agents and analysing the resulting malformations, the study aims to differentiate between the effects of chemical sensitivity and the role of gene expression in developmental disruptions. Findings from this investigation will contribute to a deeper understanding of the mechanisms driving developmental toxicity in zebrafish, with implications for broader environmental and genetic research.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf052"},"PeriodicalIF":2.2,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143951960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benzo(a)pyrene triggers cytotoxicity by disrupting cell cycle dynamics and activating Caspase-3-mediated apoptosis in multiple human cell lines.","authors":"Chul-Hong Kim, Geun-Seup Shin, Sehwan Park, Ji-Young Kim, Mi-Jin An, Hyun-Min Lee, Ah-Ra Jo, Yuna Park, Tae Kyung Hong, Jinho Kim, Yujeong Hwangbo, Jung-Woong Kim","doi":"10.1093/toxres/tfaf053","DOIUrl":"10.1093/toxres/tfaf053","url":null,"abstract":"<p><p>Benzo(a)pyrene (B(a)P), a polycyclic aromatic hydrocarbon (PAH), is a known endocrine disruptor linked to various environmentally induced diseases. While recent studies have explored its role in short- and long-term disease development, there is limited research on B(a)P's cytotoxic effects across different cell types. This study aims to evaluate the cytotoxicity of B(a)P exposure in several human cell lines under controlled conditions. We employed flow cytometry (FACS) for quantitative cytotoxicity analysis at the single-cell level. Our findings revealed that B(a)P exhibited minimal cytotoxicity in lung and liver cells, but potent toxicity in breast cells. Notably, B(a)P-induced cytotoxicity in breast cells was associated with increased cleaved caspase-3 expression, leading to cell death. This process was further linked to cell cycle arrest, as indicated by altered cyclin B1 expression in a B(a)P-dependent manner, resulting in reduced cell viability. In summary, these results suggest that breast cells are particularly sensitive to B(a)P-induced cytotoxicity, which is driven by apoptosis and cell cycle disruption.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf053"},"PeriodicalIF":2.2,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143951380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rice bran extract ameliorate heavy metal mixture induced hippocampal toxicity via inhibiting oxido-inflammatory damages and modulating Hmox-1/BDNF/Occludin/Aβ40/Aβ42 in rats.","authors":"Baridoo Donatus Dooka, Chinna N Orish, Anthonet N Ezejiofor, Theresa C Umeji, Kpobari W Nkpaa, Ifeoma Okereke, Ana Cirovic, Aleksandar Cirovic, Orish E Orisakwe","doi":"10.1093/toxres/tfaf049","DOIUrl":"10.1093/toxres/tfaf049","url":null,"abstract":"<p><p>The hippocampus executes the integration of memory and spatial learning information. This study evaluated the effect of rice bran extract (RBE) on heavy metal mixture (MM) induced hippocampal toxicity and its underlying mechanism in albino rats. Thirty five rats were exposed to MM alone at Pb 20 mg/kg, Al 35 mg/kg, and Mn 0.564 mg/kg body weight or co-exposed with RBE at 125, 250 and 500 mg/kg body weight, 125 RBE mg/kg b.wt only, and 500 RBE mg/kg b.wt only 5 days a wk for 13 wk (90 days). Subsequently, oxidative stress, inflammation (cyclooxygenase-2) and caspase-3, amyloid precursor proteins (Aβ40 and Aβ42), HMOX-1, occludin and BDNF and transcription factor Nrf-2 in the hippocampus were investigated. MM treatment resulted in significantly higher escape latency time than both the control and MM plus RBE group. MM exposure induced increased oxidative stress, inflammation resulting in enhanced hippocampal apoptosis. MM significantly increased bioaccumulation of Pb, Al, and Pb; increased caspase-3, Nrf-2, Aβ40 and Aβ42 and significantly decreased occludin, BDNF, HMOX-1 when compared with the control. All these effects were reversed by RBE. Collectively, RBE ameliorated MM - induced oxidative stress, neuro-inflammation and hippocampal apoptosis via attenuation of oxidative damages of cellular constituents, neuronal inflammation and subsequent down regulation of amyloid precursor proteins Aβ40, Aβ42 and up regulation of occludin, BDNF, HMOX-1 protein expression via Nrf-2 dependent pathways to abrogate hippocampal toxicity associated with spatial learning and memory deficits.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf049"},"PeriodicalIF":2.2,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11975361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive models assessing the impact of intensive care unit admission on the outcomes of acutely poisoned patients.","authors":"Aisha E ElMehy, Ghada N El-Sarnagawy, Basma Adel","doi":"10.1093/toxres/tfaf050","DOIUrl":"10.1093/toxres/tfaf050","url":null,"abstract":"<p><p>Although intensive care unit (ICU) admission is the cornerstone in management of critically acute poisoned patients, the decision of ICU admission is often challenging, especially with limited resources. Hence, our study aimed to assess predictive models of the impact of ICU admission on outcomes of patients with acute poisoning. This retrospective cohort study recruited records of acutely poisoned patients admitted to Tanta University Poison Control Center between 2021 and 2023. Patient demographic and toxicological data, as well as initial clinical and laboratory profiles, were retrieved. Afterward, patients were categorized according to mortality and complicated outcomes. Out of 221 acutely poisoned patients admitted to the ICU, the incidences of mortality and complications in survivors were 54.3% and 57.4%, respectively. Aluminum phosphide (ALP) was the most common cause of poisoning (59%), with a significant association with mortality and predominance in cardiac complications. However, respiratory and neurological complications were evident among illicit substances, cholinesterase inhibitors, and neuropsychiatric drugs. The model anticipating morality included time from presentation to ICU admission, mean arterial pressure (MAP), oxygen saturation, pH, and ALP poisoning. Furthermore, the complication predictive model comprised time from exposure to poison center presentation, time from presentation to ICU admission, and MAP. Both models exhibited good to excellent discrimination performance and consistent calibration. Accordingly, prompt admission of all ALP-poisoned patients to ICU with a highly standardized level of care may alleviate their deleterious outcomes. However, drug categories with reversible courses should be adequately treated with frequent respiratory and hemodynamic monitoring in less-equipped ICUs.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf050"},"PeriodicalIF":2.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Green synthesized zinc oxide nanoparticle with <i>Mentha pulegium</i> L. extracts in A549 cell line, characterization, biological activities, Genotoxicity in comet test and SMART assay in <i>Drosophila melanogaster</i>.","authors":"Dilek Akyil, Edanur Yeniyol","doi":"10.1093/toxres/tfaf046","DOIUrl":"10.1093/toxres/tfaf046","url":null,"abstract":"<p><p>In this study, zinc oxide nanoparticles (ZnO NPs) were obtained by green synthesis method using extracts prepared from <i>Mentha pulegium</i> L. species in order to investigate the cytotoxic, genotoxic and antimicrobial activities of nanoparticles. For the characterization of these nanoparticles, UV-Vis spectrophotometer, FT-IR, XRD and SEM analysis methods were used. For cell culture studies were carried out to determine the cytotoxic and genotoxic activities of ZnO NPs obtained by green synthesis with A549 cell line, which is a lung cancer cell. In the genotoxicity results determined by the Comet method, the highest DNA damage was seen at a concentration of 3.75 mg/mL. The genotoxic activity of different concentrations (0.1, 1, 5, 10 mM) of ZNO NPs were evaluated with SMART assay on <i>Drosophila melanogaster</i>. According to results ZNO NPs applications were found to be similar to the control group in all doses. On the other hand, in order to determine the antimicrobial activity, <i>Escherichia coli</i> (ATTC 25922), <i>Staphylococcus aureus</i> (ATTC 29213), <i>Candida albicans</i> (ATTC 90028), <i>Klebsiella pneumoniae</i> (ATTC 700603) and <i>Salmonella enteritidis</i> (ATTC 13076) microorganisms were cultured and disc diffusion test method was applied. In the disc diffusion test, dose application was made in the range of 15.6-500 mg/mL concentrations and it was observed that inhibition zone was formed at all concentrations.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf046"},"PeriodicalIF":2.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic efficacy to dose-dependent toxicity of Cabazitaxel in C6-induced glioblastoma model of rats.","authors":"Zahra Mohammadzadeh, Mohammad Khaksari, Mohammad Hadi Nematollahi, Reza Kheirandish, Amirhossein Moslemizadeh, Sina Delshad, Sanaz Faramarz, Sara Sheibani Tezerji, Mohammad Torkashvand, Samira Shahba, Hamideh Bashiri","doi":"10.1093/toxres/tfaf048","DOIUrl":"10.1093/toxres/tfaf048","url":null,"abstract":"<p><p>This study was designed to adjust effective chemotherapy doses of cabazitaxel (CBZ) on cognitive behaviors, inflammatory cytokines and oxidative stress parameters, and survival rate in C6-induced GBM of rats. Male Sprague-Dawley rats bearing intra-caudate nucleus (CN) C6 inoculation were randomly divided into nine groups as follows: sham, tumor, Temozolomide (TMZ) vehicle, TMZ, CBZ vehicle, CBZ at doses of 0.5, 1, 2 and 4 mg/kg. Behavioral tests survival rate, histopathology, immunohistochemistry, oxidative stress, and inflammatory cytokines were evaluated. All drug treatments reduced the volume and number of tumor cells dose-dependently and CBZ4 was able to cause the greatest reduction. The %Survival rate of animals using CBZ1 significantly increased compared to other treatment groups. CBZ1 reduced anxiety-like behaviors and increased the balance of the animal with GBM. CBZ1 and CBZ2 groups improved C6-induced learning disabilities. Treatments could ameliorate tumor-induced dysregulation of oxidative stress. TNF-α/IL-10 decreased in the CBZ1 group compared to other treatment groups, which may indicate an improvement in inflammatory balance. Our findings demonstrate that the administration of CBZ at a dosage of 1 mg/kg exerts advantageous impacts on both the survival rate and neurocognitive performance of rats within the GBM model. However, our results showed that CBZ may have toxic effects, especially in a dose of 4 mg/kg.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf048"},"PeriodicalIF":2.2,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143778521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astragaloside IV inhibits nasopharyngeal carcinoma progression by suppressing the SATB2/Wnt signaling axis.","authors":"Yinping Zeng, Tingting Duan, Jiajun Huang, Xiaofeng Wang","doi":"10.1093/toxres/tfaf047","DOIUrl":"10.1093/toxres/tfaf047","url":null,"abstract":"<p><p>Astragaloside IV (AS-IV), a major bioactive component of Astragalus membranaceus, exhibits anti-cancer and anti-inflammatory properties. However, its precise role in nasopharyngeal carcinoma (NPC) remains unclear. This study investigated the effects of AS-IV on NPC progression and its relationship with Special AT-rich binding protein-2 (SATB2), a diagnostic marker for NPC. AS-IV treatment reduced NPC cell viability in a dose-dependent manner, as assessed by CCK-8 assays. Functional experiments, including transwell, immunofluorescence, and flow cytometry assays, demonstrated that AS-IV inhibited cell migration, invasion, and autophagy while promoting apoptosis. Western blot analysis showed that SATB2 expression was significantly elevated in NPC cells, particularly in C666-1 and HK-1 cells. Overexpression of SATB2 partially reversed AS-IV's inhibitory effects on NPC progression. Further analysis revealed that AS-IV suppressed the Wnt signaling pathway by downregulating SATB2 expression, while SATB2 overexpression restored Wnt pathway activation. This effect was reversed upon treatment with the Wnt pathway inhibitor DKK-1. In vivo, AS-IV administration inhibited tumor growth in a nude mouse subcutaneous xenograft model, reduced Ki-67 positivity, and lowered LC3B expression, indicating decreased proliferation and autophagy. However, these effects were diminished upon SATB2 overexpression. These findings suggest that AS-IV exerts anti-tumor effects in NPC by downregulating SATB2 and suppressing Wnt pathway activation, highlighting its potential as a therapeutic agent for NPC.</p><p><strong>Highlights: </strong>Astragaloside IV (AS-IV) reduces nasopharyngeal carcinoma (NPC) cell vitality, suppresses cell migration, invasion and autophagy, and fosters apoptosis.SATB2 exhibits notably high levels in NPC cells.Overexpression of SATB2 counteracts the inhibition of NPC malignant progression by AS-IV.AS-IV impedes NPC progression by decreasing SATB2 and thereby hindering the Wnt pathway.AS-IV deters NPC tumor growth in nude mice.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf047"},"PeriodicalIF":2.2,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143770713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}