Environmental toxicology and pharmacology最新文献

{"title":"Polystyrene microplastics reduce honeybee survival by disrupting gut microbiota and metabolism","authors":"Han Li ,&nbsp;Wangjiang Feng ,&nbsp;Tong An,&nbsp;Pingli Dai,&nbsp;Yong-Jun Liu","doi":"10.1016/j.etap.2025.104704","DOIUrl":"10.1016/j.etap.2025.104704","url":null,"abstract":"<div><div>Polystyrene microplastics (PS-MPs) pose significant risks to honeybee health. However, how microplastics (MPs) adversely influence honeybee survival through the gut pathway, especially the metabolic processes, remains poorly understood. To conduct the experiment, the honeybees (<em>Apis mellifera</em> L.) were exposed to PS-MPs (0.5 μm and 5 μm) at environmental concentrations of 25 mg/L and 50 mg/L for 21 days. Results revealed that PS-MPs reduced honeybee survival rates and food consumption. The accumulation of PS-MPs in honeybee guts caused structural damage to gut walls and elevated oxidative stress levels. Additionally, PS-MPs altered gut microbial communities, with a decrease in <em>Lactobacillus</em> and an increase in <em>Bartonella</em>. Gut metabolomics analysis indicated that PS-MPs disrupted metabolic pathways, upregulated amino acid and carbohydrate metabolism, and downregulated alpha-linolenic acid and lipid metabolism. Our study offers important insights into the physiological effects of accumulated MPs on honeybees, highlighting the critical need for effective strategies to manage environmental pollutants.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104704"},"PeriodicalIF":4.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143867929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Bisphenol A on the neuro-immune-endocrine mechanisms controlling the reproductive axis response during an inflammatory event","authors":"Romina Penalba ,&nbsp;Juan Manuel Gamez ,&nbsp;Nancy Cardoso ,&nbsp;Rodrigo M. Bilbao ,&nbsp;Osvaldo J. Ponzo ,&nbsp;Roxana Reynoso","doi":"10.1016/j.etap.2025.104702","DOIUrl":"10.1016/j.etap.2025.104702","url":null,"abstract":"<div><div>Endotoxin-induced toxicity could increase with previous exposure to sensitizing agents like endocrine disruptors (EDs). We studied the effects on the reproductive axis on adult male rat pups exposed to BPA since gestation day (GD) 1 to final lactation and its response to LPS before sacrifice. The decrease in GnRH release caused by LPS and BPA was more pronounced in the BPA + LPS group compared to the LPS-only group. While LPS increased nitrate production, the addition of BPA lowered it compared to both the control and LPS groups. A reduction in plasma LH levels was observed in the control, BPA + LPS, and LPS groups. Plasma testosterone decreased in the LPS, BPA, and BPA + LPS groups compared to the control, and in the BPA + LPS group compared to the LPS group. In conclusion, BPA disrupts the reproductive function and sensitizes it to LPS-induced toxicity.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104702"},"PeriodicalIF":4.2,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143864763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of the impact of chlordecone and its metabolite chlordecol on genes involved in pesticide metabolism in HepG2 cell line","authors":"Gulminyam Baratzhanova ,&nbsp;Hanan EL Sheikh Saad ,&nbsp;Agnès Fournier ,&nbsp;Marion Huguet ,&nbsp;Olivier Joubert ,&nbsp;Arnaud Paul ,&nbsp;Leyla Djansugurova ,&nbsp;Céline Cakir-Kiefer","doi":"10.1016/j.etap.2025.104701","DOIUrl":"10.1016/j.etap.2025.104701","url":null,"abstract":"<div><div>Chlordecone (CLD) is an organochlorine pesticide that is highly resistant in the environment. This compound and its metabolite chlordecol (CLD-OH) still can be found in the French West Indies, after being banned 30 years ago. The novelty of this work lies in evaluating the toxicity of CLD-OH compared to CLD and examining the effects of these compounds on nuclear receptor (<em>PXR</em>, <em>PPARα</em>, and <em>CAR</em>) and metabolism-related genes (<em>CYP2B6</em>, <em>CYP3A4</em>) <em>in vitro</em> using HepG2 cell line as a model. Our study demonstrates that both compounds displayed an almost similar pattern of decrease in cell viability. Moreover, it was shown that CLD-OH can increase the expression of <em>PXR</em>, <em>CYP3A4</em>, and <em>PPARα</em> genes in comparison to CLD. The <em>AKR1C4</em> gene showed a slight decrease in expression after CLD treatment. Collectively, this study provided a new finding into the impact of CLD-OH and compares the mode of action of CLD and its metabolite<em>.</em></div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104701"},"PeriodicalIF":4.2,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143849477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolism and genotoxicity of 4,4’-oxydianiline is dependent on N-acetyltransferase 2 genetic polymorphism","authors":"Raul A. Salazar-González ,&nbsp;James T.F. Wise ,&nbsp;Mark A. Doll,&nbsp;David W. Hein","doi":"10.1016/j.etap.2025.104699","DOIUrl":"10.1016/j.etap.2025.104699","url":null,"abstract":"<div><div>4,4’-oxydianiline (ODA) is an environmental aromatic amine reasonably anticipated to be a human carcinogen. We investigated ODA genotoxicity and oxidative stress modified by N-acetyltransferase 2 (NAT2) genetic polymorphism in yeast and DNA repair deficient (UV5) Chinese hamster ovary cells (CHO) expressing human <em>NAT2*4</em> (rapid acetylator allele) or human <em>NAT2*5B</em> (slow acetylator allele) and in cryopreserved human hepatocytes from rapid, intermediate, or slow NAT2 acetylator genotypes. <em>N</em>-acetylation of ODA was both concentration- and time-dependent and significantly higher in yeast and CHO cells expressing <em>NAT2*4</em> versus <em>NAT2*5B</em>. ODA-induced DNA damage response and reactive oxygen species (ROS/RNS) were significantly higher, while intracellular reduced glutathione (GSH) and oxidized glutathione (GSSG) ratio or mitochondrial integrity were significantly lower in CHO cells expressing <em>NAT2*4</em> than <em>NAT2*5B</em>. Dose- and NAT2 phenotype-dependent responses also were observed in human cryopreserved human hepatocytes. Our findings have important implications for precise risk assessments following exposures to ODA and azo dye precursors.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104699"},"PeriodicalIF":4.2,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143839137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early life developmental effects induced by dioxins and PCBs in novel bioassays with C. elegans","authors":"Cong Bao ,&nbsp;Antoine Karengera ,&nbsp;Jan Kammenga ,&nbsp;Inez Dinkla ,&nbsp;Willemien Wieland ,&nbsp;AlberTinka J. Murk","doi":"10.1016/j.etap.2025.104697","DOIUrl":"10.1016/j.etap.2025.104697","url":null,"abstract":"<div><div>This study assessed the effects of TCDD, two PCB mixtures (Clophen A50 and Aroclor 1254), and field extracts from marine sediments and swimming crab tissues on early-life development in Caenorhabditis elegans. Gravid nematodes were exposed on agar, and isolated eggs and larvae were tested in solution. Larval development was evaluated after 72 hours. Reporter gene assays (DR-CALUX) were also used to quantify dioxin-equivalent toxicity (TEQ). Exposure to 10 pM Clophen A50 and TCDD on agar inhibited L3–L4 transition by 60 % and 50 %, respectively. Liquid exposure to 5 µM Aroclor 1254 or TCDD (10 nM and 10 µM) delayed development by 20–40 %. Field extracts contained TEQ values of 0.67–4.91 ng/kg (0.2–1.47 pM TCDD), reducing L3–L4 development by 40–60 %. Both bioassays effectively assessed the toxicity of persistent organic pollutants in environmental samples. Agar exposure mimics realistic uptake, while liquid assays offer faster, high-throughput screening.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104697"},"PeriodicalIF":4.2,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pesticide residues in honey: Agricultural landscapes and commercial wax foundation sheets as potential routes of chronic exposure for honey bees","authors":"Deicy C. Munoz Agudelo ,&nbsp;Hannah Whitehead ,&nbsp;Laura L. Figueroa ,&nbsp;Lynn S. Adler","doi":"10.1016/j.etap.2025.104700","DOIUrl":"10.1016/j.etap.2025.104700","url":null,"abstract":"<div><div>Pesticides pose significant threats to pollinators, and honey bees are frequently exposed through foraging and beekeeping practices. We assessed honey bee pesticide exposure by analyzing 92 pesticide residues in honey from 30 hobbyist apiaries across Massachusetts, along with store-bought honey and commercial wax foundation. For all samples, we calculated the risk of multiresidue toxicity to honey bees and assessed the role of landscape composition in predicting pesticides in local honey. Both honey and wax contained multiple pesticides, particularly neonicotinoids and piperonyl butoxide. Store-bought honey accumulated at least two times more residues than local, but did not differ significantly in toxicity. Overall, honey toxicity levels remained below thresholds of concern for bees and human consumption. Although our study had low agricultural land (∼6 %), croplands were positively correlated with pesticides in honey, while wetlands (∼ 15 %) were negatively correlated. Additionally, our study suggests that commercial wax exacerbates pesticide exposure.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104700"},"PeriodicalIF":4.2,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143856063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disruptive ecotoxicological effects of fluoxetine on serotoninergic signaling and enteric neurogenesis in early zebrafish larvae (Danio rerio)","authors":"Kainã Rocha Cabrera Fagundes ,&nbsp;Natalia Kasica ,&nbsp;Małgorzata Potoczna ,&nbsp;Shiho Okitsu-Sakurayama ,&nbsp;Piotr Podlasz ,&nbsp;Renata de Britto Mari","doi":"10.1016/j.etap.2025.104698","DOIUrl":"10.1016/j.etap.2025.104698","url":null,"abstract":"<div><div>This study investigated the multilevel effects of environmentally relevant concentrations of fluoxetine on serotonergic signaling and enteric neurogenesis in early zebrafish larvae (Danio rerio). To this end, zebrafish were exposed to various concentrations of fluoxetine for four days, from the 1,000-cell stage to 4 days post-fertilization (dpf).Following exposure, whole larvae were subjected to molecular, morphological, and behavioral analyses. All tested concentrations led to upregulation of the serotonin transporter (slc6a4a). At intermediate concentrations, overexpression of the serotonin receptor htr1aa was observed. The highest concentration caused a reduced total enteric neurons density, while the intermediate concentration reduced the density of serotonergic enteric neurons. Additionally, the highest concentration decreased larval locomotion and impaired their ability to differentiate between light and dark phases.Across all tested concentrations, fluoxetine disrupted serotonergic signaling, impaired enteric neurogenesis, and induced sedative-like behavioral effects.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104698"},"PeriodicalIF":4.2,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Cu(ATSM) on the expression and activity of ABC export proteins in killifish (Fundulus heteroclitus) kidney tubules","authors":"Lisa Kraus ,&nbsp;Gert Fricker","doi":"10.1016/j.etap.2025.104696","DOIUrl":"10.1016/j.etap.2025.104696","url":null,"abstract":"<div><div>ABC transporters are important for excretion of xenobiotics and metabolites into urine. They are sensitive to metallic pollutants like cadmium, mercury, zinc, or arsenic. Here, we show that copper (Cu(ATSM)) stimulates ABC transporter-mediated export in isolated renal proximal tubules from Atlantic killifish (<em>Fundulus heteroclitus</em>) with main focus on Mrp2. Transporter stimulation was reduced by cycloheximide (CHX), an inhibitor of translation, suggesting that it is partially caused by induced expression. Functional activation was reversed by modulators of the endothelin receptor (ET_B)/nitric oxide synthase/protein kinase C signaling pathway. Transporter activating effects were reversed by Gö6976 and peptide C2–4, both being PKCα inhibitors. Cu(ATSM)-induced activation was further suppressed by phosphatidylinositol 3-kinase inhibitor LY-294002 and mTOR inhibitor rapamycin. Activation was also inhibited by GSK650394, an inhibitor of serum-and-glucocorticoid-inducible-kinase-1 being a subsequent target. Given the parallelism with other metals, this ABC transporter regulation appears to be a general defense mechanism of teleosts to react on metallic pollutants.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104696"},"PeriodicalIF":4.2,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143820931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isatin-linked pyrazole K1 derivative alter the phosphatidylinositol-3-kinase pathway by enhancing the metabolic function and folliculogenesis in the triclosan-induced PCOS-like condition in zebrafish model","authors":"Karthikeyan Ramamurthy ,&nbsp;Marapatla Shiny ,&nbsp;S. Madesh ,&nbsp;Santhanam Sanjai Dharshan ,&nbsp;Girija Sastry Vedula ,&nbsp;Mansour K. Gatasheh ,&nbsp;Kathiravan Muthu Kumaradoss ,&nbsp;Jesu Arockiaraj","doi":"10.1016/j.etap.2025.104695","DOIUrl":"10.1016/j.etap.2025.104695","url":null,"abstract":"<div><div>Polycystic ovarian syndrome (PCOS), which causes hormonal imbalance, inflammation, and metabolic disorders, requires several treatments. This study aimed to examine the Isatin-linked pyrazole K1 derivative's effectiveness in PCOS induced by environmental contaminants such as triclosan, specifically assessing its biochemical, metabolic, and reproductive impacts. Isatin-linked pyrazole K1 derivative was synthesised in the lab and tested <em>in vitro</em> and <em>in vivo</em>, including cytotoxicity testing in CHO cells, apoptosis analysis in AO/PI staining, and developmental toxicity in zebrafish embryos. In addition, for network pharmacology analysis, BindingDB, GeneCard, and other databases were used to characterise the interaction of K1 derivative with PCOS-related genes and pathways, followed by examining the apoptosis in CHO cells, estimation of total cholesterol and triglycerides in adipose tissue of zebrafish. Furthermore, GSI%, follicular stage examination, collagen accumulation, nucleic acid staining by toluidine blue, and gene expression of <em>cyp19a1a</em>, <em>dennd1a</em>, <em>tox3</em>, <em>pik3ca</em>, and <em>pik3cd</em> were examined. The research found that K1 reduces various PCOS pathologies, improving folliculogenesis, overall ovarian function, and follicular growth. K1 treatment at 25 µM significantly enhanced SOD (1.470 ± 0.01533 U/ml), CAT (1.174 ± 0.008687 U/ml), and GSH (1.375 ± 0.006409 U/ml) levels while reducing LDH activity (0.9815 ± 0.01273 nmol/mg), demonstrating its ability to mitigate oxidative stress and cellular damage. In particular, K1 modulates insulin sensitivity by reducing the blood glucose level in PCOS-induced fish and lowering lipid levels, which is essential for treating PCOS metabolic symptoms. K1 derivative also significantly reduced collagen deposition in ovarian tissues, indicating K1 may reduce PCOS-related fibrosis, which suggests that the derivative may be a novel therapeutic agent for PCOS. The comprehensive approach of K1 addresses metabolic and reproductive concerns; however, clinical studies must be conducted to test these findings' efficacy and safety and understand its therapeutic molecular processes.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104695"},"PeriodicalIF":4.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of lithium on mortality and metabolite profiles in Drosophila lithium-inducible SLC6 transporter mutants","authors":"Junko Kasuya ,&nbsp;Karina Kruth ,&nbsp;Dongkeun Lee ,&nbsp;Jong Sung Kim ,&nbsp;Aislinn Williams ,&nbsp;Toshihiro Kitamoto","doi":"10.1016/j.etap.2025.104684","DOIUrl":"10.1016/j.etap.2025.104684","url":null,"abstract":"<div><div>Lithium has long been the primary treatment for bipolar disorder and shows promise for managing other neurological and psychiatric conditions. We previously identified the <em>Lithium-inducible SLC6 transporter</em> (<em>List</em>) in <em>Drosophila melanogaster</em> as a gene significantly upregulated in response to lithium chloride supplementation. <em>List</em> encodes a putative amino acid transporter belonging to the Na⁺-dependent solute carrier family 6. Here, we show that <em>List</em> is expressed in the Malpighian tubules, glia, and hindgut. RNA interference-mediated <em>List</em> knockdown in the Malpighian tubules drastically increases lithium-induced mortality. Additionally, <em>List</em> loss-of-function mutants (<em>List</em>^{<em>TG4.2</em>}) accumulate six times more internal lithium than controls after lithium exposure. Metabolomic analysis revealed disrupted amino acid metabolism and a shift toward a more oxidized cellular redox state in lithium-treated <em>List</em>^{<em>TG4.2</em>} mutants. Overall, our findings suggest that <em>List</em> protects flies from lithium toxicity by regulating internal lithium levels and maintaining metabolic and redox balance.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"116 ","pages":"Article 104684"},"PeriodicalIF":4.2,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143805179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}