Current Research in Toxicology最新文献

{"title":"Application to developmental toxicity testing of a novel method for whole-brain imaging of microglia in zebrafish","authors":"Mizuki Yuge ,&nbsp;Junko Koiwa ,&nbsp;Takashi Shiromizu ,&nbsp;Eri Wakai ,&nbsp;Akira Migoguchi ,&nbsp;Yuhei Nishimura","doi":"10.1016/j.crtox.2025.100276","DOIUrl":"10.1016/j.crtox.2025.100276","url":null,"abstract":"<div><div>Microglia, parenchymal macrophages resident in the central nervous system, regulate brain development by dynamically changing their functional and morphological states in a spatiotemporal-dependent manner. Because the function of microglia may differ depending on their location, their status should ideally be assessed within discrete brain regions. In this study, we developed a novel whole-brain imaging method to visualize microglial morphology in the forebrain, midbrain, and hindbrain of live zebrafish larvae at 5–6days post-fertilization, and quantified various morphological parameters using MorphoLibJ, a publicly available tool for mathematical analysis of three-dimensional images. We applied this method to assess the developmental toxicity of ethanol and valproic acid on microglial morphology in the zebrafish larvae, and were able to detect marked differences in the spatiotemporal effects of each compound. The duration of exposure required to detect significant changes in microglial morphology was shorter for ethanol than for valproic acid, and microglia in the forebrain diencephalon region were more susceptible to toxicity induced by ethanol compared with valproic acid. These results suggest that our whole-brain microglial imaging and modeling method may be a versatile tool to assess the developmental toxicity of chemicals in zebrafish.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100276"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145788189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multigenerational effects of uranium exposure reveal stronger testicular dysregulation in the second generation","authors":"Audrey Legendre ,&nbsp;Céline Gloaguen ,&nbsp;Dimitri Kereselidze ,&nbsp;Nawel Saci ,&nbsp;Sophia Murat El Houdigui ,&nbsp;Pascal Froment ,&nbsp;Christelle Elie ,&nbsp;Catherine Defoort ,&nbsp;Philippe Lestaevel ,&nbsp;Mohamed Amine Benadjaoud ,&nbsp;Maâmar Souidi ,&nbsp;Stéphane Grison","doi":"10.1016/j.crtox.2025.100279","DOIUrl":"10.1016/j.crtox.2025.100279","url":null,"abstract":"<div><h3>Background</h3><div>Infertility is a significant public health issue that can be influenced by environmental pollutants. As a radioactive heavy metal and environmental contaminant, uranium has the potential to impact fertility.</div></div><div><h3>Objective</h3><div>This study assesses the multigenerational reproductive effects of chronic, non-nephrotoxic uranium exposure across three generations of male rats.</div></div><div><h3>Methods</h3><div>In this study, a non-nephrotoxic uranium solution (40 mg/L) was chronically administered <em>via</em> drinking water to male and female F0 rats (n = 20 per group) throughout their lifespan. The objective was to evaluate the potential reprotoxic effects of uranium on males across three generations (F0, F1, F2), with a focus on spermatogenesis, steroidogenesis, and testicular homeostasis, including oxidative stress, inflammation, apoptosis, and vitamin D metabolism.</div></div><div><h3>Results</h3><div>Steroidogenesis was modulated in all generation, with dysregulation of sex and pituitary hormones (testosterone, estradiol, gonadotropins, Luteinizing Hormone (LH), Follicle-Stimulating Hormone (FSH). Morphological and histological changes in the testes were observed in both the F1 and F2 generations. Spermatogenesis was dysregulated by an increased proportion of seminiferous tubules at stage I-VI and reduced expression of <em>TH2B</em> and <em>eppin</em> mRNA. Interestingly, gene expression analysis of several markers involved in the regulation and protection of testicular homeostasis revealed significant effects only on the F2 generation. In this generation, uranium exposure also disrupted vitamin D metabolism in the testes.</div></div><div><h3>Conclusion</h3><div>Uranium may impair testicular function, with more pronounced effects observed in the F2 generation. These findings highlight its potential for multigenerational toxicity and underscore the need for further research into its impact on human reproductive health.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100279"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determination of the half-life of di(2-ethylhexyl) phthalate (DEHP) in a preterm neonate using blood transfusion as the source of intravenous exposure","authors":"Michael Furlong ,&nbsp;Venkata Gupta ,&nbsp;Stephanie Galanti ,&nbsp;Srinivasan Narasimhan ,&nbsp;Divya Pulivarthi ,&nbsp;Syam S. Andra ,&nbsp;Annemarie Stroustrup","doi":"10.1016/j.crtox.2026.100287","DOIUrl":"10.1016/j.crtox.2026.100287","url":null,"abstract":"<div><div>In the neonatal intensive care unit (NICU), infants face treatments that convey high-dose exposure to phthalates, a family of ubiquitous endocrine-disrupting organic chemicals. Past research shows that NICU-based phthalate exposure, particularly exposure to di (2-ethylhexyl) phthalate (DEHP), is associated with increased risk of abnormal multisystem outcomes among preterm infants. Blood product transfusion is a recognized significant source of DEHP exposure in hospitalized patients. In this pilot study we collected serial urine samples from one preterm subject following a clinically indicated blood transfusion as a sentinel DEHP exposure. Each specimen was analyzed for DEHP metabolites via liquid chromatography coupled with triple quadrupole tandem mass spectrometry. The calculated half-lives of DEHP metabolites in this subject were generally shorter than reported for adults. Our pilot data demonstrate the need for future studies to estimate population-level half-lives of DEHP metabolites in preterm infants to allow for more accurate NICU-based DEHP source identification than possible with estimates of DEHP metabolism in adults. Source identification is critical to mitigate exposure in the highly vulnerable NICU population.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100287"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147384961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel non-invasive imaging technique for mapping microplastic accumulation and distribution in different organ systems of Indian major carp Labeo rohita (Ham. 1822)","authors":"Sneha Siwach ,&nbsp;Aviral Singh ,&nbsp;Soumyadeep Paul ,&nbsp;Vanika Gupta ,&nbsp;Ishaan Gupta ,&nbsp;Ram Krishan Negi","doi":"10.1016/j.crtox.2026.100294","DOIUrl":"10.1016/j.crtox.2026.100294","url":null,"abstract":"<div><div>Microplastic (MP) pollution poses an increasing threat to the aquatic ecosystems, yet most existing detection methods remain largely destructive and spatially limited. Here, we present a novel, non-invasive imaging framework integrated with micro-computed tomography (µ-CT) and fluorescence microscopy to investigate ingestion, accumulation and internal distribution of fluorescently labelled polystyrene microplastics (PS-MP) in the commercially important fish species <em>Labeo rohita</em>. Fluorescence microscopy confirmed presence of MPs in the gastrointestinal (GI) tract, gills, muscle tissues and excreta of exposed fish, whereas, micro-computed tomography (µ-CT) facilitated non-destructive, three-dimensional whole-body imaging, allowing precise localization and visualization of internalized particles within intact organisms. A clear, progressive and exposure-dependent increase in microplastic presence was observed over the 28-day experimental period, supported by non-parametric trend and effect-size analyses, with consistently higher relative burdens under waterborne exposure compared to the dietary exposure, as revealed by complementary µ-CT and fluorescence imaging. Detection of microplastics in muscle tissue indicates systemic translocation beyond primary uptake organs, whereas their presence in excreta confirms active elimination processes. Strong spatial concordance between µ-CT and fluorescence microscopy validates the robustness of the dual-imaging approach. Collectively, this study advances microplastic ecotoxicology by establishing a scalable, high-resolution, non-invasive imaging framework for mapping and tracking microplastic fate in freshwater systems as well as organ-specific microplastic distribution and burden in freshwater fish under environmentally realistic exposure conditions.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100294"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147702655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zearalenone exposure may increase the risk of non-alcoholic fatty liver disease by activating CYP1B1-SCD1","authors":"Haonan Ruan ,&nbsp;Jing Zhang ,&nbsp;Yunyun Wang ,&nbsp;Dan Zhang ,&nbsp;Jiaoyang Luo ,&nbsp;Meihua Yang","doi":"10.1016/j.crtox.2025.100277","DOIUrl":"10.1016/j.crtox.2025.100277","url":null,"abstract":"<div><div>Zearalenone (ZEN) is an oestrogen-like mycotoxin that widely contaminates food and feed worldwide. Current research suggests that ZEN causes liver injury by disrupting hepatic lipid metabolism. Furthermore, prolonged disturbances in hepatic lipid metabolism are believed to play a role in the progression of non-alcoholic fatty liver disease (NAFLD). However, the exact association between ZEN exposure and the development of NAFLD is unclear. In this study, we established a rat model of ZEN-induced hepatic lipid accumulation (2.5, 5, 10 mg/kg/d b.w.,14 d, i.g.) to investigate the key targets of ZEN-induced hepatic lipid accumulation and to explore the potential link between ZEN exposure and NAFLD. Histological staining of rat liver showed that ZEN caused significant pathological changes and lipid accumulation; biochemical analysis showed that ZEN significantly and dose-dependently increased serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and disrupted the serum lipid profile in rats; proteomic analysis showed that ZEN significantly altered protein expression levels in rat liver, especially SOAT1, SOAT2, CYP1B1 and SCD1 (p &lt; 0.05). Through bioinformatics analyses, we combined ZEN exposure with a database of NAFLD clinical samples to reveal that ZEN exposure may increase the risk of NAFLD through activation of the CYP1B1-SCD1 pathway, and further animal experiments confirmed this. This study identifies the key target of ZEN-induced lipid accumulation and provides a basis for further research on the intrinsic link between ZEN exposure and NAFLD.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100277"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145788188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ca2+-independent cytotoxicity of menthol in the A549 lung cancer cell line","authors":"Kenji Takahashi,&nbsp;Toshio Ohta","doi":"10.1016/j.crtox.2025.100271","DOIUrl":"10.1016/j.crtox.2025.100271","url":null,"abstract":"<div><div>Menthol evokes cooling sensations by activating the transient receptor potential melastatin 8 (TRPM8) channel, resulting in relaxing, anti-inflammatory, and analgesic effects when administered through inhalation and topical application. Although the toxicity of menthol is relatively low, the mechanism underlying menthol-induced cytotoxic effects remains unclear. Thus, this study aimed to investigate the cytotoxic effects of menthol in the A549 lung cancer cell line. Menthol induced increases in intracellular Ca²⁺ concentrations ([Ca²⁺]_i) in distinct modes depending on its concentration. A relatively low concentration (0.3 mM) of menthol activated transient receptor potential ankyrin 1 (TRPA1) despite the expression of TRPM8 in A549 cells. A higher concentration (3 mM) of menthol nonspecifically induced Ca²⁺ release from intracellular stores. Menthol inhibited Ca²⁺-ATPase in the organelle membrane. At 3 mM, menthol elicited necrotic cell death accompanied by morphological changes within 60 min. This cytotoxicity was not prevented by HC-030031 (a TRPA1 blocker) or BAPTA-AM (an intracellular Ca²⁺ chelator). Furthermore, the analysis of the cytotoxicity of monoterpene analogs of menthol revealed structure-related activity in menthol-induced cytotoxicity. These findings indicate that menthol-induced cytotoxic effects are concentration-dependent and may provide valuable insights into novel therapeutic strategies for lung cancer.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100271"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145735324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scoparone induces mitophagy and apoptosis via ROS accumulation in pancreatic cancer cells","authors":"Ningna Weng ,&nbsp;Luping Lin ,&nbsp;Tong Lin ,&nbsp;Jinlu Liu ,&nbsp;Kai Zhu ,&nbsp;Sha Huang","doi":"10.1016/j.crtox.2026.100281","DOIUrl":"10.1016/j.crtox.2026.100281","url":null,"abstract":"<div><div>Pancreatic cancer (PC) is one of the deadliest malignancies worldwide. In the present study, we demonstrated that a traditional Chinese medicine extract monomer, scoparone (Scop), significantly inhibited the growth of PC cells both <em>in vitro</em> and <em>in vivo</em>. Further studies revealed that Scop could induce PINK1/Parkin-mediated mitophagy and apoptosis in PC cells; thus, inhibition of mitophagy could alleviate the anti-PC effect and apoptosis of Scop. Mechanistically, Scop exerts its anti-PC effects via the Akt/mTOR pathway. In addition, Scop increases the level of cellular reactive oxygen species (ROS) in PC cells, which may be a key factor, as the ROS inhibitor N-acetylcysteine significantly reversed the effects of mitophagy and apoptosis in PC cells. Our findings highlight Scop shows potential as a therapeutic lead candidate, offering novel insights into the antitumor potential of traditional Chinese medicine. This study elucidates the critical role of Scop in regulating mitophagy and apoptosis in PC cells, providing a foundation for future therapeutic development.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100281"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A mechanistic evaluation of the metabolism disrupting potential of methyl tert-butyl ether","authors":"A.N. Buerger ,&nbsp;M.J. Vincent ,&nbsp;S. Fitch ,&nbsp;B. Rivera ,&nbsp;N. Engel ,&nbsp;J. Zhang ,&nbsp;E.K. Rushton ,&nbsp;S.J. Borghoff","doi":"10.1016/j.crtox.2026.100290","DOIUrl":"10.1016/j.crtox.2026.100290","url":null,"abstract":"<div><div>European authoritative and regulatory assessments of endocrine disruption increasingly incorporate evaluation of metabolism disrupting potential, yet there are no regulatory- or authority-validated models or guidance to identify metabolism disrupting agents (MDAs), which are agents that increase the risk of developing metabolic disorders. Methyl <em>tert</em>-butyl ether (MTBE), a volatile organic compound utilized as a fuel additive in many countries, was recently concluded to be a suspected endocrine disruptor based on its potential to elicit insulin resistance in rodents via an endocrine mode of action (MOA) in a Regulatory Management Option Analysis (RMOA). Therefore, a thorough mechanistic assessment was conducted to evaluate the metabolism disrupting potential of MTBE. This novel approach included review of any mechanistic data including study/endpoint relevance and study reliability. Reliable data were mapped to the twelve key characteristics (KCs) of MDAs for critical evaluation of the strength of the evidence for activity within each KC. Next, the mechanistic data were contextualized and integrated within an MOA framework. No reliable epidemiological studies of MTBE were identified. Across eight KCs, largely inconsistent activity was identified in reliable <em>in vivo</em> and <em>in vitro</em> studies related to lipid, insulin, and glucose processes. MOA analysis further demonstrated inconsistent (endocrine) activity related to metabolism disruption and a lack of biologically plausible links between MTBE and metabolism disruption. Based on the current evidence identified, MTBE does not consistently perturb insulin signaling or lipid metabolism via proposed MOAs for metabolic disorders. Overall, MTBE fails to show consistent activity and adverse effects related to metabolic disruption.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100290"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating the potential carcinogenic hazard of diisononyl phthalate in humans via systematic integration of human, animal cancer studies, and mechanistic data","authors":"Isabel A. Lea ,&nbsp;Amanda N. Buerger ,&nbsp;Melissa J. Vincent ,&nbsp;Brianna N. Rivera ,&nbsp;Neepa Y. Choksi ,&nbsp;Heather Schaefer ,&nbsp;Janice Britt ,&nbsp;Seneca Fitch ,&nbsp;Laurie Haws ,&nbsp;Susan J. Borghoff","doi":"10.1016/j.crtox.2026.100295","DOIUrl":"10.1016/j.crtox.2026.100295","url":null,"abstract":"<div><div>Diisononyl phthalate (DINP) is a high molecular weight phthalate used in commercial products and polyvinyl chloride production. Herein, a systematic evaluation of DINP evidence streams (i.e., human cancer, animal cancer, and mechanistic data) was carried out to inform carcinogenic hazard in humans. Relevant data from peer-reviewed literature and publicly available laboratory reports were extracted and critically appraised. Mechanistic data were organized according to the Key Characteristics of Carcinogens (KCCs) and integrated into key events in rodent cancer modes of action (MoAs). Evidence from epidemiological studies is limited, but does not indicate an association between DINP exposure and cancer, with three studies reporting no association with breast cancer, and one reporting an imprecise increase in prostate cancer risk. Four chronic bioassays demonstrated DINP causes cancer in rodents, with increases in liver tumors in mice and rats, kidney tumors in male F344 rats, and mononuclear cell leukemia (MNCL) in F344 rats. Mechanistic data strongly support that DINP is non-genotoxic (KCC2), and that in rodents DINP induces oxidative stress (KCC5) and alters cell proliferation (KCC10). Multiple evidence stream integration and interpretation support that DINP elicits rodent-specific liver tumors through the peroxisome proliferator-activated receptor alpha, a MoA widely considered to lack human relevance. Likewise, the weak kidney tumor response in male rats was attributed to α2u-globulin nephropathy, a male rat-specific response. MNCL, a common lesion in aging F344 rats, was not considered relevant for predicting human cancer. Together, these data indicate that DINP is unlikely to pose a carcinogenic hazard to humans.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100295"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147797264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polylactic acid microplastics as metabolic disruptors: Linking gut dysbiosis to systemic toxicity by disrupting microbiota-host co-metabolism","authors":"Yumiao Li ,&nbsp;Ziyi Zhou ,&nbsp;Hui Xu ,&nbsp;Ruilin Qi ,&nbsp;Jing Xu ,&nbsp;Qihao Hu ,&nbsp;Zhi Tang","doi":"10.1016/j.crtox.2026.100298","DOIUrl":"10.1016/j.crtox.2026.100298","url":null,"abstract":"<div><div>The increasing application of polylactic acid (PLA) in consumer products leads to the widespread environmental distribution of its micro- and nano-plastics (PLA-MNPs). These particles pose potential health risks following environmental exposure, yet the mechanisms underlying their systemic toxicity remain inadequately defined. This review synthesizes current evidence demonstrating that PLA-MNPs accumulate in the intestine, compromising the gut barrier and inducing dysbiosis of the gut microbiota. We also explore the hypothetical role of disrupted gut microbiota-host co-metabolism — particularly involving aromatic amino acid pathways such as tryptophan metabolism — as a potential mechanism linking PLA-MNPs exposure to intestinal inflammation and injury, while acknowledging the current lack of direct experimental evidence for PLA-MNPs-specific effects on these pathways. By integrating literature on the gut-liver axis, we further elucidate how intestinal injury propagates to systemic metabolic disturbances. This overview aims to provide a structured synthesis of existing findings, identify key knowledge gaps, and suggest targeted approaches for future mechanistic and exposure-informed risk assessment of PLA-MNPs.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100298"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147850084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}