Toxicology Research最新文献_第3页

Curcumin nanoparticles ameliorates cardiac toxicity through modulation of oxidative stress, apoptosis, inflammation, and DNA damage in rat. 姜黄素纳米颗粒通过调节大鼠氧化应激、细胞凋亡、炎症和DNA损伤来改善心脏毒性。

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-08-08 eCollection Date: 2025-08-01 DOI: 10.1093/toxres/tfaf112

Ehab Tousson, Doha Mohammad Beltagy, Nagat Fawzy Nawar, Mona A Dora, Hamed Muhammad Abdel Bari, Ibrahim E T El-Sayed

{"title":"Curcumin nanoparticles ameliorates cardiac toxicity through modulation of oxidative stress, apoptosis, inflammation, and DNA damage in rat.","authors":"Ehab Tousson, Doha Mohammad Beltagy, Nagat Fawzy Nawar, Mona A Dora, Hamed Muhammad Abdel Bari, Ibrahim E T El-Sayed","doi":"10.1093/toxres/tfaf112","DOIUrl":"https://doi.org/10.1093/toxres/tfaf112","url":null,"abstract":"Recent studies have highlighted the toxicological impact of nanoparticles, including their role in malignancies and various organ system dysfunctions, however, the effects of nanoparticles on the cardiovascular system remain underexplored. Their fore; this study designed to investigate the therapeutic effect of Curcumin (Cur) and/or Curcumin nanoparticles (CurNPs) against Copper oxide nanoparticles (CuONPs) induced toxicity, DNA damage, oxidative stress, apoptosis and inflammation in rat cardiac tissues. A total of 60 adult male rats were assigned randomly to 6 groups [1st Gp, control; 2nd Gp; Cur; 3rd Gp, Cur NPs; 4th Gp, CuONPs; 5th Gp, CuONPs+Cur; 6th Gp, CuONPs+CurNPs]. Current results revealed, a significant elevation in serum levels of creatine kinase enzyme (CK), lactate dehydrogenase (LDH), C-reactive proteins (CRP), AST, cholesterol, triglycerides, LDL, cardiac MDA, nitric oxide (NO), DNA damage, cardiac TNFα expressions and a significant decline in HDL, cardiac total antioxidant capacity (TAC), reduced glutathione (GSH), catalase, cardiac PCNA, Bcl2 expressions when compared to control. Interestingly, treatment of CuONPs with Cur or CurNPs induced improvements of the studied parameters, heart structure and functions. CuONPs-induced toxicity, injury and oxidative stress in rat heart and the treatment with CurNPs and Cur could scavenge free radicals producing beneficial effects against CuONPs.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf112"},"PeriodicalIF":2.1,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12342465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144843814","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}

引用次数: 0

Biosynthesis of zinc oxide nanoparticles using Sideritis akmanii plant and evaluation of its biological activity. 利用黄芪植物合成氧化锌纳米颗粒及其生物活性评价。

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-08-06 eCollection Date: 2025-08-01 DOI: 10.1093/toxres/tfaf115

Arzu Özkara, Doğukan İşlek

{"title":"Biosynthesis of zinc oxide nanoparticles using Sideritis akmanii plant and evaluation of its biological activity.","authors":"Arzu Özkara, Doğukan İşlek","doi":"10.1093/toxres/tfaf115","DOIUrl":"https://doi.org/10.1093/toxres/tfaf115","url":null,"abstract":"In this study, zinc oxide nanoparticles (ZnONPs) were synthesized by green synthesis technique using the extract obtained from Sideritis akmanii plant and the obtained ZnONPs were characterized by Ultraviolet-Visible Spectrophotometry (UV-VIS), X-Ray Diffraction (XRD) spectrophotometer, Scanning Electron Microscopy (SEM) and Fourier Transform Infrared Spectroscopy (FT-IR) techniques. Cytotoxic effects of both ZnONPs and Sideritis akmanii plant extract on A549 cells were investigated by MMT assay and genotoxic effects by Comet assay method. It was observed that the cytotoxic activity of ZnONP doses was higher than Sideritis akmanii plant extracts. In the comet test, the highest DNA damage (62.25 ± 10.15) was observed in the 10 mg/mL ZnONP application at 48 h of application, DNA damage did not exceed the negative control group at 3 different plant extract doses. Moreover, the genotoxic effects of 4 different concentrations of ZnONPs (0.1, 1, 5, 10 mM) were evaluated on Drosophila melonagaster with the SMART test. The results obtained as a result of ZnONP application were found to be close to the control group and it was determined that no statistically significant genotoxic effect was observed. The antimicrobial activity of ZnONPs on Escherichia coli (ATCC 25922), Staphylococcus aureus (ATCC 29213), Salmonella enteritidis (ATCC 13076), Klebsiella pneumoniae (ATCC 700603) and Candida albicans (ATCC 90028) microorganisms was analyzed using disk diffusion method. According to the antimicrobial and antifungal activity data, it was determined that the synthesized ZnONPs were effective on all microorganism strains used in the study and the inhibition zone diameters ranged from 8 to 13.67 mm.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf115"},"PeriodicalIF":2.1,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144843813","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}

引用次数: 0

Exploring the causal relationship and molecular mechanisms between Methyl-4-hydroxybenzoic acid (MEP) and Alzheimer's disease: a mendelian randomization, multi-omics, and network toxicology approach. 探索甲基-4-羟基苯甲酸（MEP）与阿尔茨海默病之间的因果关系和分子机制：孟德尔随机化、多组学和网络毒理学方法

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-08-06 eCollection Date: 2025-08-01 DOI: 10.1093/toxres/tfaf113

Hong Gong, Jiayu Li, Rong Pu, Jian Huang

{"title":"Exploring the causal relationship and molecular mechanisms between Methyl-4-hydroxybenzoic acid (MEP) and Alzheimer's disease: a mendelian randomization, multi-omics, and network toxicology approach.","authors":"Hong Gong, Jiayu Li, Rong Pu, Jian Huang","doi":"10.1093/toxres/tfaf113","DOIUrl":"10.1093/toxres/tfaf113","url":null,"abstract":"The pathogenesis of Alzheimer's disease remains incompletely understood. Methyl-4-hydroxybenzoic acid, a common chemical additive, may play a role, though its mechanisms are unclear. This research investigated the potential causal link between Methyl-4-hydroxybenzoic acid and Alzheimer's disease and examined underlying molecular mechanisms. Mendelian randomization analysis evaluated causality, using Cochran's Q test, the Mendelian Randomization-Egger intercept test, and Mendelian Randomization Pleiotropy RESidual Sum and Outlier to assess heterogeneity and sensitivity. Methyl-4-hydroxybenzoic acid targets were identified through multiple databases, and a related target library was constructed using Weighted Gene Co-expression Network Analysis, differential gene expression analysis, and the Genecards database. A Protein-Protein Interaction network identified core genes, validated by molecular docking. Transcriptomic analysis and single-cell expression data explored cell-type-specific expression patterns. Results showed a significant positive causal association between Methyl-4-hydroxybenzoic acid and Alzheimer's disease. We identified 198 Methyl-4-hydroxybenzoic acid targets, with 99 genes associated with both Methyl-4-hydroxybenzoic acid and Alzheimer's disease. Six core genes (EGFR, ESR1, MAPK3, MMP9, PTGS2, TP53) were pinpointed. Functional enrichment implicated neuronal signaling, inflammation, and metabolism. Multi-omics and single-cell analyses revealed differential expression of core genes in key brain regions. Molecular docking confirmed stable interactions between Methyl-4-hydroxybenzoic acid and these proteins. This research confirms a causal relationship between Methyl-4-hydroxybenzoic acid and Alzheimer's disease, revealing potential molecular mechanisms and core gene functions, offering insights into pathogenesis and therapeutic targets.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf113"},"PeriodicalIF":2.1,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833430","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}

引用次数: 0

Influence of senescence on the sensitization potential of chemicals detected by local lymph node assays in aged mice. 衰老对衰老小鼠局部淋巴结检测的化学物质致敏电位的影响。

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-08-01 DOI: 10.1093/toxres/tfaf110

Koji Ishida, Mao Kaneki, Chiharu Ohira, Mana Ichikawa, Ibuki Yasuda, Chizuki Usui, Yoshiichi Takagi, Tomoki Fukuyama

{"title":"Influence of senescence on the sensitization potential of chemicals detected by local lymph node assays in aged mice.","authors":"Koji Ishida, Mao Kaneki, Chiharu Ohira, Mana Ichikawa, Ibuki Yasuda, Chizuki Usui, Yoshiichi Takagi, Tomoki Fukuyama","doi":"10.1093/toxres/tfaf110","DOIUrl":"https://doi.org/10.1093/toxres/tfaf110","url":null,"abstract":"The global population is aging rapidly, posing new challenges for the safety evaluation of chemicals. Most toxicity studies use suitably aged animals that resemble healthy adults if they have similar responses. However, this assumption may not be valid because aging affects various physiological functions, such as immunity. The objective of this study was to compare the skin sensitization potential of chemicals in healthy adult mice, aged mice, and an aging mouse model using local lymph node assays (LLNA). Initially, eight-week-old female CBA/Ca, C3H/He (historical control for SAMP1 mice), senescence-accelerated mouse prone 1 (SAMP1), and C57BL6/N mice were compared to verify any differences among these strains. Next, 20-wk-old C3H/He and SAMP1 mice were compared with 80-wk-old C57BL6/N mice. Several concentrations (2.76, 8.3, and 25%) of α-hexyl cinnamaldehyde (HCA) were used as a positive substance for LLNA to determine the skin sensitization potential in each strain. The proliferation of T and B cells and related cytokine production were also measured. A dose-dependent correlation was observed, and a threshold of 1.8 for positive criteria for skin sensitization in LLNA, was surpassed in the CBA/Ca, C3H/He, and C57BL6/N strains, but not in the SAMP1 strain. In 20-wk-old mice, a positive response was observed only in C3H/He mice, whereas no positive response was observed in aged C57BL6 mice and SAMP1 mice. Our findings imply that senescence affects the skin sensitization potential of chemicals as measured using LLNA.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf110"},"PeriodicalIF":2.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774379","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}

引用次数: 0

Albiflorin improves diabetic retinopathy by mitigating oxidative stress and inflammation via the TLR-4/NF-kB signaling pathway. Albiflorin通过TLR-4/NF-kB信号通路减轻氧化应激和炎症，改善糖尿病视网膜病变。

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-08-01 DOI: 10.1093/toxres/tfaf105

Liuyi Xie, Yingjun Wang, Yudan Gong

{"title":"Albiflorin improves diabetic retinopathy by mitigating oxidative stress and inflammation via the TLR-4/NF-kB signaling pathway.","authors":"Liuyi Xie, Yingjun Wang, Yudan Gong","doi":"10.1093/toxres/tfaf105","DOIUrl":"10.1093/toxres/tfaf105","url":null,"abstract":"This study was to investigate the effects of Albiflorin (ALB) on oxidative stress and inflammation in diabetic retinopathy (DR) and explore its potential mechanism involving the Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway. Human retinal microvascular endothelial cells (HRMECs) were treated with high glucose (HG) and ALB. Cell viability was assessed by MTT assay. Oxidative stress markers and inflammatory cytokines were measured by ELISA. TLR4/NF-κB pathway proteins were analyzed by Western blot. A streptozotocin (STZ)-induced diabetic rat model was established to examine retinal histological changes. Serum metabolic parameters, oxidative stress markers, and inflammatory cytokines were evaluated in the DR model and ALB intervention groups. Results showed that ALB improved HRMEC viability under HG induction and reduced oxidative stress and inflammation. ALB inhibited the TLR4/NF-κB pathway in HG-induced HRMECs. Overexpression of TLR4 partially reversed the protective effects of ALB. In diabetic rats, ALB ameliorated metabolic disorders, improved retinal histological structure, and reduced oxidative stress and inflammation. ALB also suppressed the TLR4/NF-κB signaling pathway in vivo. In conclusion, ALB improves DR by resolving oxidative stress and inflammation through inhibiting the TLR4/NF-κB signaling pathway. These findings suggest ALB as a potential therapeutic agent for DR.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf105"},"PeriodicalIF":2.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774378","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}

引用次数: 0

Molecular mechanisms of non-pharmaceutical chemicals exposure-induced liver injury: a network toxicology approach. 非药物化学物质暴露诱导肝损伤的分子机制：网络毒理学方法。

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-08-01 DOI: 10.1093/toxres/tfaf096

Tao Chen, Xing Qian, Zhi Wu

{"title":"Molecular mechanisms of non-pharmaceutical chemicals exposure-induced liver injury: a network toxicology approach.","authors":"Tao Chen, Xing Qian, Zhi Wu","doi":"10.1093/toxres/tfaf096","DOIUrl":"https://doi.org/10.1093/toxres/tfaf096","url":null,"abstract":"The exposure to non-pharmaceutical chemicals has been increasingly associated with liver injury, yet the underlying molecular mechanisms remain unclear. This study investigates the impact of three such chemicals-sunset yellow (SUN), tartrazine (TART), and triclosan (TRI)-on human HepaRG cells to elucidate potential toxicological targets and pathways. We conducted differential expression analysis on HepaRG cells exposed to SUN, TART, and TRI, identifying differentially expressed genes (DEGs). Intersection analyses were performed to uncover common targets, followed by heatmap visualization and enrichment analyses using GO and KEGG pathways. Protein-protein interaction (PPI) and immune cell infiltration analyses further elaborated the effects, complemented by molecular docking studies to assess chemical binding affinities. Our findings identified 47 upregulated and 123 downregulated DEGs as common targets across all chemical exposures. Enrichment analysis revealed significant alterations in biological processes related to liver metabolism and development. Four core toxic targets (KNG1, PLG, SERPINE1, SERPINF2) were identified with significant connectivity in PPI analysis, confirmed by altered gene expression. Immune cell infiltration analysis indicated modulation of various immune cell populations. The molecular docking study highlighted strong binding of TART and SUN to PLG, suggesting a potential mechanism of liver injury. This study provides insights into the molecular mechanisms of liver injury induced by non-pharmaceutical chemical exposure, identifying key toxicological targets and pathways. The results suggest that chemicals like SUN and TART can significantly alter liver function through specific gene expression changes and immune modulation, offering potential biomarkers and therapeutic targets for mitigating such toxic effects.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf096"},"PeriodicalIF":2.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774380","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}

引用次数: 0

Protective effect of L-carnitine on cadmium induced neurotoxicity in rats. 左旋肉碱对镉致大鼠神经毒性的保护作用。

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-08-01 DOI: 10.1093/toxres/tfaf111

Yan Wang, Yuan Hu, Chunxia Guo, Yuanjing Ma, Qizhong Qin

{"title":"Protective effect of L-carnitine on cadmium induced neurotoxicity in rats.","authors":"Yan Wang, Yuan Hu, Chunxia Guo, Yuanjing Ma, Qizhong Qin","doi":"10.1093/toxres/tfaf111","DOIUrl":"https://doi.org/10.1093/toxres/tfaf111","url":null,"abstract":"Cadmium (Cd), a well-known environmental pollutant, widely exists in water, soils, sediments, and air, and produces various system dysfunctions including those affecting the nervous system. L-carnitine (L-CAR) is an antioxidant that plays neuroprotective roles by improving enzyme functions. The purpose of our study was to evaluate whether L-CAR could efficiently protest against neurotoxicity induced by Cd. Rats were exposed to different concentrations of Cd (0, 25, 50, 100 mg/l) for 4 weeks. We used the open-field test (OFT) and forced-swimming test (FST) to observe the rats'spontaneous locomotor activity and exploration behavior; brain histopathological section to observe the damage of cortical neurons in the brain; Oxidative stress indicators reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) were determined at terminal time-points. The protective effects of L-CAR(1.5 g/l) were evaluated in parallel. Here, we corroborated that that L-CAR is a potential pharmacological agent that protests against the neurotoxicity of Cd. The results of brain histopathological sections show that with the increase of cadmium dosage in drinking water, but the damage to cortical neurons becomes more severe;the Cd(100 mg/l) + L-CAR(1.5 g/l) group, the neuronal cell membrane was intact, the cell outline was clear. The Cd-induced oxidative stress in the cerebral cortex was proven by elevation of ROS, MDA levels, and reduction of SOD activity. However, those effects on oxidative stress were attenuated if L-CAR(1.5 g/l) was simultaneously administrated. The results suggested that L-CAR is a potential pharmacological agent that protects the neurotoxicity of Cd.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf111"},"PeriodicalIF":2.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774381","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}

引用次数: 0

Puerarin alleviates high glucose-induced lens epithelial cell damage by activating the Nrf2 Signaling pathway to inhibit oxidative stress. 葛根素通过激活Nrf2信号通路抑制氧化应激，减轻高糖诱导的晶状体上皮细胞损伤。

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-08-01 DOI: 10.1093/toxres/tfaf109

Juan Xia, Mingli Zhou, Yuandong Ma, Song Zhang, Shanshan Tang, Jie Zhang

{"title":"Puerarin alleviates high glucose-induced lens epithelial cell damage by activating the Nrf2 Signaling pathway to inhibit oxidative stress.","authors":"Juan Xia, Mingli Zhou, Yuandong Ma, Song Zhang, Shanshan Tang, Jie Zhang","doi":"10.1093/toxres/tfaf109","DOIUrl":"https://doi.org/10.1093/toxres/tfaf109","url":null,"abstract":"This study investigated Puerarin's protective effects and mechanisms against high glucose (HG)-induced damage in human lens epithelial cells (HLECs), which are relevant to diabetic complications. Using an HG-exposed HLEC model, varying doses of Puerarin (10 μM, 20 μM, 50 μM) were tested. While non-toxic to normal HLECs, both 20 μM and 50 μM Puerarin significantly and dose-dependently restored cell viability reduced by HG (P < 0.05). Puerarin effectively reversed HG-induced apoptosis and mitigated oxidative stress by increasing levels of antioxidant enzymes (SOD, GSH-Px) and decreasing malondialdehyde (MDA) concentrations. Mechanistically, Puerarin significantly upregulated the expression of the transcription factor Nrf2, with the strongest effect observed at 50 μM. Crucially, when Nrf2 expression was knocked down using shRNA Nrf2 transfection in HG-treated HLECs, the protective effects of high-dose Puerarin were completely abolished. This loss of protection resulted in significantly increased cell death and oxidative stress markers compared to control cells transfected with shRNA Ctrl and treated with Puerarin. The findings demonstrate that Puerarin, particularly at doses of 20 μM and 50 μM, protects HLECs from HG-induced damage in a dose-dependent manner. This protection involves preserving cell viability, reducing apoptosis, and enhancing cellular antioxidant defenses. The Nrf2 signaling pathway is identified as a key mechanism mediating Puerarin's beneficial effects. These results suggest that Puerarin has potential as a therapeutic agent for preventing diabetic complications affecting the lens epithelium.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf109"},"PeriodicalIF":2.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774382","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}

引用次数: 0

Nitrate protects against methotrexate-induced liver injury by activating Wnt/β-catenin Signaling in mice. 硝酸通过激活小鼠Wnt/β-catenin信号通路，保护小鼠免受甲氨蝶呤诱导的肝损伤。

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-07-30 eCollection Date: 2025-08-01 DOI: 10.1093/toxres/tfaf107

Xin Wen, Ying Liu, Chunmei Zhang, Jinsong Wang, Guangyong Sun, Dong Zhang, Songlin Wang, Shaorong Li

{"title":"Nitrate protects against methotrexate-induced liver injury by activating Wnt/β-catenin Signaling in mice.","authors":"Xin Wen, Ying Liu, Chunmei Zhang, Jinsong Wang, Guangyong Sun, Dong Zhang, Songlin Wang, Shaorong Li","doi":"10.1093/toxres/tfaf107","DOIUrl":"10.1093/toxres/tfaf107","url":null,"abstract":"Methotrexate (MTX) is a drug used to treat autoimmune diseases and certain cancers. However, its untreatable hepatotoxic effect severely limits its clinical use. Therefore, further studies are required to combat MTX-induced liver injury. Nitrate, abundant in green vegetables, possesses anti-inflammatory, antioxidant, and immunoregulatory effects. Our study investigated the preventive effects of nitrate on MTX-induced liver injury. Liver injury in mice was induced by administering a single dose of MTX (20 mg/kg body weight) intraperitoneally (i.p.). Pre-treatment of mice with 2 mM nitrate in drinking water 5 days prior effectively mitigated the MTX-elevated serum aminotransferase activities, attenuated hepatic pathological injury, reduced hepatic apoptosis and restored the proliferative capacity of hepatocytes. RNA sequencing analysis indicated that the molecular mechanism may involve the activation of the Wnt/β-catenin pathway. The AML 12 cell line was employed for in vitro validation. In this study, the hepatoprotective effect of nitrate against drug-induced liver injury (DILI) was identified for the first time, providing a new approach to preventing DILI in clinical practice.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf107"},"PeriodicalIF":2.1,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144751907","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}

引用次数: 0

Accuracy of Pediatric new poisoning mortality score versus poisoning severity score in prediction of in-hospital mortality of acutely poisoned children admitted to Pediatric intensive care unit. 儿科新发中毒死亡率评分与中毒严重程度评分预测儿科重症监护病房急性中毒儿童住院死亡率的准确性

IF 2.1 4区医学

Toxicology Research Pub Date : 2025-07-30 eCollection Date: 2025-08-01 DOI: 10.1093/toxres/tfaf108

Meray Medhat Shokry Zaghary, Hend Gamal Aref, Wafaa Abdel-Ghaffar Ali

{"title":"Accuracy of Pediatric new poisoning mortality score versus poisoning severity score in prediction of in-hospital mortality of acutely poisoned children admitted to Pediatric intensive care unit.","authors":"Meray Medhat Shokry Zaghary, Hend Gamal Aref, Wafaa Abdel-Ghaffar Ali","doi":"10.1093/toxres/tfaf108","DOIUrl":"https://doi.org/10.1093/toxres/tfaf108","url":null,"abstract":"Acute pediatric poisoning is a severe global public health issue that represents a leading cause of morbidity and mortality in pediatrics. The study discussed the accuracy rate of the new PMS to be applied to pediatric acutely poisoned patients after modification to be called the pediatric new poisoning mortality score (pediatric new-PMS) and compared it to the poisoning severity score (PSS). The study was conducted on acutely pediatric intoxicated patients admitted to a pediatric intensive care unit (PICU) during the period from January 2021 to January 2024 (181 cases). 48.6% of cases were males, and 51.4% were females; the median age was 5 years. Regarding the fate of cases, 65.2% recovered completely, 16.57% recovered with a complicated course, and 18.23% died. The pediatric new-PMS above 50 points had an accuracy rate of 85.3% with good discrimination for mortality, sensitivity of 78.8%, specificity of 77.7%, positive predictive value of 44%, and negative predictive value of 94%. The PSS above 2 had an accuracy rate of 84.5% with good discrimination for mortality, sensitivity of 97%, specificity of 71.6%, positive predictive value of 43.2%, and negative predictive value of 99%. The study concluded that the PSS and pediatric new PMS can be used efficiently to predict mortality in acute pediatric intoxicated patients. The pediatric new-PMS score is easy to calculate even before admission to PICU, as it depends on objective markers that can be obtained even in the prehospital stage, such as vital signs, mental state, demographics, and poisoning-related variables.","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 4","pages":"tfaf108"},"PeriodicalIF":2.1,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144758740","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}

引用次数: 0