Journal of Applied Toxicology最新文献

{"title":"Hepatic Biotransformation in Climbing Perch Anabas testudineus Exposed to Polystyrene Microplastics at Environmentally Relevant Concentrations.","authors":"Reeha Mashirin, Kumari Chidambaran Chitra","doi":"10.1002/jat.4772","DOIUrl":"https://doi.org/10.1002/jat.4772","url":null,"abstract":"<p><p>Polystyrene microplastics (PS-MPs) are an emerging environmental pollutant posing significant risks to aquatic organisms. This study investigates the hepatic biotransformation responses and histopathological changes in the liver tissues of Anabas testudineus exposed to environmentally relevant concentrations of PS-MPs (13.6 and 23.6 mg L^-1) over durations of 1, 7, 15, 30, and 60 days, followed by a 60-day depuration phase. The study assessed the activities of key phase I and phase II detoxification enzymes in cytosolic and microsomal fractions, including ethoxyresorufin-O-deethylase (EROD), pentoxyresorufin O-dealkylase (PROD), flavin-containing monooxygenase (FMO), NADPH-cytochrome P450 reductase (CPR), sulfotransferase (SULT), UDP-glucuronosyltransferase (UGT), and glutathione S-transferase (GST), alongside mRNA expression analysis of Cyp1a1 and Ugt. Results indicated significant induction of phase I enzymes, particularly EROD, and a subsequent alterations in phase II enzyme activities, reflecting an adaptive detoxification response. Histopathological examination revealed persistent lesions, necrosis, vacuolization, and melanomacrophage aggregation, even after the depuration period, indicating liver tissue damage. The findings highlight the adverse effects of A. testudineus to MP exposure and suggest potential risks to other aquatic organisms, emphasizing the importance of mitigating plastic pollution in aquatic environments.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Samarium Oxide Exposure Induces Toxicity and Cardiotoxicity in Zebrafish Embryos Through Apoptosis Pathway.","authors":"Yan Liu, Ruxia Pu, Bo Zou, Xiaojia Zhang, Xiaohui Wang, Haijing Yin, Jing Jin, Yabin Xie, Yuting Sun, Xiaoe Jia, Yannan Bi","doi":"10.1002/jat.4774","DOIUrl":"https://doi.org/10.1002/jat.4774","url":null,"abstract":"<p><p>As a light rare earth element, Sm and Sm₂O₃ are widely used in various fields such as electronics, chemistry, and medicine. Their distribution in the environment, accumulation in biological organisms and exposure through medicinal pathways have attracted increasing public attention. It is crucial to clarify the impact of Sm₂O₃ on human health. In this study, we applied Sm₂O₃ to 24 h post-fertilization (hpf) zebrafish embryos and investigated the toxic effects and mechanisms of Sm₂O₃. The results showed that Sm₂O₃ induced developmental abnormalities in zebrafish embryos, such as prominent pericardial swelling, slight curvature of the spine, and decreased body length. The incidence of abnormalities in zebrafish significantly increased. The scanning electron microscopy and transmission electron microscopy results showed that Sm₂O₃ accumulated in the zebrafish induced the shortening or disappearance of microcrest in zebrafish skin cells. The Lyz-fish system results demonstrated that macrophages migrated to the skin, suggesting that Sm₂O₃ caused damage. Laser confocal microscopy revealed that the heart ventricles of zebrafish embryos exhibited compensatory swelling, ventricular atrophy, and abnormal heart rates. Acridine orange (AO) staining showed obvious green fluorescence. Embryos proteins at 96 hpf were extracted after Sm₂O₃ treatment, revealing that the anti-apoptosis bcl-2 protein decreased with an increase in the Sm₂O₃ concentration. The caspase-3 apoptosis executioner protein also showed concentration-dependent expression, indicating that Sm₂O₃ promotes apoptosis in cardiac tissue cells. DCFH-DA staining showed significant reactive oxygen species (ROS) accumulation in the hearts and brains in zebrafish. In summary, Sm₂O₃ caused ROS accumulation and activated apoptotic pathways in zebrafish embryos, thereby inducing developmental abnormalities and exhibiting biological toxicity. This study demonstrated that 3-day exposure of 24 hpf zebrafish embryos to Sm₂O₃ resulted in pericardial edema, body length reduction, macrophage migration, and shortened micro-ridges of skin cells. Notably, cardiac anomalies included ventricular swelling, atrophy, and arrhythmia, which correlated with elevated ROS levels and apoptotic signals. Mechanistically, Sm₂O₃ promoted apoptosis through downregulation of Bcl-2 and upregulation of caspase-3 expression. These findings collectively reveal that Sm₂O₃ induces developmental toxicity via ROS accumulation and activation of caspase-dependent apoptotic pathways, highlighting its potential biological hazards in early vertebrate development.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic Insights and Pharmacological Approaches for Nitrogen and Sulfur Mustards and Their Implications as Therapeutic Agents.","authors":"Madison Owens, Anita Thyagarajan, Jeffrey B Travers, Ravi P Sahu","doi":"10.1002/jat.4770","DOIUrl":"https://doi.org/10.1002/jat.4770","url":null,"abstract":"<p><p>Nitrogen and sulfur mustards, often acting as vesicants, have significant consequences for public health. Skin is a common site for exposure to these vesicants that can result in considerable morbidity and mortality. Given that the treatment options are limited, new insights into the mechanisms for the toxicity of these vesicants that can be translated into preventative/therapeutic strategies are desperately needed. Importantly, like most antineoplastic agents, including chemotherapy, the cytotoxic activity of vesicants such as nitrogen mustard (i.e., mustargen/mechlorethamine) and sulfur mustard is primarily mediated via their ability to act as alkylating agents. The current review highlights the underlying mechanisms, effects as well as approaches to mitigate sulfur and nitrogen mustard-induced effects, and their potential to be explored as therapeutic agents. Insights into the mediating roles and impacts of mustard agents could lead to future research and interventions that raise public health awareness to circumvent their adverse events and exploit desirable effects against proliferative diseases such as cancer.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prolonged Low-Dose Chromium (VI) Exposure Induces Oxidative Stress, Apoptotic Genes and Epigenetic Modification of DNA Repair Genes in the Brain and Kidney of Swiss Albino Mice.","authors":"Shehnaz Islam, Sunanda Mukherjee, Olivia Sarkar, Sreejata Kamila, Ansuman Chattopadhyay","doi":"10.1002/jat.4769","DOIUrl":"https://doi.org/10.1002/jat.4769","url":null,"abstract":"<p><p>Hexavalent chromium (Cr (VI)) poses a major health risk due to its high solubility and cell permeability, often exceeding permitted drinking water limits globally. Research has highlighted a strong correlation between Cr (VI) exposure through drinking water and increased cancer rates, particularly in near chrome industries. Our previous research demonstrated that chronic low-dose Cr (VI) exposure (2, 5 and 10 ppm) via drinking water stimulated hepatotoxicity in Swiss albino mice. In this study, we investigated the effects of the same doses over 4 and 8 months on the brain and kidney tissues of Swiss albino mice. It was found that oxidative stress markers, including catalase activity, malondialdehyde (MDA) and reduced glutathione (GSH) levels, were significantly elevated in both the tissues post-treatment. Prolonged exposure to Cr (VI) led to DNA fragmentation and a reduced organo-somatic index in the affected tissues. Additionally, histoarchitectural alterations were observed in the brain and kidney. Apoptotic gene expression was significantly upregulated after 8 months of exposure, confirmed by immunohistochemical studies indicating apoptosis. DNA repair genes (Rad51, Mutyh, Ogg1, and Mlh1) and genes coding enzymes regulating epigenetics (Sirt1, Dnmt1, Kdm1a, and Ezh2) showed significantly varied expression patterns compared to control. Methylation-specific PCR revealed DNA hypermethylation as a factor in the transcriptional reduction of specific DNA repair genes in these tissues. This study denotes that long-term low-dose Cr (VI) exposure not only surges oxidative stress and changes histoarchitecture and gene expression but also results in epigenetic modifications via DNA hypermethylation, impacting organs like the brain and kidney.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to Polystyrene Nanoplastics Compromise Ovarian Reserve Function and Endometrial Decidualization in Early Pregnant Mice.","authors":"Qian-Feng Qiao, Li-Qing Wang, Qiong-Jun Xu, Xiao-Mei Wu, Qi-Duo Chen, Tao-Yu Sheng, Man-Xue Cui, Jing-Ai Li, Xiao-Qing Pang, Yong-Jiang Zhou","doi":"10.1002/jat.4765","DOIUrl":"https://doi.org/10.1002/jat.4765","url":null,"abstract":"<p><p>In the environment, nanoplastics (NPs) have been shown to adversely impact reproductive health, yet research on their effects during early pregnancy is scarce. This study investigated the impact of NPs on endometrial decidualization in early pregnant mice and fertility. Female mice were administered polystyrene nanoplastics (PS-NPs) orally for 90 days before pregnancy. Our findings indicated that PS-NPs exposure decreased the live birth rate and neonatal crown-rump length. Decreased embryo implantation sites and uterine wet weight were observed post PS-NPs exposure. Histological examination revealed structural defects in the uteri of early pregnant mice and a significant reduction in follicular count across all stages in the PS-NPs-treated groups. Serum levels of estradiol (E₂) and progesterone (P) were elevated, while follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were diminished post-exposure. Additionally, PS-NPs exposure upregulated the expression of the endometrial decidualization marker HOXA10 in uterine decidua. In conclusion, our results suggest that exposure to PS-NPs may disrupt endometrial decidualization during early pregnancy. This disruption is likely due to the perturbation of hormonal balance within the hypothalamic-pituitary-ovary including FSH, LH, E₂, and P levels. These hormonal alterations may arrest follicular development, consequently leading to detrimental pregnancy outcomes and compromised neonatal birth conditions. Our study provided a new perspective on understanding the possible effects of microplastics on female fertility.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subchronic Toxicity Test of Transgenic Herbicide-Tolerant Soybean ZH10-6 in Rats.","authors":"Chao Han, JinPeng Zhao, Chen Chen, Yan Li, LiLi Shi","doi":"10.1002/jat.4766","DOIUrl":"https://doi.org/10.1002/jat.4766","url":null,"abstract":"<p><p>The herbicide-tolerant soybean ZH10-6 was developed by modifying the Zhonghuang 10 (ZH10) variety with the G2-EPSPS and GAT genes, conferring resistance to glyphosate. This study aimed to assess the potential health effects of ZH10-6 in Sprague-Dawley rats through a 90-day subchronic toxicity test. Seven groups of rats (n = 10/sex/group) were fed a commercial AIN93G diet or diets containing 7.5%, 15%, or 30% ZH10-6 or ZH10 soybeans. General behavior, body weight, and food consumption were monitored weekly. At the end of the study, clinical pathology, including hematology, serum chemistry, urinalysis, and histopathology, were conducted. Throughout the study, all rats remained healthy and showed no abnormal clinical signs. Although some coagulation and serum biochemistry parameters showed statistical differences between groups, all values fell within the historical control ranges and were considered normal biological variability rather than treatment-related effects. The results indicate that ZH10-6 soybean consumption did not cause any adverse health effects in rats. These findings suggest that ZH10-6 is as safe as its nontransgenic parental variety, ZH10, with no evidence of toxicity after 90 days of exposure.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Preliminary Quantitative Risk Assessment for Inhalation Exposure to Glutaraldehyde.","authors":"Sudha P Pandalai, David A Dankovic","doi":"10.1002/jat.4761","DOIUrl":"https://doi.org/10.1002/jat.4761","url":null,"abstract":"<p><p>Glutaraldehyde (Chemical Abstracts Service [CAS] registry number 111-30-8) has various occupational uses and is associated with adverse health effects including respiratory tract irritation, asthma, and chronic obstructive pulmonary disease. A quantitative risk assessment was conducted to evaluate the likelihood of adverse health effects associated with differing levels of occupational inhalation exposure to glutaraldehyde. Dose-response models were fit to data from a 2-year glutaraldehyde inhalation exposure bioassay conducted by the National Toxicology Program. The benchmark concentration lower bound values of 32 and 44 parts per billion (ppb) were based on bioassay data for female rats and mice that developed squamous epithelium inflammation and respiratory epithelium squamous metaplasia, respectively. These values were used as a point of departure to determine exposure levels relevant to the occupational setting. Extrapolation from rodents to humans assumed a 40-h workweek and an 8-fold uncertainty factor to account for interspecies and interindividual variability. Adjusted benchmark lower bound concentrations of 3 and 4.1 ppb were calculated for inhalation exposure to glutaraldehyde using the endpoints observed in rat and mouse models. Due to the extrapolation parameters used in deriving this result, these findings have applicability for exposure to glutaraldehyde in the occupational setting.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intestinal Bacterial Dysbiosis and Liver Fibrosis in Mice Through Gut-Liver Axis and NLRP3 Inflammatory Pathway Caused by Fine Particulate Matter.","authors":"Pengfei Fu, Mei Zhang, Lirong Bai, Shanshan Chen, Wenqi Chen, Zhiping Li, Jianwei Yue, Chuan Dong, Ruijin Li","doi":"10.1002/jat.4767","DOIUrl":"https://doi.org/10.1002/jat.4767","url":null,"abstract":"<p><p>Fine particulate matter (PM_2.5) is associated with risks of liver diseases and intestinal bacterial dysbiosis, in which the gut-liver axis regulation mechanisms induced by PM_2.5 exposure are still limited so far. In this study, after 12 weeks of exposure to atmospheric PM_2.5 (64 μg/m³) and clean air in winter in Taiyuan, China, we collected liver and intestinal tissues and serum in male mice to perform toxicology experiments. The results showed that PM_2.5 significantly exacerbated the pathological injury in the liver and intestine and liver fibrosis in mice, along with elevated levels of pro-inflammatory cytokines and lipopolysaccharide (LPS) levels in the serum. PM_2.5 caused abnormal liver function and activated TLR4/NF-κB/NLRP3 pathway in mouse liver. PM_2.5 also significantly inhibited the expression of intestinal mucosal tight junction proteins such as ZO-1 and occludin. Besides, from 16S rRNA gene sequencing results in intestinal and fecal samples, we found that PM_2.5 decreased the diversity and abundance of intestinal bacteria, along with reducing Shannon, Chao1 and Ace indices and increasing Simpson indices. Principal component analysis (PCA) showed that mice's intestinal bacterial composition and β-diversity in the PM_2.5-exposed group significantly differed from the control group. KEGG pathway analyzed key functional genes and metabolic pathways in important mouse bacterial communities in the PM_2.5-exposed group. It suggested that PM_2.5 exposure exacerbates liver fibrosis in mice via the NLRP3 pathway. PM_2.5 caused intestinal mucosal injury, intestinal bacterial disorders and increased LPS levels, leading to the activation of inflammatory pathways, which can exacerbate liver fibrosis via the gut-liver axis.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mechanism of Bisphenol S-Induced Atherosclerosis Elucidated Based on Network Toxicology, Molecular Docking, and Machine Learning.","authors":"Bing Guo, Xuan He","doi":"10.1002/jat.4768","DOIUrl":"https://doi.org/10.1002/jat.4768","url":null,"abstract":"<p><p>The increasing prevalence of environmental pollutants has raised public concern about their potential role in diseases such as atherosclerosis (AS). Existing studies suggest that chemicals, including bisphenol S (BPS), may adversely affect cardiovascular health, but the specific mechanisms remain unclear. This study aims to elucidate the effects of BPS on AS and the underlying mechanisms. Through an extensive search of databases such as ChEMBL, STITCH, SwissTargetPrediction, SuperPred, SEA, and GEO, we identified 34 potential targets related to BPS-induced AS. A target network was constructed using the STRING platform and Cytoscape software. GO and KEGG functional enrichment analysis using the DAVID database revealed that BPS may promote the occurrence of AS by interfering with critical biological processes such as glutathione metabolism, nitrogen metabolism, and tyrosine metabolism. This was followed by the selection of 4 core targets-aminopeptidase n (ANPEP), alcohol dehydrogenase 5 (ADH5), lysosomal pro-x carboxypeptidase (PRCP), and microsomal glutathione s-transferase 1 (MGST1)-using five machine learning methods. These core targets play a pivotal role in BPS-induced AS. Furthermore, molecular docking confirmed the tight binding between BPS and these core targets. In conclusion, this study provides a theoretical framework for understanding the molecular mechanisms of BPS-induced AS and contributes scientific evidence for the development of prevention and treatment strategies for cardiovascular diseases triggered by BPS exposure.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subchronic Inhalation of TiO₂ Nanoparticles Leads to Deposition in the Lung and Alterations in Erythrocyte Morphology in Mice.","authors":"Pavel Kulich, Soňa Marvanová, Radim Skoupý, Miša Škorič, Jan Vysloužil, Omar Šerý, Pavel Mikuška, Lukáš Alexa, Pavel Coufalík, Kamil Křůmal, Pavel Moravec, Zbyněk Večeřa, Miroslav Machala","doi":"10.1002/jat.4759","DOIUrl":"https://doi.org/10.1002/jat.4759","url":null,"abstract":"<p><p>TiO₂ nanoparticles (NPs) are extensively used in various applications, highlighting the importance of ongoing research into their effects. This work belongs among rare whole-body inhalation studies investigating the effects of TiO₂ NPs on mice. Unlike previous studies, the concentration of TiO₂ NPs in the inhalation chamber (130.8 μg/m³) was significantly lower. This 11-week study on mice confirmed in vivo the presence of TiO₂ NPs in lung macrophages and type II pneumocytes including their intracellular localization by using the electron microscopy and the state-of-the-art methods detecting NPs' chemical identity/crystal structure, such as the energy-dispersed X-ray spectroscopy (EDX), cathodoluminescence (CL), and detailed diffraction pattern analysis using powder nanobeam diffraction (PNBD). For the first time in inhalation study in vivo, the alterations in erythrocyte morphology with evidence of echinocytes and stomatocytes, accompanied by iron accumulation in spleen, liver, and kidney, are reported following NP's exposure. Together with the histopathological evidence of hyperaemia in the spleen and kidney, and haemosiderin presence in the spleen, the finding of NPs containing iron might suggest the increased decomposition of damaged erythrocytes. The detection of TiO₂ NPs on erythrocytes through CL analysis confirmed their potential systemic availability. On the contrary, TiO₂ NPs were not confirmed in other organs (spleen, liver, and kidney); Ti was detected only in the kidney near the detection limit.</p>","PeriodicalId":15242,"journal":{"name":"Journal of Applied Toxicology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}