{"title":"Neurotoxic and metabolic effects of chronic aspartame consumption in rodent models: a systematic review and meta-analysis.","authors":"Arbind Kumar Choudhary, Nishant Singh","doi":"10.1080/15376516.2026.2662931","DOIUrl":"10.1080/15376516.2026.2662931","url":null,"abstract":"<p><p>Aspartame (ASP), a widely used artificial sweetener, remains the subject of scientific scrutiny regarding its long-term safety. While regulatory agencies assert safety at established acceptable daily intake (ADI) levels, accumulating preclinical rodent data suggests potential adverse effects under chronic exposure conditions. This systematic review and meta-analysis synthesized evidence from 13 rodent studies investigating neurotoxic and metabolic endpoints. Our quantitative meta-analysis of the oxidative stress domain (<i>k</i> = 8) demonstrated a very large and statistically significant increase in oxidative damage (pooled Hedges' g = +4.44; 95% CI: 2.94 to 5.94), suggesting oxidative stress as a major hypothesized mechanism of aspartame-induced injury. Qualitatively, chronic exposure was associated with neurobehavioural deficits, including spatial learning and memory impairments, alongside metabolic dysfunction such as glucose intolerance and dyslipidaemia. Notably, these effects were observed in several studies utilizing doses equivalent to the human ADI. However, the interpretation of these findings is constrained by high statistical heterogeneity (I<sup>2</sup> = 85.4%) and a lack of detailed reporting in primary studies, resulting in uncertain internal validity across several risk-of-bias domains. While these results provide a critical signal regarding the neurotoxic and metabolic potential of aspartame, they underscore the urgent need for improved reporting standards in preclinical toxicology and long-term human epidemiological studies to fully clarify its safety profile.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1045-1058"},"PeriodicalIF":2.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730138","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":"Characterization of unusual immunoassay cross-reactive cannabinoid metabolites in canine urine via gas chromatography-mass spectrometry.","authors":"Chris Pickard, John P Buchweitz, Andreas F Lehner","doi":"10.1080/15376516.2026.2665315","DOIUrl":"10.1080/15376516.2026.2665315","url":null,"abstract":"<p><p>Recent increases in cannabis use and dog ownership have elevated the risk of canine cannabis intoxication, prompting a need for efficient diagnostic tools. Enzyme immunoassays (EIAs) that employ monoclonal antibodies specific to 11-nor-9-carboxy-Δ<sup>9</sup>-tetrahydrocannabinol (THC-COOH) are commonly employed for preliminary screening and frequently return positive results in canine urine, yet these are not corroborated by gas chromatography-mass spectrometry (GC-MS), suggesting immunoassay cross-reactivity that raises concerns about false positives. The present study incorporated confirmatory GC-MS and GC-MS/MS analyses with mass spectral deconvolution to investigate EIA-positive, GC-MS-negative samples. Two novel compounds with molecular weights of 446 and 460 were identified following trimethylsilylation in the corresponding urine samples. Structural analysis suggests these compounds may be metabolic derivatives of tetrahydrocannabivarin (THCV), a cannabinoid with growing presence in consumer products. These compounds are structurally distinct from Δ<sup>9</sup>-THC-COOH yet exhibit EIA-reactivity. Ion fragmentation patterns, derivatization behavior, and comparison to established mass spectral libraries support the possibility of 11-hydroxylated and 9-carboxylated THCV analogs. The findings point to THCV metabolism as a plausible source of EIA-cross-reactivity in canines, raising important implications for veterinary toxicology and drug screening protocols. This study contributes crucial insights into canine cannabinoid metabolism and highlights limitations of existing immunoassays when influenced by structurally similar analytes.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1162-1182"},"PeriodicalIF":2.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147821177","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}
Zehra Keskin, Can Özgür Yalçın, Engin Yenilmez, Ezgi Öztaş, Mahmoud Abudayyak
{"title":"Copper-based nanoparticles-associated neurotoxicity: ions or particles?","authors":"Zehra Keskin, Can Özgür Yalçın, Engin Yenilmez, Ezgi Öztaş, Mahmoud Abudayyak","doi":"10.1080/15376516.2026.2664036","DOIUrl":"10.1080/15376516.2026.2664036","url":null,"abstract":"<p><p>The widespread use of engineered nanomaterials raises concerns regarding their potential toxicity to human health and the environment. Among metal oxide nanoparticles, copper-based nanoparticles (Cu-based NPs) are extensively produced and utilized due to their unique physicochemical properties. The dissolution of NPs leads to the release of ionic species, and still, there is no clear consensus on whether metal-based NPs' toxicity arises primarily from the nanoparticles themselves or from the ionic species generated through metal ion dissolution. This study systematically evaluated the cellular uptake and toxicological profiles of various Cu-based NPs (Cu, CuO, Cu<sub>2</sub>O, and CuFe<sub>2</sub>O<sub>4</sub>) in comparison to ionic copper (CuCl<sub>2</sub>) using the PC12 neuronal model. ICP-MS analysis demonstrated that cellular uptake was both dose- and particle-dependent; notably, CuO NPs yielded the highest intracellular copper accumulation. Cytotoxicity assays (MTT and NRU) revealed that all Cu-based NPs showed significantly higher toxicity than CuCl<sub>2</sub>. Furthermore, Cu-based NP exposure, particularly with Cu<sub>2</sub>O, triggered a robust oxidative stress response characterized by significant alterations in GSH, CAT, and MDA levels. This oxidative imbalance was closely associated with a marked increase in apoptosis and necrosis and substantial DNA damage. Our findings elucidate that the oxidation state and chemical formulation of copper nanoparticles significantly dictate their neurotoxic potential, with Cu<sub>2</sub>O NPs exhibiting the most pronounced geno- and cytotoxicity. These results highlight the necessity of considering nanoparticle-specific effects beyond simple ion dissolution in the safety assessment of engineered nanomaterials.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1145-1161"},"PeriodicalIF":2.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147843239","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":"Advances in artificial intelligence and machine learning for toxicity prediction in computational toxicology: a comprehensive review.","authors":"Gerald Shija","doi":"10.1080/15376516.2026.2712550","DOIUrl":"10.1080/15376516.2026.2712550","url":null,"abstract":"<p><p>Over the past three decades, artificial intelligence (AI) and machine learning (ML) have revolutionized computational toxicology, providing powerful tools for predicting chemical toxicity and supporting safer assessments for human health and the environment. This review offers a critical 30-year synthesis (1995-2025) that distinguishes itself from narrower prior works through its interdisciplinary integration of historical evolution, multi-omics data fusion, nanotoxicity challenges, regulatory frameworks, multi-stakeholder perspectives, and emerging hybrid and generative models. Key findings reveal a clear progression from early artificial neural networks capturing non-linear patterns in the 1990s to modern deep learning architectures such as convolutional neural networks and graph neural networks that have achieved over 85% accuracy, primarily in retrospective benchmarks on ToxCast and Tox21 datasets for endpoints including hepatotoxicity, cardiotoxicity, and nanotoxicity. However, prospective validation on novel compounds remains limited, representing a critical translational gap. Traditional machine learning methods (random forests and support vector machines) effectively handle imbalanced high-throughput screening data, facilitating multi-omics integration and applications across pharmaceuticals, pesticides, cosmetics, and nanoparticles. These approaches strengthen read-across strategies, Integrated Approaches to Testing and Assessment (IATA), and Threshold of Toxicological Concern (TTC) frameworks. Regulatory acceptance, guided by OECD principles, increasingly emphasizes explainable AI to ensure transparency and validation. In conclusion, AI/ML approaches can substantially reduce animal testing, accelerate safety evaluations, and address data gaps, yet require ongoing attention to biases, model opacity, and limited prospective performance. Hybrid mechanistic-AI models, federated learning, and strengthened cross-sector collaboration represent the most promising path forward.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-19"},"PeriodicalIF":2.7,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148621482","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}
Marwa Qadri, Daniyah A Almarghalani, Abdulaziz Alarifi, Bassim M S A Mohamed, Hany M Fayed
{"title":"Remogliflozin attenuates thioacetamide-induced nephrotoxicity: association with Nrf2/HO-1, SIRT1/AMPK, and TLR4/NF-κB pathway modulation.","authors":"Marwa Qadri, Daniyah A Almarghalani, Abdulaziz Alarifi, Bassim M S A Mohamed, Hany M Fayed","doi":"10.1080/15376516.2026.2718918","DOIUrl":"10.1080/15376516.2026.2718918","url":null,"abstract":"<p><p>Thioacetamide (TAA) induces renal injury <i>via</i> oxidative stress and inflammation. Remogliflozin (Remo), an SGLT2 inhibitor, was evaluated for potential renoprotection. Twenty-four male Wistar rats were assigned to control, TAA (100 mg/kg IP twice weekly), TAA + Remo 25 mg/kg, or TAA + Remo 50 mg/kg (oral daily). Outcomes included renal function, oxidative stress (GSH, SOD, MDA), antioxidant biomarkers (Nrf2, HO-1), inflammatory mediators (TLR4/NF-κB, TNF-α, IL-1β), metabolic/kinase biomarkers (SIRT1, AMPK, PI3K, AKT), and histopathology/immunohistochemistry (mTOR, MYD88, Nrf2). Remogliflozin was associated with lower serum creatinine, urea, and uric acid, with endpoint-specific differences between doses. Remo was associated with higher renal Nrf2, HO-1, SIRT1, and p-AMPK, and lower MDA, TLR4, NF-κB, TNF-α, IL-1β, PI3K, and AKT. Histopathology and IHC showed associations with reduced tissue injury, lower mTOR and MYD88 immunoreactivity, and increased Nrf2 staining. While the 50 mg/kg group showed changes in more markers, this does not establish uniform dose superiority or a formal dose-response relationship; at 25 mg/kg, effects differed among AMPK-related endpoints. Direct 25-versus-50 mg/kg comparisons were included in the Tukey-Kramer analysis for each endpoint. No pharmacokinetic measurements or formal dose-response analyses were performed. In this exploratory model, remogliflozin was associated with attenuation of TAA-induced renal injury and modulation of related biomarkers. Causal mechanisms remain to be confirmed by targeted intervention studies. Findings are limited to young male Wistar rats and should not be generalized to other populations or clinical settings. Remogliflozin warrants further preclinical investigation in TAA-associated renal injury.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-22"},"PeriodicalIF":2.7,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148724265","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 study on the influence of environmental toxicants on the luminol/KSCN/H<sub>2</sub>O<sub>2</sub>/Cu oscillator.","authors":"C André, F Gagné","doi":"10.1080/15376516.2026.2708117","DOIUrl":"10.1080/15376516.2026.2708117","url":null,"abstract":"<p><p>Oscillatory reactions involving periodical oxido-reduction reactions are commonly found in lifeforms. The purpose of this study consisted in using the luminol-KSCN-H2O2-Cu(II) oscillator to probe the capacity of known environmental xenobiotics to alter these oscillatory reactions. The above oscillator was studied in the presence of increasing concentrations of ascorbate (a reducer), cerium (Ce IV; an oxidant), samarium oxide (SmO), nanocerium (nCeO2), zinc oxide nanoparticles (nZn), polyethylene nanoplastics (PE), cadmium tellurium quantum dots (CdTe) and copper-zinc-iron composite (nCuZnFeO) to monitor changes in the cyclic luminescent profiles. In normal conditions, 4 amplitude changes were generated during the first 15 min with luminescence spikes occurring at each 2.5-3 min. Following Fourier transformation, the amplitudes of the major oscillations were obtained for the first 9 frequencies and showed negative slope β between amplitudes and frequencies, which is related to the fractal dimension fD. The addition of the above compounds in the reaction media produced characteristic changes in oscillations with the appearance of amplitudes at higher frequencies at various intensity thereby decreasing the slope β and increasing the fD. The data also revealed that the fD followed the reported toxicity values of these compounds in fish suggesting that electron flow occurring in increased fD is associated to toxicity. Although more research is needed, the use of chemical oscillators based on oxido-reduction reactions could serve as a proxy to identify potential toxicity of xenobiotics.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-8"},"PeriodicalIF":2.7,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148593482","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}
Michaela Nicole Siebrits, David Fisher, Chontrelle Willemse, Khayelihle Brian Makhathini
{"title":"The effects of methylprednisolone on non-inflamed and inflamed <i>In vitro</i> brain endothelial cells.","authors":"Michaela Nicole Siebrits, David Fisher, Chontrelle Willemse, Khayelihle Brian Makhathini","doi":"10.1080/15376516.2026.2714946","DOIUrl":"https://doi.org/10.1080/15376516.2026.2714946","url":null,"abstract":"<p><p>The blood-brain barrier (BBB) is primarily regulated by highly selective endothelial cells. Inflammation of the brain capillaries can compromise the BBB's functioning. Methylprednisolone (M-Pred), a synthetic glucocorticoid, is clinically prescribed to treat systemic inflammation; however, little is known about its effect on both non-inflamed and inflamed brain capillaries. This study evaluated the effectiveness of M-Pred in ameliorating the lipopolysaccharide (LPS)-induced inflammatory response using the <i>in vitro</i> BBB model (bEnd.3). Cultured brain endothelial cells (BECs) were exposed to LPS (500, 1000, 2000 ng/ml) and co-treated with selected concentrations of M-Pred (10, 20, 40 µM). Cell proliferation, quantification of pro-inflammatory cytokines TNF-α and IL-1β (ELISA), and monolayer permeability (Transendothelial Electrical Resistance) were investigated. LPS decreased live cell number, increased dead cell number, and increased cell monolayer permeability; LPS increased pro-inflammatory cytokine secretion. These data confirmed the experimental functionality of the <i>in vitro</i> inflammatory BBB model. In the absence of inflammation, M-Pred decreased bEnd.3 cell monolayer permeability and pro-inflammatory cytokine secretion. M-Pred failed to alleviate LPS-induced inflammation across all tested concentrations. Chronic M-Pred treatment in the absence of inflammation proved detrimental to bEnd.3 cells' physiology.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-18"},"PeriodicalIF":2.7,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148713071","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}
Jingze Niu, Stefan Wagner, Robert Preissner, Priyanka Banerjee
{"title":"Data-driven <i>in silico</i> toxicity profiling of marketed drugs and retrospective analysis of post-marketing withdrawal risk.","authors":"Jingze Niu, Stefan Wagner, Robert Preissner, Priyanka Banerjee","doi":"10.1080/15376516.2026.2704958","DOIUrl":"https://doi.org/10.1080/15376516.2026.2704958","url":null,"abstract":"<p><p>Drug safety remains a central challenge in drug development and post-marketing surveillance, as the limited size and duration of pre-approval trials constrain detection of rare or delayed adverse effects, leaving patients exposed to residual risk after launch. Using ProTox 3.0 <i>in silico</i> toxicity predictions and statistical modeling, we analyzed an observational cohort of nearly 2,000 historically marketed small-molecule drugs and identified hepatotoxicity as a robust and consistent determinant of pharmaceutical post-marketing withdrawal probability after adjustment for therapeutic context. Other organ toxicities and structural descriptors of the drug molecules exhibited additional, indication-specific associations with withdrawal status, indicating that <i>ex-ante</i> toxicity liability is heterogeneous across therapeutic areas. While our analysis does not establish causality, the stable correlations observed across toxicity profiles, structural characteristics, and clinical indications suggest that a substantial fraction of withdrawal risk is statistically predictable. Embedding these quantitative risk signals into early-stage decisions and targeted safety evaluation strategies offers a data-driven approach to reduce late-stage attrition and post-marketing withdrawals, thereby contributing to safer and more efficient drug development.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-13"},"PeriodicalIF":2.7,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707718","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}
Yuchen Hua, Chang Su, Xian Zhang, Xuwei He, Ke Li, Zhongqiu Lu, Jianping Ye
{"title":"Comparison of machine learning and logistic regression in predicting mortality from acute poisoning in young adults: a multicenter study identifying herbicide exposure as the predominant risk determinant.","authors":"Yuchen Hua, Chang Su, Xian Zhang, Xuwei He, Ke Li, Zhongqiu Lu, Jianping Ye","doi":"10.1080/15376516.2026.2713207","DOIUrl":"10.1080/15376516.2026.2713207","url":null,"abstract":"<p><strong>Objective: </strong>Compare the effectiveness of machine learning algorithms and traditional logistic regression in predicting the mortality risk of young patients with acute poisoning, and establish a risk stratification nomogram.</p><p><strong>Methods: </strong>This multicenter retrospective study derived a derivation cohort of 406 young adults with acute poisoning from Wenzhou and an external validation cohort of 150 patients from Lishui. LASSO regression was used to screen predictive factors from 43 candidate variables. Compare the predictive performance of 14 machine learning algorithms (including RandomForest, XGBoost, CatBoost, LightGBM, SVM, etc.) with logistic regression on a training set (7:3 random split). The model evaluation indicators include AUC, sensitivity, specificity, and calibration, and conduct internal and external verification.</p><p><strong>Results: </strong>LASSO identified six independent predictive factors: white blood cell count, creatinine, herbicide poisoning, invasive mechanical ventilation, liver dysfunction, and shock. The discriminative power of the final logistic regression is comparable to that of the optimal machine learning model (internal validation AUC 0.885, external validation AUC 0.971), and it is well calibrated (Brier score 0.058-0.082, Hosmer Lemeshow test <i>p</i> > 0.05). A nomogram for predicting the 28-day mortality risk of young patients was constructed based on Logistic regression.</p><p><strong>Conclusion: </strong>Logistic regression performs similarly to complex machine learning algorithms in predicting the risk of death from acute poisoning in young adults, with better interpretability and clinical practicality. The nomogram constructed based on this is a simple and effective early risk stratification tool, which can serve as one of the reference tools for clinical decision-making assistance.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-13"},"PeriodicalIF":2.7,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148664189","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 thyroid toxicity of atrazine and its potential mechanisms: a review.","authors":"Haoyan Ma, Xinyi Wang, Xijun Zhang, Xiaoyu Jia, Jiasong Yang, Yue Qi, Chuyuan Liu, Yuezhu Zhang","doi":"10.1080/15376516.2026.2711721","DOIUrl":"https://doi.org/10.1080/15376516.2026.2711721","url":null,"abstract":"<p><p>Atrazine (ATR) is a globally used herbicide with a long environmental half-life, resulting in its widespread persistence in various environmental media. ATR has been recognized as an environmental endocrine disruptor. The thyroid gland, the largest endocrine organ in the human body, regulates essential physiological processes, including metabolism, growth, and development, through the secretion of thyroid hormones. Accumulating evidence indicates that ATR can adversely affect thyroid function through multiple pathways, including disruption of the hypothalamic-pituitary-thyroid axis, interference with thyroid hormone synthesis and metabolism, and induction of oxidative stress. This review aims to comprehensively summarize the effects of ATR on thyroid morphology and function, as well as its potential toxicological mechanisms. It also seeks to provide references for a deeper understanding of ATR-induced thyroid toxicity and to offer a scientific basis for the development of relevant risk assessment and prevention strategies.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-10"},"PeriodicalIF":2.7,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148713101","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}