Archives of Toxicology最新文献

{"title":"Role of PANoptosis in cancer: molecular mechanisms and therapeutic insights.","authors":"Yi Zhang, Xue-Li Wang, Yan-Wen Wang, Ti Chu, Lei Cao, Yong-Qi Fan, Yu-Hang Chen, Yan-Ge Li, Wei-Rong Si, Qi-Ying Jiang, Dong-Dong Wu","doi":"10.1007/s00204-026-04567-w","DOIUrl":"https://doi.org/10.1007/s00204-026-04567-w","url":null,"abstract":"<p><p>Dysregulated cell death signaling profoundly influences oncogenesis, making the targeted elimination of malignant cells a cornerstone of modern oncological interventions. Insights into programmed cell death kinetics have revealed cross-talk among apoptosis, pyroptosis, and necroptosis, establishing the conceptual framework of PANoptosis. As an inflammatory death modality, PANoptosis is orchestrated by a multi-subunit protein platform termed the PANoptosome, which integrates and executes these distinct death programs. This review outlines the fundamental molecular cascades governing PANoptosis, alongside its multifaceted involvement in tumorigenesis, immune microenvironment remodeling, and metastatic dissemination. Although PANoptosis potentiates host antitumor defense mechanisms, its impact on malignant progression remains context-dependent. Pharmacological intervention directed at central node molecules or combined with radiation and immune checkpoint blockade represents a compelling strategy. Notably, suppressing ZBP1 attenuates chemotherapy-induced systemic toxicities, whereas multimodal therapies synergistically augment therapeutic efficacy. Nevertheless, precise regulatory networks demand further elucidation, and clinical translation requires rigorous validation. Ultimately, PANoptosis offers novel insights into cancer biology and paves the way for personalized therapeutic paradigms.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N-nitroso-hydrochlorothiazide: in vivo mutagenicity evaluation in a transgenic rodent model.","authors":"Gregory R Ott, Troy Griffin, Kate Bebb, Marina Marinkovic, Raphael Nudelman, Jason M Roper, Safra Rudnic-Glick, Tunde Szabo, Mojdeh Yousefi, Valerie Niddam-Hildesheim","doi":"10.1007/s00204-026-04584-9","DOIUrl":"https://doi.org/10.1007/s00204-026-04584-9","url":null,"abstract":"<p><p>N-nitrosamine drug substance related impurities (NDSRIs) are considered to be within the \"cohort of concern\" (CoC) due to their potential mutagenic carcinogenicity. However, increasing evidence indicates variability in mutagenic potency across this class. N-nitroso-hydrochlorothiazide (N-nitroso-HCTZ), an impurity associated with hydrochlorothiazide, has shown positive results in bacterial mutagenicity (Ames) assays, although mechanistic studies suggest these findings are likely driven by reactive degradation products rather than the parent compound. To further characterize mutagenic potential in vivo, a transgenic rodent (TGR) gene mutation assay was conducted in the Muta™Mouse test system. Male mice were administered N-nitroso-HCTZ by oral gavage at 0, 18.5, 55.7, 167, 500, or 750 mg/kg/day for 28 consecutive days. Mutant frequency (lacZ) was evaluated in liver and glandular stomach at 167, 500, and 750 mg/kg/day. Systemic exposure was confirmed in a toxicokinetic study following a single 750 mg/kg dose. N-nitroso-HCTZ was well tolerated, and no statistically significant increases in mutant frequency were observed in either tissue at any evaluated dose. All values were within historical control ranges, while the positive control demonstrated the anticipated response. Under the conditions of this study, N-nitroso-HCTZ did not induce gene mutations in vivo.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic effects of lead on the differentiation of human embryonic stem cells into ectoderm: implication for adverse pregnancy outcomes and neurodevelopmental disorders.","authors":"Tyler Eng, Christopher Porter, Xiaolei Jin, Hing Man Chan","doi":"10.1007/s00204-026-04571-0","DOIUrl":"https://doi.org/10.1007/s00204-026-04571-0","url":null,"abstract":"<p><p>Epidemiological studies revealed associations between maternal lead (Pb) exposure and adverse pregnancy and birth outcomes as well as neurodevelopmental disorders. However, the underlying mechanisms remained unclear, and thus was investigated at the transcriptional level in this study using human embryonic stem cells (hESCs). Differentiation of hESCs to ectoderm was induced for 7 days using STEMdiff™ Trilineage Differentiation Kit containing 0 (water), 6.2 (geometric mean concentration of Pb in human maternal blood), or 118 µg Pb²⁺/L, in the form of lead chloride (PbCl₂), followed by bulk RNA sequencing. Both doses of PbCl₂ altered gene expression related to protein metabolism and trafficking, while also causing changes in genes involved in gastrulation, proliferation, DNA repair, stress response, and immune-cell development. PbCl₂ at the low dose induced gene changes predicting decreased cell proliferation and increased sensory loss. Cells exposed to the high dose of PbCl₂ had a distinct global gene expression profile from that of control cells with specific changes predicting increased neurodegeneration. The differences in expression of ectoderm lineage marker genes (ELMG) between control and PbCl₂ treated cells did not reach statistical significance. However, expression of some genes downstream of ELMG differed markedly between control and PbCl₂ treated cells. Multiple adverse outcome pathways involving WNT, IGF-1, RHO-PKN, CDK5, MAP kinase, and Ca²⁺ signaling, cell cycle control, protein metabolism and trafficking, DNA double strand break and repair, and immune response were detected in PbCl₂ treated cells. Overall, the findings suggest that Pb exposure disrupted early ectodermal development by prioritizing genome preservation over fate execution.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrodotoxin (TTX): What do we currently know? The state of the art.","authors":"Łukasz Niżnik, Kamil Kuca, Eugenie Nepovimová, Kamil Jurowski","doi":"10.1007/s00204-026-04548-z","DOIUrl":"https://doi.org/10.1007/s00204-026-04548-z","url":null,"abstract":"<p><p>Tetrodotoxin (TTX) is one of the most potent naturally occurring neurotoxins and continues to attract considerable scientific, clinical, forensic, and regulatory attention. Historically associated with pufferfish poisoning in East and Southeast Asia, TTX has recently emerged as a global food safety concern due to its detection in an increasing number of marine and terrestrial organisms and its expanding geographical distribution, including European coastal waters. Despite decades of research, important questions regarding its biosynthesis, ecological origin, toxicokinetics, and environmental dissemination remain unresolved. This review provides a comprehensive overview of current knowledge on TTX. The chemical structure, physicochemical properties, proposed biosynthetic origin, and diversity of naturally occurring TTX analogues are discussed. Attention is devoted to the toxin's mechanism of action, which involves high-affinity binding to voltage-gated sodium channels and subsequent inhibition of sodium ion conductance, leading to neuromuscular paralysis and potentially fatal respiratory failure. Current evidence regarding toxicokinetics, tissue distribution, elimination pathways, and the suitability of different biological matrices for laboratory confirmation of exposure is also summarized. The review further examines the analytical challenges associated with TTX determination, including its high polarity, occurrence at trace concentrations, rapid elimination from blood, and frequent co-occurrence with structurally related analogues. The evolution of analytical methodologies is presented, from early bioassays and chromatographic techniques with fluorescence or UV detection to advanced liquid chromatography-mass spectrometry platforms, high-resolution mass spectrometry, capillary electrophoresis, immunochemical assays, and emerging biosensor-based approaches. Finally, current regulatory perspectives and risk assessment strategies are discussed in the context of the increasing occurrence of TTX in seafood and the growing need for harmonized monitoring programs. Collectively, this review summarizes the current state of the art, identifies key knowledge gaps, and highlights future directions in TTX research.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cysteine-based molecular switches: a focus on KEAP1 and BACH1 in regulating the antioxidant response.","authors":"Jialin Feng, Albena T Dinkova-Kostova","doi":"10.1007/s00204-026-04562-1","DOIUrl":"https://doi.org/10.1007/s00204-026-04562-1","url":null,"abstract":"<p><p>Due to the chemical properties of their thiol groups and the surrounding amino acid environment, specific cysteines in proteins serve as the principal intracellular sensors for oxidants and electrophiles. In this review, we focus on the ubiquitin ligase substrate adaptor Kelch-like ECH-associated protein 1 (KEAP1) and the transcriptional repressor BTB and CNC homology 1 (BACH1) as representative cysteine-based molecular switches, both of which have critical functions in the cellular antioxidant response. KEAP1 is a protein endowed with a number of highly reactive cysteines, which can be covalently and preferentially modified by a wide array of reactive oxygen species, reactive nitrogen species and reactive electrophilic species, from endogenous as well as exogenous origin. Covalent cysteine modifications are also involved in the regulation of the localisation, stability and turnover of BACH1. Both KEAP1 and BACH1 antagonize the constitutively expressed transcription factor NF-E2 p45-related factor 2 (NRF2), the master regulator of the cellular antioxidant response, thus keeping the transcriptional activity of NRF2 low at homeostatic state. Cysteine modifications within KEAP1 and BACH1 render the repressor proteins inactive, resulting in rapid NRF2 activation that does not rely on de novo transcription of NFE2L2, the gene encoding NRF2. Consequently, NRF2 induces the transcriptional upregulation of a large network of genes encoding cytoprotective proteins, many of which have antioxidant functions, restoring the redox homeostasis.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Demonstrating the reliability of in vivo metabolomics-based chemical grouping: Part 2 - Consistency of group-specific metabolic effects.","authors":"G R Lloyd, C Sands, A Kende, V Haake, E Amstalden, M Bouhifd, T Ebbels, F Lai, P E G Leonards, U Simanainen, T Sobanski, A D Southam, L Swindale, R J M Weber, F M Zickgraf, H Kamp, M R Viant","doi":"10.1007/s00204-026-04570-1","DOIUrl":"https://doi.org/10.1007/s00204-026-04570-1","url":null,"abstract":"<p><p>Previously, the MetAbolomics ring-Trial for CHemical groupING (MATCHING) demonstrated high inter-laboratory reproducibility in the blinded application of rat plasma metabolomics to group eight substances (aniline, 2-chloroaniline, 4-chloro-3-nitroaniline, dichlorprop-p, fenofibrate, 17α-methyl-testosterone, trenbolone, WY-14643). Each ring-trial partner applied their preferred metabolomics workflows to acquire, process, quality assess and statistically analyse their data. All five partners whose datasets passed quality control correctly clustered the substances into three groups according to previously established toxicological effects, both for female and male rats. However, to ensure high confidence in each grouping hypothesis, metabolomics data should support a plausible toxicological interpretation by linking changes in annotated metabolite profiles to known toxicological effects associated with the substances. In this follow-up study, our first data-driven objective was to determine the consistency of group-specific discriminatory metabolites (including lipids) across partners. For all six cases (three groups in female and male rats), statistically significant consistency was observed, confirming that all partners discovered similar metabolic perturbations underpinning each group. Strikingly, this was achieved even though a range of statistical and computational approaches were used for both discovering and annotating discriminatory metabolites. Secondly, we evaluated whether pre-existing toxicological knowledge, organised using an Adverse Outcome Pathway-informed framework of metabolomic associative events (mAEs), could provide plausible toxicological interpretations of the partner's discriminatory metabolite profiles, for each toxicological effect (androgen receptor activity (AR), peroxisome proliferation (PP), anaemia). Binomial distribution analysis revealed statistically significant detection of characteristic mAEs for all six cases, albeit with insufficient specificity across the three effects. Consequently, a third objective was developed, to refine the mAEs by combining the pre-existing toxicological knowledge with partner-to-partner detection reproducibility of metabolites and their directional change, thereby significantly enhancing mAE detection specificity. Overall, the discovery by the five partners of significantly consistent metabolic perturbations underpinning each group further demonstrates the reliability of metabolomics for chemical grouping. Moreover, an integrated knowledge and data-driven approach is presented as a basis for deriving metabolomic signatures that were used to support plausible toxicological interpretations of the metabolomics data. Considering the broader implications of this study, we propose the development of a collaborative framework to facilitate community-driven contributions to a shared knowledgebase of metabolomic signatures.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methodological considerations for pharmacovigilance signal prediction in drug-induced lung injury: comment on Zhao et al.","authors":"Juan Zhang, Linlin Zhang","doi":"10.1007/s00204-026-04559-w","DOIUrl":"https://doi.org/10.1007/s00204-026-04559-w","url":null,"abstract":"","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2-Amino-3-methylimadazo[4,5-f]quinoline (IQ) induces cytochrome P450 1A through the canonical AhR-XRE pathway in human hepatocytes.","authors":"Minna A Choi, Medjda Bellamri, Arnaud Tete, Etienne B Blanc, Sophie Langouët","doi":"10.1007/s00204-026-04565-y","DOIUrl":"https://doi.org/10.1007/s00204-026-04565-y","url":null,"abstract":"<p><p>Heterocyclic aromatic amines (HAAs) are procarcinogens formed during the cooking of meat and fish and could potentially contribute to hepatocellular carcinoma. Although several HAAs are classified as possible or probable human carcinogens, most mechanistic studies have relied on rodent models, despite well-documented interspecies differences in HAA bioactivation by cytochrome P450 (CYP) isoforms. In this study, we investigated the regulation of CYP1A by the HAA 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) using complementary primary human hepatocytes and Hepoid® with HepaRG cells, a long-term 3D liver spheroid model. IQ at concentrations ranging from 0.1 to 20 µM strongly induced CYP1A1 and CYP1A2 expression and enzymatic activity following acute and chronic exposure, whereas other major hepatic CYP isoforms remained unaffected. This response was specific to IQ among other HAAs tested and to human hepatocytes and persisted for up to 28 days in 3D spheroids. IQ-induced CYP1A expression required transcriptional activation and involved the aryl hydrocarbon receptor (AhR). Using complementary pharmacological and genetic approaches, luciferase reporter assays and ligand-binding assays, we demonstrate that IQ is a direct AhR ligand that activates the canonical AhR-xenobiotic response element (XRE) signaling pathway in human hepatocytes. These findings indicate that IQ is a potent and selective inducer of CYP1A through the AhR and induces a sustained human-specific response upon repeated treatment. Persistent CYP1A induction and AhR activation may enhance the bioactivation of IQ and other co-occurring CYP1A substrates, highlighting the value of long-term human-relevant models to improve risk assessment of chemical carcinogens.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetogenic effects of arsenic exposure in C57BL/6 N mice carrying the human AS3MT gene: the role of sex and exposure window.","authors":"Navkaran Singh, Christelle Douillet, Yelyzaveta Minaieva, Bingzhen Shang, Fernando Pardo-Manuel de Villena, Rebecca C Fry, Miroslav Styblo","doi":"10.1007/s00204-026-04568-9","DOIUrl":"https://doi.org/10.1007/s00204-026-04568-9","url":null,"abstract":"<p><p>Chronic exposure to inorganic arsenic (iAs) has been linked to diabetes in both humans and laboratory mice. Prior studies highlight that the mechanism underlying the diabetogenic effects of iAs and the manifestation of iAs-associated diabetes depend, in part, on the exposure window. We have shown that exposure to iAs prior to conception or in utero consistently produced diabetic phenotypes in wild-type (WT) C57BL/6J mice and that this phenotype was characterized primarily by insulin resistance. The effects of postnatal iAs exposures have been less consistent. However, significance of these findings for human exposure remains unclear because WT mice metabolize and detoxify iAs more efficiently than humans. The present study describes the diabetogenic effects of iAs in humanized C57BL/6 N mice that express the human arsenic methyltransferase and exhibit human-like patterns of iAs metabolism. We examined diabetes indicators in male and female offspring of parents exposed to 0 (controls) or 200 ppb iAs (arsenite) prior to conception (PC), and offsprings exposed to iAs in utero (IU), or during the whole life, including the PC and IU windows. We found that only PC exposure produced diabetic phenotype in male offspring. This phenotype was characterized by elevated fasting blood glucose (FBG) and decreased HOMA-B, the indicator of beta cell function. However, fasting plasma insulin and HOMA-IR, the indicator of insulin resistance, were not affected. FBG was also higher in male mice after IU exposure as compared to control male mice, but this difference was not statistically significant. LL exposure had no significant effects in male offspring. No differences in diabetes markers were found between iAs-exposed and control female mice regardless of exposure window. These results suggest that PC exposure produced fasting hyperglycemia in the humanized male mice by impairing the function of insulin secreting beta cells. However, postnatal iAs exposure appeared to attenuate these effects, suggesting that activation of compensatory mechanisms may take place after birth. These findings may inform designs of population studies that examine iAs-associated diabetes, as well as the interpretation of data collected in these studies.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Publisher intervention in editorial decision-making: when established editorial procedures no longer determine publication decisions.","authors":"Jan G Hengstler","doi":"10.1007/s00204-026-04560-3","DOIUrl":"https://doi.org/10.1007/s00204-026-04560-3","url":null,"abstract":"<p><p>The credibility of scientific journals is often attributed to rigorous peer review and editorial independence. In reality, however, scientific publishing, like every human institution, is shaped by competing interests, institutional incentives, and errors of judgment. Its credibility therefore depends less on the presumed virtues of authors, reviewers, editors, and publishers than on transparent procedures, clearly defined responsibilities, and institutional arrangements that make departures from established standards visible and open to scientific scrutiny. This Editorial examines a revealing recent case in which publication of a Guest Editorial that had successfully completed the established editorial procedures of Archives of Toxicology was ultimately prevented by the Publisher. Rather than discussing the scientific merits of the underlying manuscript, the present analysis focuses on how the publication decision changed after the manuscript had already been formally accepted. The documented events show how the publication process was progressively compromised through a succession of additional procedural requirements, each introduced only after the preceding requirement had been fulfilled. As a consequence, publication no longer depended on completion of the journal's published editorial process but on successive interventions outside that process. The case illustrates that transparent editorial procedures alone are insufficient to safeguard editorial integrity. Effective institutional self-correction requires a second, equally important safeguard: the guaranteed possibility that alleged departures from editorial procedures can themselves be subjected to unobstructed public scientific scrutiny through mechanisms such as Commentaries or Opinion Articles. In the present case, both safeguards were compromised simultaneously. The established editorial procedures were progressively displaced, while the very mechanism intended to permit public examination of alleged procedural failures was itself prevented from operating. The present analysis argues that departures from editorial procedures are not corrected automatically. They become self-correcting only when independent publication pathways remain available in which transparent editorial governance is preserved. The long-term credibility of scientific publishing therefore rests not primarily on confidence in individuals but on institutional structures that make procedural departures visible, increase the expected cost of abusing institutional power, and guarantee that alleged failures of governance can themselves be subjected to public scientific scrutiny. Transparency without the guaranteed possibility of such scrutiny remains incomplete.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}