Environmental Toxicology最新文献

{"title":"Correction to \"Combined Exposure of Nano-Titanium Dioxide and Polystyrene Nanoplastics Exacerbate Oxidative Stress-Induced Liver Injury in Mice by Regulating the Keap-1/Nrf2/ARE Pathway\".","authors":"","doi":"10.1002/tox.70097","DOIUrl":"10.1002/tox.70097","url":null,"abstract":"","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":"373-374"},"PeriodicalIF":3.2,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Exposure to Inheritance: Persistent Microplastic-Induced Neural and Mitochondrial Dysfunction in Subsequent Generations of Drosophila melanogaster.","authors":"Mustafa Munir Mustafa Dahleh, João Vitor Aguirre de Pereira, Pamela Piardi Almeida, Julianna do Amaral Ritter, Gustavo Petri Guerra, Marina Prigol","doi":"10.1002/tox.70114","DOIUrl":"https://doi.org/10.1002/tox.70114","url":null,"abstract":"<p><p>Microplastic contamination poses a critical intergenerational threat to ecosystems and human health, with pervasive infiltration into food chains. This study investigates the developmental and intergenerational consequences of polystyrene microplastic (1.0 μm) exposure (0-25 ppm) in Drosophila melanogaster, evaluating both directly exposed F0 flies and their unexposed F1 offspring. Developmental exposure in F0 adults caused concentration-dependent lifespan shortening (≥ 0.1 ppm) and neurobehavioral impairments (≥ 10 ppm), characterized by reduced locomotion, exploratory deficits, and stress tolerance, with microplastic accumulation detected in heads at ≥ 0.1 ppm. Molecular analyses of F0 heads revealed disrupted acetylcholine metabolism, including elevated acetylcholine (AChE) activity at ≥ 1 ppm, and altered mitochondrial dynamics, characterized by activation of the intrinsic apoptotic pathway, with elevated drICE and Dcp-1 levels, alongside suppression of fusion protein Mfn-2 and ATP5A1. In addition, exposure also reduced F0 adult emergence rates at ≥ 1 ppm. To evaluate indirect intergenerational effects, unexposed F1 offspring were assessed. F1 displayed lifespan reduction at ≥ 10 ppm with persistent locomotor and exploratory deficits at ≥ 1 ppm, though stress tolerance remained unaffected. Notably, no microplastics were detected in F1, yet mitochondrial dysregulation was observed starting at ≥ 1 ppm, with elevated AChE activity. At this concentration, mitochondrial dysregulation persisted: Dcp-1 and Mfn-2 levels were altered at ≥ 1 ppm, and ATP5A1 was suppressed at ≥ 10 ppm, while drICE remained unchanged. No significant changes were observed in F2 adult emergence. Developmental microplastic exposure induces mitochondrial and cellular stress, driving neurobehavioral impairments and lifespan reduction in Drosophila melanogaster, with parental effects persisting in unexposed offspring.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antimicrobial Residues in a Key Cerrado River: Distribution, Persistence, and Effects on Zebrafish Embryo-Larval Development.","authors":"Náthala Maria Simão, Igor Romeiro Dos Santos, Jerônimo Raimundo de Oliveira Neto, Flávio Olimpio Sanches Neto, Felipe Cirqueira Dias, Jéssyca Moreira Morais, Lorranny Pereira de Assis Valadares, Naiara Raica Lopes de Oliveira, Mirelle Garcia Silva Bailão, Luiz Carlos da Cunha, Valter Henrique Carvalho-Silva, Thiago Lopes Rocha, Elisa Flávia Luiz Cardoso Bailão","doi":"10.1002/tox.70100","DOIUrl":"https://doi.org/10.1002/tox.70100","url":null,"abstract":"<p><p>The current study aimed to quantify the antimicrobials amoxicillin (AMX), cefazolin (CFZ), chloramphenicol (CHL), metronidazole (MTZ), and sulfamethoxazole (SX) in effluents and surface water of an important Cerrado river, calculate their half-lives, and analyze their ecotoxicity following single and combined exposures. Four sampling surveys were carried out to identify the antimicrobials employing HPLC-MS/MS. Surface water was collected from the river's spring to the mouth, and effluent samples were taken at a sewage treatment plant (STP). The pySiRC tool was used to predict the half-life of antimicrobials in aqueous media under •OH-attack. Ecotoxicity was assessed using a zebrafish embryo-larval toxicity assay at environmentally relevant concentrations of the detected antimicrobials. Just MTZ (0.1 to 45.5 ng L^-1) and SX (0.1 to 502.7 ng L^-1) were detected in this study. The persistence of MTZ and SX in the aqueous environment was estimated at 14 to 139 days and 9 to 88 days, respectively. The single exposure to MTZ induced cardiotoxicity and changes in the swim bladder and tail curvature. MTZ and SX induced sensory and physiological morphometric changes compared to the control. MTZ, alone or combined with SX, affected the larvae's behavior. Our findings contribute to the understanding of the presence, persistence, and ecotoxicity of antimicrobials in aquatic environments.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EE2 and the Fish Brain: Age-Dependent Impact of 17α-Ethinylestradiol on Brain Cell Proliferation and Behavior in Sea Bass Larvae.","authors":"Soloperto Sofia, Stephanie Olivier, Céline Thomasse, Christophe Minier, Marie-Pierre Halm-Lemeille, Christelle Jozet-Alves, Salima Aroua","doi":"10.1002/tox.70115","DOIUrl":"https://doi.org/10.1002/tox.70115","url":null,"abstract":"<p><p>Endocrine-disrupting chemicals (EDCs), such as 17α-ethinylestradiol (EE2), have raised concerns about their potential effects on aquatic organisms, particularly during early developmental stages. In this context, the study of behavioral disruption has gained considerable attention, as it may have consequences on individual fitness and ultimately influence key ecological processes. However, little is known about the potential link between behavioral disruption and neurodevelopmental alteration in nonmammalian vertebrates. This study aimed to assess the effects of EE2 exposure on the larvae of the marine teleost, European sea bass (Dicentrarchus labrax), during two distinct larval periods (30-38 and 40-48 days posthatch (dph)), focusing on behavioral and neurodevelopmental outcomes. Our findings revealed that exposure to EE2 during the 30-38 dph period resulted in a positive correlation between gene expression of the brain aromatase, brain cell proliferation, and behavioral changes. In contrast, exposure between 40 and 48 dph led to an increase in brain cell proliferation without behavioral alterations. These results suggest that the age of exposure plays a critical role in the neurodevelopmental and behavioral outcomes of EE2, with distinct molecular pathways involved. Future research should further investigate the mechanisms underlying the observed age-dependent effects, particularly the relationship between the brain aromatase activity, gh expression, and brain cell proliferation.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic Toxicity of Low-Concentration Metal Mixture on Male Rats: Reproductive, Renal, and Hepatic Effects.","authors":"Kalinka Helóra Gomes de Almeida,Thalita Tofanin Sargiani D'Assumpção,Ana Priscila Gomes Silva,Carolina Rocha Moreira de Oliveira,Tailisi Hoppe Trevizani,Rubens Cesar Lopes Figueira,Lucas Buruaem Moreira,Juliana Elaine Perobelli","doi":"10.1002/tox.70117","DOIUrl":"https://doi.org/10.1002/tox.70117","url":null,"abstract":"Mining plays a crucial role in economic development, but improper management can lead to severe environmental degradation. Particularly for iron ore, mining generates vast amounts of tailings often stored in unstable dams. This study aims to investigate the toxicological impacts of environmentally relevant concentrations of metals mixture-specifically Manganese (Mn), Arsenic (As), Cadmium (Cd), and Lead (Pb)-on male reproductive health and hepato-renal morpho-physiology using a rat model. Both acute and sub-chronic exposure scenarios were assessed to better reflect typical human environmental exposure. Acute exposure caused significant liver and kidney damage, with notable accumulation of Cd and Pb, while sub-chronic exposure led to more pronounced reproductive effects, impairing sperm quality and hormonal balance. These findings reveal endocrine-disrupting effects from the metal mixture, even at low concentrations, emphasizing the risks of prolonged environmental exposure to mining-related contaminants.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"33 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147754612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Silico Transcriptomic Analysis Suggests That Nickel Exposure Upregulates NINJ1 Expression: Implications for Lytic Cell Death.","authors":"Sukran Yagmur Avcioglu,Busra Nur Ozdemir,Caglar Berkel","doi":"10.1002/tox.70113","DOIUrl":"https://doi.org/10.1002/tox.70113","url":null,"abstract":"Nickel (Ni) has been shown to induce cell death in multiple studies, by the involvement of different programmed cell death mechanisms such as apoptosis and pyroptosis. NINJ1 (Ninjurin 1) is a recently identified transmembrane protein, mediating plasma membrane rupture and the loss of plasma membrane integrity during lytic cell death or following mechanical strain. The involvement of NINJ1-mediated plasma membrane rupture in nickel-induced cell death has not been previously studied. Here, by performing in silico transcriptomics analysis of publicly available datasets in the R programming environment, we observed that nickel exposure/treatment increases the expression of NINJ1 at the transcription (mRNA) level in various cell types such as human PBMCs and endothelial cells, and rat liver cells (fold changes of 1.1, 2.61, and 1.02, respectively). Besides, we observed that in skin biopsies of individuals who were exposed to nickel, those with nickel allergy have higher NINJ1 mRNA expression compared to those without nickel allergy (nonallergic controls) (fold change of around 1.05), pointing to the potential involvement of NINJ1 in nickel allergy in skin. Combined, based on computational data analyses, we here hypothesized that nickel-induced increases in NINJ1 mRNA expression might possibly lead to higher levels of NINJ1-mediated plasma membrane rupture and lytic cell death in these nickel-exposed cells, likely resulting in increased inflammation. However, since this bioinformatics study is solely based on computational reanalysis, and functional NINJ1-mediated plasma membrane rupture following nickel exposure was not experimentally demonstrated, additional experimental data is required to support the findings. Further research is needed to identify cellular mechanisms by which nickel induces NINJ1 mRNA expression and possibly lytic cell death, contributing to the nickel-induced inflammation.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"25 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147751350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sargassum Lung Syndrome: Air Flow Obstruction and Bronchial Inflammation Are Observed After Prolonged Exposure to Sargassum Gas Emissions in the Eastern Caribbean.","authors":"Rishika Banydeen,Jonathan Florentin,Maxime Boutourlinsky,Remi Nguyen,Fatima Radouani,Moustapha Agossou,Gary Lutin,Thierry Lebrun,Remi Neviere,Dabor Resiere","doi":"10.1002/tox.70110","DOIUrl":"https://doi.org/10.1002/tox.70110","url":null,"abstract":"Sargassum inundation of Caribbean and American shorelines is a growing environmental hazard. Hydrogen sulfide (H2S) and ammonia (NH3) produced by decomposing Sargassum could be involved in airway obstruction and bronchial inflammation. The study was undertaken to evaluate the effects of exposure to H2S and NH3 gases emitted during Sargassum decomposition based on measures of airflow obstruction and bronchial inflammation in a study population from the French Caribbean Island of Martinique. Ambient air exposure was estimated by the closest ground H2S/NH3 sensor. Lung function and bronchial inflammation were evaluated by spirometry and fractional measurement of nitric oxide in the exhaled air (FeNO), respectively. Multivariate logistic and linear regression were applied to analyze associations between cumulative Sargassum H2S/NH3 exposure and risk of airway obstruction and FeNO changes. The analyses also took into account the effects of confounding factors, notably air pollution. Among the 335 study patients, 72% were living in Sargassum-impacted zones. Compared with nonexposed patients, exposed patients had lung measures showing airway obstruction and increased FeNO levels. Exposed patients with asthma presented a two-fold rise in FeNO levels. Multivariate modeling retained mean cumulative concentrations of Sargassum H2S and NH3 as independent predictors of increased risk of airway obstruction and bronchial inflammation. The present study highlights a potential association between impaired lung function and exposure to Sargassum H2S and NH3 during coastal stranding episodes. Present study results strongly support the deleterious effect on the respiratory health of individuals chronically exposed to Sargassum gas emissions.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"30 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147751353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION : Ameliorative Effect of N‐acetyl Cysteine on Alpha‐Cypermethrin‐Induced Pulmonary Toxicity in Male Rats","authors":"","doi":"10.1002/tox.70112","DOIUrl":"https://doi.org/10.1002/tox.70112","url":null,"abstract":"","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"4 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined Toxicity of Polyamide Microplastics and Fenitrothion Impairs Growth, Intestinal Integrity, and GH-IGF Axis in Nile Tilapia.","authors":"Mobassir Bin Anwar,Md Ahsanul Haque,Md Mahiuddin Zahangir,Md Shahjahan","doi":"10.1002/tox.70111","DOIUrl":"https://doi.org/10.1002/tox.70111","url":null,"abstract":"The pervasive contamination of aquatic ecosystems by microplastics (MPs) and organophosphate pesticides raises concerns about their combined impacts on fish physiology, yet empirical evidence remains limited. This study investigated the coexposure effects of polyamide microplastics (PA-MPs, 10 mg/L) and the insecticide fenitrothion (0.3 mg/L) on growth performance, intestinal integrity, and GH-IGF axis regulation in juvenile Nile tilapia (Oreochromis niloticus) over 42 days. Coexposure markedly suppressed somatic growth (weight gain and specific growth rate) and feed efficiency (feed conversion ratio; FCR), exceeding the adverse effects observed under single exposures. Histopathological evaluation revealed significant depletion of goblet cells and enterocytes per villus, indicating pronounced disruption of intestinal epithelium. At the molecular level, gh, igf-1, and igf-2 transcripts were substantially downregulated in the coexposed group, reflecting coordinated impairment of the somatotropic axis. Principal component analysis demonstrated a strong interrelationship among growth, intestinal cellular integrity, and gene expression, collectively delineating the severity of chemical stress. These results suggest potential combined toxicity of co-occurring MPs and organophosphate pesticides, emphasizing their capacity to compromise aquaculture productivity and ecosystem health.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"67 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prosopis africana Pod Methanolic Extract Attenuates Multi-Metal Oxidative Injury in Thyroid and Thymus: Evidence for Nrf2/NF-κB Modulation and Implications for Environmental Toxicity.","authors":"Harrison A Ozoani,Kenneth O Okolo,Barido Donatus Dooka,Cecilia N Obasi,Prosper Manu Abdulai,Orish E Orisakwe","doi":"10.1002/tox.70108","DOIUrl":"https://doi.org/10.1002/tox.70108","url":null,"abstract":"Heavy metal mixtures (HMMs) containing lead (Pb), cadmium (Cd), and arsenic (As) induce oxidative stress and inflammation in thyroid and thymic tissues, disrupting endocrine and immune homeostasis. While Prosopis africana pod methanolic extract (PA) exhibits antioxidant properties, its protective mechanisms against multi-metal toxicity remain undefined. This study investigated PA's efficacy in mitigating HMM-induced organ injury in rats. Male Sprague-Dawley rats (n = 5/group) received environmentally relevant HMM [PbCl2 (20 mg/kg), CdCl2 (1.61 mg/kg), Na2AsO3 (10 mg/kg)] via drinking water with concurrent daily oral gavage of PA extract (500, 1000, or 1500 mg/kg) for 60 days. Tissue metal accumulation was quantified by atomic absorption spectrophotometry and oxidative stress markers spectrophotometrically. Inflammatory mediators (TNF-α), apoptotic markers (caspase-3), and pathway regulators (Nrf2, NF-κB) were measured by ELISA. Histopathological evaluation and multivariate analyses were performed. PA extract, rich in flavonoids and tannins, exhibited dose-dependent protective effects. Co-treatment significantly reduced Pb, Cd, and As accumulation in thyroid and thymus (up to 82% reduction in thyroid Cd at 1500 mg/kg compared to HMM controls, p < 0.05). Oxidative balance was restored, evidenced by a 79% decrease in malondialdehyde and recovery of antioxidant enzyme activities (SOD, CAT, GSH, GPx). PA normalized dysregulated Nrf2 expression and suppressed NF-κB activation, restoring functional antioxidant responses, resulting in marked attenuation of TNF-α (95% reduction) and caspase-3 (76% reduction). These biochemical improvements correlated with the prevention of HMM-induced organomegaly and preservation of normal histoarchitecture. Prosopis africana pod methanolic extract confers significant protection against HMM-induced thyroid and thymic injury through dual mechanisms: (i) substantial reduction of tissue metal bioaccumulation (up to 82% reduction in thyroid Cd), and (ii) restoration of functional Nrf2-mediated antioxidant responses while suppressing NF-κB-driven inflammation. Critically, PA normalized suggesting dysregulated compensatory Nrf2 elevation while enhancing antioxidant enzyme activities, demonstrating functional pathway restoration rather than mere suppression. These findings highlight PA's potential as a multi-targeted phytotherapeutic agent for mitigating heavy metal toxicity, warranting further mechanistic and translational studies.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"148 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}