Archives of Toxicology最新文献

{"title":"Circadian rhythm, oxidative stress, and cancer immunosuppression","authors":"Li You,&nbsp;Eugenie Nepovimova,&nbsp;Qinghua Wu,&nbsp;Kamil Kuca","doi":"10.1007/s00204-026-04500-1","DOIUrl":"10.1007/s00204-026-04500-1","url":null,"abstract":"<div><p>Circadian rhythm and oxidative stress are fundamental biological regulators whose intricate interplay plays a pivotal role in cancer progression and immunosuppression. These two factors engage in a bidirectional, self-reinforcing pathological loop that drives tumor progression and fosters an immunosuppressive tumor microenvironment. In the context of cancer, circadian rhythm disruption promotes immunosuppression by reducing cytotoxic CD8⁺ T cell infiltration while expanding populations of immunosuppressive cells such as regulatory T cells and myeloid-derived suppressor cells. Oxidative stress acts as a pivotal effector with dual roles, it promotes immunosuppression by polarizing macrophages toward an M2 phenotype, yet it is also strategically harnessed to disrupt immunosuppressive networks. Critically, oxidative stress serves as a central link, wherein circadian rhythm disruption, through the accumulation of ROS, drives the recruitment of immunosuppressive cells and upregulates immune checkpoints such as PD-L1, thereby suppressing anti-tumor immunity. Furthermore, emerging evidence highlights the potential of circadian rhythm as a prognostic biomarker and underscores the promise of chrono-immunotherapy, which strategically times interventions to align with the circadian rhythm to optimize anti-tumor immune function. Collectively, the circadian rhythm and redox balance represent novel therapeutic targets, with pharmacological agents that restore circadian rhythm and enable cell-selective modulation of oxidative stress. Thus, integrating circadian rhythm and oxidative stress into oncology offers a promising strategy to improve cancer prevention, prognosis, and treatment outcomes.</p></div>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":"100 9","pages":"3857 - 3881"},"PeriodicalIF":10.9,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410003","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":"When remediation creates toxicological risk: transformation products and the soil exposome in contaminated agroecosystems.","authors":"Wajid Zaman, Asma Ayaz","doi":"10.1007/s00204-026-04504-x","DOIUrl":"10.1007/s00204-026-04504-x","url":null,"abstract":"<p><p>Remediation is often considered successful when parent contaminants decline, visible pollution disappears, or extractable concentrations fall below target values. In contaminated agroecosystems, however, contaminant disappearance does not necessarily mean toxicological risk disappearance. Agricultural soils are reactive exposure interfaces where pollutants interact with minerals, organic matter, enzymes, microbes, and plant roots, often generating transformation products with different mobility, persistence, bioavailability, and toxicity from their parent compounds. This commentary proposes the soil exposome as a framework for evaluating remediated agroecosystems as dynamic exposure systems shaped by chemical mixtures, transformation pathways, microbial responses, plant uptake, and potential dietary exposure. We argue that remediation can create or obscure risk when assessment remains limited to removal efficiency or parent-compound monitoring. A toxicology-oriented evaluation should therefore integrate transformation-product profiling, effect-based bioassays, bioavailability testing, microbial and soil-function indicators, phytotoxicity assessment, and crop-safety verification. Moving from pollutant removal to verified exposure-system recovery is essential for ensuring that remediation reduces toxicological hazard while supporting soil function, crop safety, and long-term environmental sustainability.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148395579","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":"TEAD inhibitor induced switch in energy metabolism drives human podocyte injury in vitro.","authors":"Alexander Zielinski, Julia Hauptstein, Bernd Baier, Peter Schaarschmidt, Natalie Ketter, Daniel R Dietrich, Florian Meier","doi":"10.1007/s00204-026-04497-7","DOIUrl":"https://doi.org/10.1007/s00204-026-04497-7","url":null,"abstract":"<p><p>Early detection and understanding of the potential adverse effects of a drug candidate is of utmost importance to reduce the attrition rate during drug development while delivering safe medications to patients. The kidney is one of the most frequently challenged organs involved in drug-induced toxicity, including general glomerulopathy and podocyte- specific cytotoxicity with ensuing overt proteinuria. Whilst TEAD inhibitors address the need for treatment of mesotheliomas and other tumours unaffected by approved drugs, animal testing and clinical trials provide evidence of renal toxicity induced by this novel class of drugs. Here we present an in vitro test system consisting of immortalized human podocytes PODO/TERT256 to characterize the potential adverse effects of TEAD inhibitors. We demonstrate that TEAD inhibitors K-975, IK-930 and VT-107 affect the podocyte monolayer in a wide dose range (33.3-100 µM), disrupt the cellular vesicle system, and subsequently induce cell death, especially after exposure to pan-TEAD inhibitors (VT-107 and K-975). Of note, low micromolar concentrations of TEAD inhibitors lowered mitochondrial oxidative phosphorylation directly after exposure which was confirmed by reduced basal ATP levels after 3 d of exposure. In summary, the in vitro human podocyte model presented can characterize glomerular filtration functionality decline subsequent to TEAD inhibitor exposure and thus represents a promising model for early detection and prediction of potential drug related glomerulopathy in humans.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148434934","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":"Developmental exposure to a human-relevant PCB mixture: impacts on PCB congeners, metabolites, and drug-metabolizing enzymes in the bladder of post-weaning mice.","authors":"Hui Wang, Alex Goskowicz, Audrey Spiegelhoff, Conner L Kennedy, Monica M Ridlon, Rachel F Marek, Hans-Joachim Lehmler, Kimberly P Keil Stietz","doi":"10.1007/s00204-026-04498-6","DOIUrl":"10.1007/s00204-026-04498-6","url":null,"abstract":"<p><p>Many women suffer from symptoms associated with dysfunction of the lower urinary tract, including incontinence and overactive bladder, especially during pregnancy. While causes are likely multifactorial, environmental factors, such as exposure to polychlorinated biphenyls (PCBs), have been shown to alter voiding in adult female mice. However, the distribution of PCBs and their metabolites to the bladder and urine, as well as their effects on bladder drug-metabolizing enzyme expression after dosing with PCB mixtures, remains largely unexplored. Female C57BL/6J mice were exposed to MARBLES PCB mixture (0, 0.1, 1, and 6 mg/kg/d) through gestation and lactation, and post-weaning bladder, urine, blood, adipose, and liver were collected for measurement of PCBs and OH-PCBs, and for abundance of cytochrome P450 (Cyp) transcripts in liver and bladder. PCBs and OH-PCBs were detected in all tissues in a dose-dependent manner. Bladder, adipose, and liver retained parent PCBs while OH-PCBs were predominant in urine and blood. Cyp1a2 mRNA abundance was elevated in the liver of the high dose PCB group versus the vehicle, and the same trend was observed in the bladder. These results define the signatures of PCBs and OH-PCBs in the bladders and urine of post-weaning dams exposed to the MARBLES mixture of PCBs and provide a reference for comparison with accumulation in more commonly studied tissues. Our results also provide new insights into the regulation of Cyp1a2 in the liver and bladder, changes that may play a role in how environmental exposures in adulthood alter voiding function.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13637031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network toxicology deciphers micro- and nanoplastics-mediated mixture hazard, predictive risk assessment, and regulatory translation.","authors":"Wenjuan Wu, Yán Wāng","doi":"10.1007/s00204-026-04496-8","DOIUrl":"https://doi.org/10.1007/s00204-026-04496-8","url":null,"abstract":"<p><p>Micro- and nanoplastics (MNPs) are pervasive environmental contaminants and efficient carriers of coexisting pollutants, including heavy metals, organic chemicals, and antibiotics. Their capacity to adsorb, transport, and release contaminants has raised growing concern over mixture toxicity under realistic exposure scenarios. This review systematically examines the mechanistic basis of MNPs-mediated combined toxicity and evaluates the emerging role of network toxicology as a systems-based tool for hazard assessment. MNPs alter the bioavailability, environmental fate, tissue distribution, and intracellular delivery of associated pollutants through hydrophobic, electrostatic, and other intermolecular interactions. Carrier-mediated uptake, particularly the \"Trojan horse\" effect, appears to be a major driver of non-additive toxicity in co-exposure systems. We then outline the core workflow of network toxicology, encompassing target identification, network construction, pathway enrichment, and experimental validation, and discuss its application in decoding mixture toxicity. Oxidative stress, inflammatory signaling, metabolic disturbance, barrier dysfunction, and programmed cell death emerge as conserved and interconnected pathways underlying synergistic multi-organ injury. These findings indicate that toxicity in complex exposure systems is governed not only by the intrinsic properties of particles or chemicals, but also by their dynamic physicochemical and biological interactions. We further assess current advances and limitations in network toxicology and propose a next-generation risk assessment (NGRA)-oriented framework to support mechanism-based risk assessment and regulatory decision-making. Although current evidence is dominated by binary, high-dose laboratory studies, network toxicology offers strong potential as a new approach methodology (NAM) for predictive evaluation of environmentally relevant mixtures. Future priorities include standardized multi-omics integration, dose-time-response modeling, human-relevant validation, and regulatory translation.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374332","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":"Scientific approach to derive occupational exposure limits for formaldehyde releasers.","authors":"Sandra Michaelsen, Britta Laube, Rüdiger Bartsch, Stephan Baumgärtel, Dietmar Breuer, Rolf Grebenstein, Edgar Leibold, Ruth Lohmann, Hans Merk, Carsten Schleh, Manigé Fartasch, Michael Bader, Hans Drexler, Brunhilde Blömeke, Andrea Hartwig","doi":"10.1007/s00204-026-04489-7","DOIUrl":"https://doi.org/10.1007/s00204-026-04489-7","url":null,"abstract":"<p><p>Formaldehyde is highly reactive, causing irritation and acute and chronic toxicity in target tissues (the eyes, respiratory tract, and skin) following inhalation and/or skin contact. Moreover, formaldehyde is a local carcinogen after inhalation exposure. It induces nasal squamous cell carcinoma in laboratory animals and nasopharyngeal carcinoma in humans, albeit less convincingly. While formaldehyde has been evaluated and classified by different organizations and committees in recent years, the question has arisen of how to deal with substances that release formaldehyde. These releasers decompose in aqueous media and are frequently used as biocides in water-miscible metalworking fluids, adhesives, paints, disinfectants, and cosmetics. In this context, the MAK Commission has developed a concept for differential evaluation regarding carcinogen classification and MAK value derivation. This approach is based on hydrolysis rates as a function of pH, temperature, and concentration under physiological conditions. Furthermore, vapor pressure is considered to determine whether the formaldehyde releaser will be present as a vapor or aerosol upon inhalation. This concept is demonstrated using four examples that lead to different carcinogen classifications and MAK value derivations. Additionally, the releasers were evaluated for percutaneous absorption and sensitization.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374263","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":"Molecular dosimetry of hemoglobin adducts in mice exposed to ethylene oxide.","authors":"Chih-Wei Liu, Jiahao Feng, Jingya Peng, Haoduo Zhao, Xueying Wang, B Bhaskar Gollapudi, Abby A Li, James S Bus, Christopher Kirman, Kun Lu","doi":"10.1007/s00204-026-04419-7","DOIUrl":"10.1007/s00204-026-04419-7","url":null,"abstract":"<p><p>Ethylene oxide (EtO) is a widely used industrial compound with known carcinogenic potential in humans. Due to its high reactivity and short biological half-life, occupational exposure assessments (> 1 ppm) rely on the detection of stable biomarkers, such as N-(2-hydroxyethyl)-L-valine (HE-V), formed as hemoglobin adducts in blood. Existing analytical methods for HE-V detection often require large volumes of blood and purified hemoglobin due to limited sensitivity, restricting their application in characterizing the dose-response relationship between EtO exposure and HE-V accumulation-particularly at low environmental exposure levels relevant to assessing potential general population health risks. In this study, we aimed to characterize the molecular dosimetry of HE-V formation in B6C3F1 mice exposed by whole body inhalation to a broad range of concentrations of EtO: 0, 0.05, 0.1, 0.5, 1, 50, 100, and 200 ppm, 7 days/week for 4 weeks. To achieve this, we developed a sensitive LC-MS-based workflow for HE-V quantification, incorporating hemoglobin purification, HE-V release plus enrichment, and targeted mass spectrometric detection from as little as 10 μL of blood and 50 μg of extracted hemoglobin. A clear, dose-dependent increase in HE-V levels was observed following EtO exposure, with statistically significant elevations detected even at 0.05 ppm compared to endogenous background levels. At lower concentrations (0.5 to 1 ppm), HE-V levels increased linearly with dose, while higher concentrations (50 to 200 ppm) exhibited an upward-bending (increasing slope) dose response. No sex-specific differences were observed. Taken together, these findings indicate EtO exhibits linear systemic toxicokinetics at lower exposures that transition to nonlinear toxicokinetics in the range of higher exposures (likely due to saturation of glutathione-mediated detoxification), thus providing new quantitative insights to support improved risk assessments and toxicological evaluations of EtO exposure.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148359147","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":"From data mining to mechanistic prediction: a study on drug-induced lung injury integrating FAERS, machine learning, and network toxicology.","authors":"Yihuan Zhao, Jiawang Yan, Yaofeng Zhou","doi":"10.1007/s00204-026-04488-8","DOIUrl":"10.1007/s00204-026-04488-8","url":null,"abstract":"<p><p>Drug-induced lung injury (DLI) is a serious and potentially fatal adverse drug reaction that remains difficult to detect early and continues to challenge both drug development and clinical safety. Because current diagnosis relies largely on exclusion and lacks specific early warning biomarkers, there is an urgent need for an integrated strategy that enables both risk prediction and mechanistic interpretation. To address this unmet need, we for the first time develop and validate a comprehensive integrated research strategy that combines FAERS database mining, XGBoost-based machine learning, and network toxicology, and is specifically designed for early DLI risk assessment and in-depth exploration of the underlying mechanisms. DLI-related adverse event reports were systematically extracted and standardized from FAERS to construct a curated small-molecule drug dataset. An optimized XGBoost model was then built using structural, physicochemical, and target-based features to predict DLI risk. In parallel, network toxicology was applied to construct drug-target-pathway networks for high-risk compounds and to identify key toxicological mechanisms. Our results highlighted MMP9 and ERBB2 as core targets associated with the pulmonary toxicity of Sunvozertinib and Zongertinib, and subsequent molecular docking and molecular dynamics simulations further suggested stable binding between the compounds and the above targets. This integrated framework enables efficient early prediction of DLI risk while providing mechanistic insights into drug-induced pulmonary toxicity. Overall, our study offers a practical and reproducible computational strategy for DLI risk assessment in drug development and supports safer clinical medication and rational drug design.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148343788","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":"Copper oxide nanoparticles: from EU-regulatory landscape and mechanistic toxicity towards a cuproptosis-linked adverse outcome pathway.","authors":"Sophie Scholz, Julia Prinz, Linde Sevenants, Andrea Holzwarth, Birgit Mertens, Robert Pieper, Vera Ritz, Kirsten Schulz, Holger Sieg, Aswin Mangerich, Linda Böhmert","doi":"10.1007/s00204-026-04465-1","DOIUrl":"https://doi.org/10.1007/s00204-026-04465-1","url":null,"abstract":"<p><p>Copper is an essential trace element, yet concerns regarding its toxic potential have gained increasing attention, particularly with regard to nanoparticulate forms of copper oxides. Both CuO and Cu₂O are currently authorised in the EU for use in agriculture, biocides, and animal nutrition, but regulatory clarity regarding their nanoforms remains limited. This comprehensive review-combining narrative, bibliometric, and systematic approaches-addressed three key questions: (i) whether CuO and Cu₂O nanoparticles are sufficiently considered within EU regulations to prevent unintentional oral exposure via the food and feed chain, (ii) whether these nanoparticles can cross the intestinal barrier as intact particles and accumulate in tissues, and (iii) whether they elicit distinct biological responses, including regulated cell death pathways such as cuproptosis. With respect to question (i), a detailed analysis of EU legal frameworks revealed a heterogeneous regulatory landscape and a lack of binding provisions that would preclude unintended presence of copper oxide nanoforms in regulated materials. Although some nano-specific data requirements exist, empirical information on nanoparticulate fractions in commercial products is still lacking. With respect to questions (ii) and (iii), our systematic literature analysis supports consistent intracellular uptake of CuO and Cu₂O nanoparticles, yet direct evidence for transport of intact particles across the intestinal barrier is scarce. Mechanistic evidence supports cuproptosis as a key pathway for CuO nanoparticle toxicity, while the extent to which these effects differ quantitatively from ionic copper remains unclear due to insufficient data using appropriate experimental controls. Notably, a pronounced data gap was identified for Cu₂O nanoparticles across all evaluated domains. Finally, to organise and integrate the mechanistic evidence presented, we developed an adverse outcome pathway (AOP), registered as AOP 590 in the AOP Wiki, describing how increased intracellular copper can induce cuproptosis via disruption of energy metabolism. Collectively, these findings highlight the need for coordinated analytical, mechanistic, and regulatory research to support evidence-based risk assessment of CuO and Cu₂O nanoparticles in the food and feed context.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337558","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":"Chemical components of tattoo inks and their potential role in carcinogenesis and their side effects.","authors":"Luiza Czaczkowska, Ewa Jabłońska, Julia Bury, Natalia Szurant, Wioletta Ratajczak-Wrona","doi":"10.1007/s00204-026-04484-y","DOIUrl":"https://doi.org/10.1007/s00204-026-04484-y","url":null,"abstract":"<p><p>Tattooing is an invasive procedure that has gained popularity, particularly among individuals. Growing attention has been directed toward the safety of tattoo ink ingredients, which are complex mixtures of synthesis precursors and byproducts. These inks may contain classified carcinogens, heavy metals, polycyclic aromatic hydrocarbons (PAHs), and phthalates, often at concentrations exceeding permissible limits. Tattooing involves the insertion of needles 1-3 mm into the dermis. While part of the pigment is eliminated with epidermal turnover, approximately 25% is transported to lymph nodes and subsequently into the bloodstream. The remaining pigment is engulfed by phagocytic cells involved in innate immunity. Repeated needle punctures trigger local inflammation, recruitment of immune cells, and release of inflammatory mediators, followed by tissue regeneration and remodelling driven by keratinocytes, fibroblasts, and endothelial cells. Cases of malignant melanoma, squamous cell carcinoma, keratoacanthoma, and lymphoma have been reported in individuals with tattoos. However, the relationship between tattooing and cancer is not fully understood. It is suspected that the cause may be the transfer of toxic substances to lymph nodes and then to organs. The possible carcinogenic effects of tattoo ink ingredients will be discussed based on available scientific reports.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337574","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}