Toxicology Research最新文献

{"title":"Screening of Salsola imbricata extract impacts against acrylamide induced hepatic toxicity in rats through the regulation of different global gene expression.","authors":"Ahmed M El-Shehawi, Samy Sayed, Mona M Elseehy, Saqer Alotaibi, Siraj B Alharthi, Ghadi Alsharif, Mohamed Soliman","doi":"10.1093/toxres/tfaf038","DOIUrl":"10.1093/toxres/tfaf038","url":null,"abstract":"<p><p>Acrylamide (A) is known for its biological toxicity and <i>S. imbricata</i> is recognized for its various biological activities. The leaf extract of <i>S. imbricata</i> was utilized as a protective approach from acrylamide-induced oxidative stress at the transcriptome level by analyzing global gene expression, biological processes and pathways. Three groups of rats were used to investigate the protective effect of <i>S. imbricata</i> leaf extract on the liver transcriptome: Group C (Control), group A (received acrylamide), and group A_S (received acrylamide and <i>S. imbricata</i> extract). Transcriptome analysis was conducted using RNAseq with the Illumina NovaSeq 6,000. The results identified 53 differentially expressed genes (DEGs) in A/C and 91 genes in A_S/C comparisons. Various GO terms were significantly enriched, with 19 terms in the A/C comparison and 6 terms in the A_S/C comparison. In addition, several pathways were enriched, including ATP biosynthesis, mitochondrial inner membrane, and iron binding. The extract of <i>S. imbricata</i> exhibited various effects, including A-like, A-antagonistic, or A-agonistic on gene expression. This explains the observed contradiction of <i>S. imbricata</i> extract on the global gene expression of rat liver. The identified DEGs in the current study are associated with various pathways, including electron transport chain, mitochondrial apoptosis, ribosome function, iron binding, and homeostasis. The findings indicate an A-like transcriptomic toxicity of <i>S. imbricata,</i> although its previously reported antioxidant and anti-inflammatory activities. This raises concerns about the safety of medicinal plants and their widespread use in food supplements and alternative medicine, emphasizing the need for their assessment at various biological levels.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf038"},"PeriodicalIF":2.2,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143655689","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":"Genotoxicity evaluation in fish (<i>Rutilus rutilus</i>) collected from rivers Drenica and Sitnica in the Kosovo.","authors":"Fisnik H Asllani, Avdulla J Alija, Peter M Eckl, Nikolaus Bresgen","doi":"10.1093/toxres/tfaf032","DOIUrl":"10.1093/toxres/tfaf032","url":null,"abstract":"<p><p>Our previous investigations on the cyto- and genotoxic properties of the water samples from the rivers Drenica and Sitnica in the Kosovo revealed an increased mutagenic potential. More recently we reported genotoxic effects induced in fish (erythrocytes) collected in five locations along the rivers Drenica and Sitnica during 2016 and 2017. In this paper, the data obtained from the assessment of the genetic damages in the erythrocytes of fish (<i>Rutilus rutilus</i>) collected in spring 2017 (May-June) and in two sampling rounds in spring 2018 (March-April and May-June) are presented. The fish specimens were collected in three locations along the river Drenica and two locations along the Sitnica river while the fish specimens from Lake Badovc were used for comparison. Erythrocytes of collected fish were investigated using the Comet assay and micronucleus formation as indicators of the genotoxic potential of the river water. The obtained data show differences as regard to the genetic damages in the erythrocytes of individuals which are specific as regard to the location and seasons as well as for the type of damages (% of DNA in tail and/or micronucleated cells). Together with the data published previously, a more complete picture of the season and location associated variations in the genotoxicity was obtained showing that variations are specific and attributable also to the influence of the non-point pollution sources with various chemistry and amount as well as the hydrological characteristics which are not monitored and investigated at satisfactorily level.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf032"},"PeriodicalIF":2.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584046","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":"Coenzyme Q10 alleviates AlCl₃ and D-galactose induced Alzheimer via modulating oxidative burden and TLR-4/MAPK pathways and regulation microRNA in rat brain.","authors":"Nagat F Nawar, Doha M Beltagy, Ehab Tousson, Mai M El-Keey, Tarek M Mohamed","doi":"10.1093/toxres/tfaf031","DOIUrl":"10.1093/toxres/tfaf031","url":null,"abstract":"<p><p>Alzheimer's disease (ad) is the most progressive form of neurodegenerative disease resulting in cognitive and non-cognitive deficits. Coenzyme Q10 (CoQ10) is an anti-inflammatory and anti-oxidative stress supplement that can improve inflammation and oxidative stress associated with ad. This study aimed to explore the protective potential of coenzyme Q10 (CoQ10). It also sought to uncover any synergistic effects when combined with donepezil, an acetylcholinesterase inhibitor, in treating Alzheimer's disease in rats, focusing on the modulation of the TLR-4/MAPK pathway and regulation of microRNA. The experiment involved seventy rats categorized into different groups: control, Reference group (donepezil 10 mg/kg/P.O.), CoQ10 alone (1,200 mg/kg/P.O.), ad-model (D-galactose (120 mg/kg/i.p) + Alcl₃ (50 mg/kg/P.O.)), donepezil co-treatment, CoQ10 co-treatment, and CoQ10 + donepezil co-treatment. Behavioral parameter was defined using the Morris-Maze test (MMT) and various assessments, such as GABA, oxidative stress, Aβ_1-42, ion homeostasis, toll-like receptor-4 (TLR-4), mitogen-activated protein kinase-1 (MAPK-1), micro-RNA (mir-106b, mir-107, and mir-9) were measured. Immunohistological staining was used to assess structural abnormalities in hippocampus. CoQ10 treatment demonstrated memory improvement, enhanced locomotion, and increased neuronal differentiation, mainly through the activation of the TLR-4/MAPK pathway and regulation of mir-106b, mir-107, and mir-9.</p><p><strong>Highlights: </strong>Coenzyme Q10 (CoQ10) improved the rats' passive avoidance memory impairment caused by D-gal and AlCl₃. ad led to the alteration of the TLR-4/MAPK pathways.CoQ10 as a protective agent, diminishes oxidative burden, improve ion homeostasis.CoQ10 counteracts Alzheimer's disease by enhancing neurotransmitter parameter and regulating the MicroRNA.CoQ10 lowered accumulation of Aβ plaque in the hippocampal neurons of D-Gal and AlCl₃-treated rats.One promising therapeutic method was the combination of donepezil and CoQ10 therapy.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf031"},"PeriodicalIF":2.2,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143571728","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":"Fasudil protects spiral ganglion neurons and hair cells against cisplatin-induced apoptosis by inhibiting reactive oxygen species accumulation and regulating the ROCK/PTEN/AKT signaling pathway.","authors":"Peng Yin, Zhenhua Jiang, Xue Wang, Shusheng Gong, Cui Zhang, Zhaomin Fan","doi":"10.1093/toxres/tfaf030","DOIUrl":"10.1093/toxres/tfaf030","url":null,"abstract":"<p><p>Cisplatin causes hearing loss in at least 60% of chemotherapy patients, leading to impairments in the patient's life quality. Spiral ganglion neurons (SGNs) and hair cells (HCs) are the main cell types affected by cisplatin accumulation in the inner ear. Fasudil is an FDA-approved drug and has been reported to exert neuroprotective effects in previous research. However, whether fasudil possesses protective effects in cisplatin-induced SGN and HC damage and the potential mechanisms remain unknown. In this study, we investigated whether fasudil has a protective effect on cisplatin-induced damage to inner ear SGNs and HCs. We first observed the effect of different concentrations of fasudil on cisplatin-induced cell loss of SGNs and HCs. We also studied the effects of fasudil on cisplatin-induced apoptosis of SGNs and HCs and detected the mitochondrial reactive oxygen species (ROS) level. Furthermore, we investigated the mechanisms of fasudil in protecting the SGNs and HCs from cisplatin- induced cells apoptosis. We found that fasudil treatment significantly ameliorated SGNs and HCs loss and attenuated cell apoptosis after cisplatin exposure. Moreover, fasudil attenuated the cisplatin-induced ROS generation in SGN- and HC-explants culture. Further mechanistic studies revealed that fasudil regulated the ROCK/PTEN/AKT signaling pathway in SGN- and HC-explants after cisplatin exposure. This study indicates that fasudil might be a novel therapeutic target for preventing cisplatin-induced SGNs and HCs damage.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf030"},"PeriodicalIF":2.2,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143571729","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":"Melatonin may protect the gastrointestinal system from cadmium chloride toxicity during pregnancy.","authors":"Erhan Şensoy","doi":"10.1093/toxres/tfaf003","DOIUrl":"10.1093/toxres/tfaf003","url":null,"abstract":"<p><p>Cadmium is absorbed into the body through food consumption. Since food intake increases during pregnancy, Cadmium consumption from food also increases. Melatonin, secreted by the pineal gland, is an antioxidant hormone with therapeutic effects. This research aims to reveal how Cadmium Chloride (CdCl₂) affects antioxidant capacity by histological and biochemical methods and to test the effect of Melatonin in treating CdCl₂-induced lesions in pregnant mice's stomach and small intestine. Control, CdCl₂, Melatonin, and CdCl₂ + Melatonin groups were created using pregnant mice (n: 6). CdCl₂ (2 mg/kg/bw) and Melatonin (3 mg/kg/bw) were administered. The investigation was terminated after birth. Stomach and small intestine tissues were pull out and fixed in 10% formaldehyde. They were routinely histologically processed and dyed via Hematoxylin-Eosin. The tissues were appraised under light and electron microscopy, and biochemical analyses were carried out. A one-way analysis of variance (ANOVA) was applied to compare the groups, and LSD tests were used for pairwise comparisons (<i>P</i> < 0.05). While a reduction in body weight was noted in CdCl₂ group (<i>P</i>: 0.01), no decrease was observed in the Melatonin group (<i>P</i>: 0.02). CdCl₂ caused pathologies such as degeneration of gland cells, vacuole formation, and hemorrhage in the stomach. Although CdCl₂ caused rupture and breakage of the villi in the intestine, these degenerations were minimal in CdCl₂ + Melatonin group. CdCl₂ also caused a significant decrease in antioxidant enzyme levels; however, the enzyme levels approached normal values in CdCl₂ + Melatonin group. Melatonin may be an effective therapeutic agent for gastrointestinal organs lesions caused by increased CdCl₂ during pregnancy.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf003"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565649","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":"Meta-analysis of studies testing the association between air pollution and live birth rates in women undergoing assisted reproductive technology.","authors":"Juan Hu, Huiqiu Zheng, Yan Wu, Qing Yan, Minghao Zhang, Shikun Sun, Meidi Gong, Rao Zheng, Shujing Jia, Rui Zhou, Jing Wu","doi":"10.1093/toxres/tfaf028","DOIUrl":"10.1093/toxres/tfaf028","url":null,"abstract":"<p><p>Amidst a proliferation of research on air pollutants and negative pregnancy outcomes, uncertainty lingers regarding their impact on live birth rates in women receiving assisted reproductive technology (ART). This meta-analysis aims to clarify this vital issue. We searched EMBASE, PubMed, and Web of Science databases, targeting articles published prior to 2023 August 2. We pooled relative risks (RRs) and their corresponding 95% confidence intervals (95%CIs) across all included studies to assess the relationship between exposure to air pollutants and live birth rates. From an initial 5,785 citations, we identified five eligible papers with a total sample size of approximately 282,000 participants. In the year prior to oocyte retrieval, for every 10 μg/m³ increase in fine particulate matter (PM_2.5) (RR: 0.94, 95%CI: 0.92-0.97) and coarse particulate matter (PM₁₀) (RR: 0.95, 95%CI: 0.92-0.97), the probability of live birth decreased by 6% and 5%, respectively. For every additional ppb increase in nitrogen dioxide (NO₂) (RR: 0.92, 95%CI: 0.87-0.98), the likelihood of live birth decreased by 8%. This meta-analysis demonstrates adverse associations between air pollution and live birth rates in women undergoing ART. These findings highlight further elucidate the observed associations, as well as to explore potential mechanisms and implications for reproductive health.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 1","pages":"tfaf028"},"PeriodicalIF":2.2,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565497","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":"Comparative in vitro and in silico evaluation of the toxic effects of metformin and/or ascorbic acid, new treatment options in the treatment of Melasma.","authors":"Hülya Tezel Yalçın, Deniz Arca Çakır, Anıl Yirün, Sonia Sanajou, Gözde Işık, Özlem Bozdemir, İbrahim Özçelik, Merve Güdül Bacanlı, Naciye Dilara Zeybek, Terken Baydar, Pınar Erkekoğlu","doi":"10.1093/toxres/tfaf025","DOIUrl":"10.1093/toxres/tfaf025","url":null,"abstract":"<p><p>Melasma is a chronic condition that leads to the buildup of melanin pigment in the epidermis and dermis due to active melanocytes. Even though it is considered a non-life-threatening condition, pigment disorders have a negative impact on quality of life. Since melasma treatment is not sufficient and complicated, new treatment options are sought. Research on metformin and ascorbic acid suggested that they might be used against melasma in the scope of \"drug repositioning.\"The MNT-1 human melanoma cell line was used to assess the effects of metformin, ascorbic acid, and metformin+ascorbic acid combination on cytotoxicity and oxidative stress. Melanin, cAMP, L-3,4-dihydroxyphenylalanine (L-DOPA) and tyrosinase levels were determined by commercial ELISA kits and tyrosinase gene expression was analyzed with RT-qPCR. Cytopathological evaluations were performed by phase contrast microscopy. Tyrosinase expression was determined by immunofluorescence (IF) staining of MNT-1 cells. The online service TargetNet was used for biological target screening. The parameters were not significantly altered by ascorbic acid applied at non-cytotoxic concentrations. On the contrary, metformin dramatically raised tyrosinase and intracellular ROS levels. Moreover, intracellular ROS levels and tyrosinase levels were found to be considerably elevated with the combined treatment. Also, potential metformin and ascorbic acid interactions were determined. According to the results, it can be said that these parameters were not significantly altered by ascorbic acid. On the contrary, metformin dramatically raised tyrosinase and intracellular oxidative stress levels. Moreover, intracellular oxidative stress and tyrosinase levels were elevated with the combined treatment. In conclusion, individual treatments of ascorbic acid or metformin may only provide a limited effect when treating melasma and extensive in vitro and in vivo research are required.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 1","pages":"tfaf025"},"PeriodicalIF":2.2,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555325","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":"Toxicity assessment of imatinib mesylate and a related impurity: in vitro and in vivo approaches.","authors":"Cássia Franciele Rosa da Silva Rocha, Bruna Saraiva Hermmann, Juliana Machado Kayser, Gabriela Zimmermann Prado Rodrigues, Günther Gehlen, Fernanda Brião Menezes Boaretto, Jaqueline Nascimento Picada, Juliane Deise Fleck, Mariele Feiffer Charão, Simone Gasparin Verza","doi":"10.1093/toxres/tfaf029","DOIUrl":"10.1093/toxres/tfaf029","url":null,"abstract":"<p><p>Imatinib mesylate (IM) is a widely used anticancer drug, mainly for treating chronic myeloid leukemia. However, pharmaceutical formulations may contain impurities, which in some cases can be more toxic than the parent compounds. This study aimed to compare the toxicity of IM and one of its impurities (IMP), N-(2-methyl-5-aminophenyl)-4-(3-pyridyl)-2-pyrimidine amine, using progressively complex models. Cytotoxicity was evaluated using 3-(4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium, neutral red uptake and sulforhodamine B colorimetric assays. Mutagenic activity was assessed using the Ames test<i>.</i> In vivo assays were performed using both the invertebrate <i>C. elegans</i> and vertebrate zebrafish embryo models. In Vero cell cultures, the cytotoxicity of IM and IMP was found to be similar across the colorimetric assays tested. Neither IM nor IMP showed mutagenic effects in the Ames test. In the <i>C. elegans</i> lethality and development assay the toxicity profiles of the compounds were similar. However, in the Fish Embryo Acute Toxicity assay, the LC₅₀ value for IMP (0.735 μg/mL) was significantly lower than that for IM (60.86 μg/mL), indicating greater toxicity for IMP. Furthermore, sublethal effects such as yolk-sac edema, pericardial edema, and tail deformities, were observed in embryos treated with IMP, even at low concentrations, indicating potential hazards associated with IMP. This study is the first to evaluate the toxicity of an IM subproduct, previously reported in pharmaceutical formulations, using different models. The Zebrafish model demonstrated higher sensitivity in predicting the toxic response of the TKI subproduct.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 1","pages":"tfaf029"},"PeriodicalIF":2.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565503","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":"The effect and mechanism of atorvastatin regulating PI3K-Akt-mTOR pathway on radiosensitivity of hepatocellular carcinoma cells.","authors":"Zhengzheng Deng, Jinjing Guo, Zihao Zhu, Qiancheng Qing, Dangting Wan, Pengyuan Lei, Qi Liu, Bo Huang","doi":"10.1093/toxres/tfae202","DOIUrl":"10.1093/toxres/tfae202","url":null,"abstract":"<p><p>Radiation therapy is an important method to treat liver cancer, but because of the strong DNA repair ability of liver cancer cells, even after receiving high doses of radiation still can not get satisfactory results. Atorvastatin (ATO) is a lipophilic and tissue-selective inhibitor of HMG-CoA reductase whose anticancer effects have been validated in various cells, but its effect on the radiation sensitivity of hepatocellular carcinoma cells remains unclear. Therefore, Therefore, this study explored the radiosensitivity of ATO and its possible mechanism by pretreating HepG2 with ATO and collecting HepG2 cells after irradiation. It was found that atorvastatin can not only affect the survival of liver cancer cells when used alone, but also enhance the radiation sensitivity of HepG2 cells. The study found that ATO significantly exacerbated the inhibitory effects of IR on the growth, proliferation, and migration of HepG2 cells. Measurement of ROS, SOD, GPx, and MDA levels indicated that ATO enhanced IR-induced oxidative stress, further promoted the decrease of Mitochondrial Membrane Potential, increased the rate of apoptosis in HepG2, upregulating pro-apoptotic proteins Bax and Cleaved-Caspase 3, and downregulating anti-apoptotic proteins Bcl-2. Western blot analysis showed that the PI3K-Akt-mTOR pathway was inhibited, leading to the activation of cytotoxic autophagy in HepG2 and an increase in the expression of the LC-3II protein. In summary, ATO, in combination with IR, enhances the oxidative stress response of HepG2 induced by IR, promotes autophagy by inhibiting the PI3K-Akt-mTOR pathway, and thereby potentially enhances the radiosensitivity of HepG2 as a pharmacological intervention.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 1","pages":"tfae202"},"PeriodicalIF":2.2,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11851483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514290","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":"Editorial.","authors":"Shirley Price","doi":"10.1093/toxres/tfaf018","DOIUrl":"https://doi.org/10.1093/toxres/tfaf018","url":null,"abstract":"","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 1","pages":"tfaf018"},"PeriodicalIF":2.2,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11848837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497730","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}