Comparative Biochemistry and Physiology C-toxicology & Pharmacology最新文献

{"title":"Multigenerational effects of selected environmental contaminants in fishes: A comprehensive review","authors":"Md Helal Uddin ,&nbsp;Jinnath Rehana Ritu ,&nbsp;Som Niyogi ,&nbsp;Douglas P. Chivers","doi":"10.1016/j.cbpc.2026.110453","DOIUrl":"10.1016/j.cbpc.2026.110453","url":null,"abstract":"<div><div>The pervasive presence of environmental contaminants in aquatic ecosystems has raised significant concerns regarding their long-term impacts on aquatic organisms, particularly fishes. While ecotoxicological studies have traditionally focused on single-generation or single-life-stage exposures, such approaches may underestimate or overestimate population-level consequences. This review critically evaluates the current state of knowledge on the multigenerational effects of both traditional and emerging contaminants in fishes. The study includes five major contaminant groups: pesticides, pharmaceuticals and personal care products (PPCPs), metals and metalloids, microplastics and plasticizers, and <em>per</em>- and polyfluoroalkyl substances (PFASs). Most multigenerational studies have been conducted on freshwater species, including <em>Danio rerio</em>, <em>Oryzias latipes</em>, <em>Oryzias melastigma</em>, <em>Oncorhynchus mykiss</em>, <em>Menidia beryllina</em>, <em>Nothobranchius furzeri</em>, <em>Pimephales promelas</em>, and <em>Paramisgurnus dabryanus</em>, highlighting a substantial research gap in marine fish species. Findings consistently reveal that multigenerational exposure to these contaminants can lead to developmental, behavioural, reproductive, and neurodevelopmental impairments, which may reduce reproductive success, population growth, and overall fitness. Moreover, emerging evidence points to epigenetic modifications, such as DNA methylation and histone alterations, as potential mechanisms underlying these multigenerational effects. Notably, our review identifies considerable variability across studies, with some contaminants exhibiting pronounced multigenerational toxicity, while others show limited or inconsistent outcomes. Given the increasing global concern over aquatic pollution and its far-reaching effects on biodiversity, food security, and public health, this review underscores the urgent need to integrate multigenerational endpoints into ecological risk assessments.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"302 ","pages":"Article 110453"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988564","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":"Review: Synergistic effects of environmental pollutants: Multiple stressors driving the transmission of vector-borne diseases and the vicious cycle","authors":"Tingting Liu ,&nbsp;Jia Wang ,&nbsp;Minghao Yu ,&nbsp;Yining Li ,&nbsp;Huan Lin ,&nbsp;Dan Deng ,&nbsp;Xiaolu Shi ,&nbsp;Xiaoping Xiao","doi":"10.1016/j.cbpc.2025.110442","DOIUrl":"10.1016/j.cbpc.2025.110442","url":null,"abstract":"<div><div>This review systematically examines the mechanisms through which multiple environmental pollutants-including microplastics, heavy metals, atmospheric particulates, pesticide residues, water eutrophication, and artificial light at night-synergistically exacerbate the transmission risk of mosquito-borne diseases. A conceptual framework of the “pollution - resistance - transmission” vicious cycle is proposed, illustrating how pollutants not only directly impair mosquito physiology and drive the evolution of insecticide resistance but also systematically enhance pathogen transmission efficiency by reshaping vector-host-environment interactions, altering host behavior, compromising immune function, and extending mosquito activity periods. Interactions among pollutants, such as the role of microplastics as “Trojan horses” that carry other contaminants, further amplify ecological and health risks through combined exposure. The review also highlights species-specific and context-dependent variations in responses, identifies key research bottlenecks, and proposes multi-level intervention strategies integrating technological innovation with systematic governance-encompassing source control, process interruption, and ecological restoration-to provide a scientific basis for harmonizing public health and ecological security.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"302 ","pages":"Article 110442"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932575","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":"Rab10 GTPase from the mud crab Scylla paramamosain is involved in the host immune response against V. parahaemolyticus infection","authors":"Chang-Hong Cheng ,&nbsp;Hai-Peng Qin ,&nbsp;Si-Gang Fan ,&nbsp;Hong-Ling Ma ,&nbsp;Guang-Xin Liu ,&nbsp;Dong-Lin Yao ,&nbsp;Wen-Fan Luo ,&nbsp;Xian-Feng Yang ,&nbsp;Zhi-Xun Guo","doi":"10.1016/j.cbpc.2026.110463","DOIUrl":"10.1016/j.cbpc.2026.110463","url":null,"abstract":"<div><div>Rab GTPases are pivotal regulators of organelle trafficking and host immune responses, which are critical for bacterial defense. However, little is known of the function of Rab in crustacean responses to bacterial infection. In this study, a Rab10 gene (<em>Sp-Rab10</em>) was identified from the mud crab <em>Scylla paramamosain</em>. The full open reading frame of consisted of 612 bp, encoding a 203-amino acid polypeptide that shared 98% sequence identity with <em>Portunus trituberculatus Rab10</em>. Quantitative real-time PCR (qRT-PCR) analysis showed that <em>Sp-Rab10</em> exhibited broad tissue distribution, with the highest expression detected in the hepatopancreas. Notably, <em>Sp-Rab10</em> expression was markedly up-regulated following <em>V. parahaemolyticus</em> infection, implying its potential involvement in the innate immune response against bacterial challenge. To explore the regulatory mechanism of Sp-Rab10, an RNA interference (RNAi) experiment was conducted. Silencing of Sp-Rab10 resulted in significant down regulation of 3 phagocytosis-related genes (<em>c-type lysozyme</em>, <em>crustin</em> and <em>anti-lipopolysaccharide factor</em>). Additionally, in vivo knockdown of <em>Sp-Rab10</em> increased bacterial load in the hemolymph and mortality of mud crabs after <em>V. parahaemolyticus</em> infection. Collectively, these findings demonstrated that <em>Sp-Rab10</em> played a critical role in antimicrobial defense in crustaceans.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"302 ","pages":"Article 110463"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146060591","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":"Selenium regulates pyroptosis through the ROS-mtDNA-cGAS-STING axis to alleviate trimethyltin chloride-induced inflammation in chicken kidneys","authors":"Huiling Zheng ,&nbsp;Xinyu Huo ,&nbsp;Wenwen Zhang ,&nbsp;Shuang Lou ,&nbsp;Mingyue Li ,&nbsp;Chenxi Huang ,&nbsp;Kang Yang ,&nbsp;Tong Xu ,&nbsp;Hongjin Lin","doi":"10.1016/j.cbpc.2026.110452","DOIUrl":"10.1016/j.cbpc.2026.110452","url":null,"abstract":"<div><div>Trimethyltin chloride (TMT) is a highly toxic and environmentally ubiquitous organotin compound. Selenium (Se) mitigates toxin-induced injury by alleviating oxidative stress, whereas mitochondrial DNA (mtDNA) leakage activates pyroptosis and inflammation via the mtDNA–cGAS–STING pathway. Yet, the precise mechanism by which selenium antagonizes TMT-induced renal inflammation in chickens through ROS–mtDNA–cGAS–STING-mediated pyroptosis remains elusive. We generated a chicken TMT model (10 μg kg⁻¹ gavage) ± Se-enriched diet (2 mg kg⁻¹). Primary chicken embryo kidney (CEK) cells were used for in vitro validation. Both in vivo and in vitro data revealed that TMT suppressed antioxidants (CAT, GSH-Px, SOD, T-AOC), raised H₂O₂/MDA, and provoked excessive ROS. TMT also depolarized mitochondrial membrane potential (ΔΨm), elevated mitochondrial ROS (mtROS), induced mtDNA release, and disturbed mitochondrial dynamics, culminating in severe mitochondrial dysfunction. Cytoplasmic mtDNA activated the cGAS–STING pathway, up-regulating key signaling molecules and increasing pyroptosis markers (Caspase1, NLRP3, GSDMD, IL-18) and pro-inflammatory cytokines (TNF-α, ASC, IL-1β, IL-6). Se supplementation reversed these alterations. Importantly, the Se-mediated protection was abolished by the oxidative stress inducer sanguinarine, the cGAS–STING agonist STING-Agonist 12, or the pyroptosis activator nigericin. Collectively, our results demonstrate that Se alleviates TMT-induced renal pyroptosis and inflammation by reducing ROS, preserving mitochondrial homeostasis, preventing mtDNA leakage, and restraining the cGAS–STING pathway. These findings not only elucidate the molecular basis of TMT nephrotoxicity but also support Na₂SeO₃ as a candidate therapeutic for TMT-induced kidney injury.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"302 ","pages":"Article 110452"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145958684","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":"IGF-1/AKT signaling attenuates arsenic-induced neuronal apoptosis and DNA fragmentation","authors":"Nourhan Elsayed","doi":"10.1016/j.cbpc.2026.110456","DOIUrl":"10.1016/j.cbpc.2026.110456","url":null,"abstract":"<div><div>Chronic arsenic exposure is a major environmental cause of neurotoxicity, linked to oxidative stress and apoptosis. While its toxicity is established, protective strategies are limited. Insulin-like growth factor-1 (IGF-1) is a key neurotrophic factor, but its potential to counteract arsenic-induced neuronal apoptosis and DNA fragmentation remains largely unexplored. The neuroprotective role of IGF-1 against sodium arsenite (NaAsO₂) was investigated in human SH-SY5Y neuroblastoma cells. Differentiated cells were employed to study IGF-1/AKT signaling, while undifferentiated cells were employed for apoptosis assays. Cells were exposed to NaAsO₂ with or without IGF-1 treatment. AKT phosphorylation status at Thr308 and Ser473 was assessed by Western blot. Apoptosis was evaluated via flow cytometric analysis of the sub-G1 population and by immunoblotting for key apoptotic markers, including cleaved caspase-3, cleaved PARP, p53, and Bcl-2. Arsenic exposure significantly suppressed AKT phosphorylation and induced concentration-dependent apoptosis, evidenced by increased p53, cleaved caspase-3, PARP cleavage, and a compensatory increase in Bcl-2. Treatment with IGF-1 significantly attenuated these effects. IGF-1 restored AKT signaling, reduced pro-apoptotic markers (p53, cleaved caspase-3), diminished PARP cleavage, and significantly decreased apoptotic cell death and DNA fragmentation (sub-G1 population). The observed reduction in Bcl-2 following IGF-1 treatment suggests a restoration of apoptotic equilibrium. The findings present novel evidence that IGF-1 confers protection against arsenic-induced neuroapoptosis and DNA fragmentation by reactivating the PI3K/AKT pathway. This reactivation rebalances apoptotic regulators and suppresses p53-mediated apoptosis. The findings highlight IGF-1 signaling as a promising therapeutic target for arsenic-related neuronal damage, warranting further investigation in vivo.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"302 ","pages":"Article 110456"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145974218","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":"Toxicity and transcriptome sequencing analyses of Daphnia magna under multi-walled carbon nanotubes (MWCNTs) stress","authors":"Jiaqi Shen ,&nbsp;Zhenyang Zhang ,&nbsp;Xudong Zheng ,&nbsp;Pinpin Lv ,&nbsp;Yong Huang ,&nbsp;Xiaochan Gao","doi":"10.1016/j.cbpc.2026.110460","DOIUrl":"10.1016/j.cbpc.2026.110460","url":null,"abstract":"<div><div>Due to the rapid development of the power battery industry, the potential pollution of carbon nanotubes (CNTs) has drawn great attention in recent years. In this study, the toxicity of multi-walled CNTs (MWCNTs) on antioxidant capacity, digestive capacity, and transcriptome in <em>Daphnia magna</em>, which is a model organism of plankton, was conducted. <em>D. magna</em> individuals were exposed to different concentrations (0, 0.53 mg/L, and 5.3 mg/L) of MWCNTs for 48 h. The results showed that 5.3 mg/L MWCNTs induced obvious oxidative stress reflected by significantly increased malondialdehyde content, and significantly decreased activities of superoxide dismutase, catalase, and glutathione. There were marked reductions in digestive enzyme activities, including lipase activity, trypsin activity, and amylase activity, in the 5.3 mg/L-exposed group relative to those in the control group. KEGG function annotation analysis showed that MWCNTs at both concentrations disturbed two pathways, including metabolism of xenobiotics by cytochrome P450 and the fatty acid elongation signaling pathway. However, the protein digestion and absorption pathway was disturbed in the 5.3 mg/L MWCNTs-exposed group but not in the 0.53 mg/L MWCNTs-exposed group. Overall, we deduce that oxidative damage, impairment of detoxification function, and disorders of protein metabolism and lipid metabolism are associated with CNTs toxicity on <em>D. magna</em>.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"302 ","pages":"Article 110460"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017672","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":"Metabolomic insights into gut–brain axis dysregulation under unpredictable chronic stress in zebrafish","authors":"Zhang Yizhu ,&nbsp;Zaynab Mando ,&nbsp;Zenab Aldurrah ,&nbsp;Roziana Mohamed Hanaphi ,&nbsp;Ahmad Syahir Abd Halim Hapiz ,&nbsp;Muhammad Ariff Azmi ,&nbsp;Adriana Sofia Abdul Latip ,&nbsp;Sarah Idris ,&nbsp;Azira Muhamad ,&nbsp;Fauziahanim Zakaria","doi":"10.1016/j.cbpc.2026.110457","DOIUrl":"10.1016/j.cbpc.2026.110457","url":null,"abstract":"<div><div>Growing evidence indicates that depression is closely associated with disturbances in the gut-brain axis. Although rodent models are currently widely utilised in depression pathophysiology research, the zebrafish (<em>Danio rerio</em>) has become a valuable and promising alternative model species. This study examined changes in neuroendocrine and neurochemical markers associated with behavioural modifications in a zebrafish model of unpredictable chronic stress (UCS). Following a 14-day UCS procedure, the open-field test (OFT), social interaction test (SIT), and light-dark test (LDT) were conducted. Whole-body cortisol and IL-1β levels, along with metabolomics analysis of brain and intestinal tissues, were performed for neuroendocrine and neurochemical assessment. Depression-like behaviours such as increased immobility time (<em>P</em> = 0.0009) and impaired social interaction (<em>P</em> = 0.0306) were observed, alongside elevated levels of cortisol (<em>P</em> &lt; 0.0001) and IL-1β (<em>P</em> = 0.0255). NMR-based metabolomics analysis revealed alterations in valine, alanine, glutamate, and choline in both brain and intestinal tissues in UCS zebrafish, indicating disruption of amino acid metabolism, highlighting the involvement of bidirectional gut-brain axis communication. The glycine, serine, and threonine pathways were most significantly perturbed in UCS zebrafish, suggesting compromised redox homeostasis leads to neuroinflammation in the pathophysiology of depression-related chronic stress related to the gut-brain axis. This study demonstrates that zebrafish is a valuable alternative vertebrate model for exploring the systemic impacts of unpredictable chronic stress (UCS) on the gut-brain axis.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"302 ","pages":"Article 110457"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017508","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":"Parental exposure to phenanthrene induces thyroid disruption in zebrafish offspring","authors":"Liqiao Zhong ,&nbsp;Fengyue Zhu ,&nbsp;Luyin Wu ,&nbsp;Baoshan Ma ,&nbsp;Huijun Ru ,&nbsp;Xinbin Duan","doi":"10.1016/j.cbpc.2025.110439","DOIUrl":"10.1016/j.cbpc.2025.110439","url":null,"abstract":"<div><div>Polycyclic aromatic hydrocarbons (PAHs) constitute extensively studied pollutants present throughout environmental and food matrices. Phenanthrene (PHE), ranking among the most prevalent PAHs detected in food items and aquatic ecosystems, causes reproductive and developmental toxicity in zebrafish. However, the potential for PHE to transfer to zebrafish offspring and disrupt the thyroid endocrine system remains unclear. To investigate intergenerational thyroid disruption, adult zebrafish underwent PHE treatment (0, 0.85, 8.5, and 85 μg/L) for 60 days, with embryos (F1) subsequently cultured in clean water until 5 days postfertilization (dpf) and 14-dpf. Results demonstrated that PHE accumulated in zebrafish offspring through parental transmission. Parental PHE exposure induced developmental toxicity in zebrafish offspring, characterized by elevated deformation rates, diminished survival rates, and reduced body length. PHE exposure altered thyroid hormone levels and caused thyroid disruption in the F1 generation. Among F1 generation specimens (including 5 and 14-dpf larvae), L-thyroxine (T4) concentrations elevated, whereas 3,5,3′-L-triiodothyronine (T3) levels decreased. Additional investigation revealed that hypothalamic-pituitary-thyroid (HPT) axis gene transcription patterns underwent alteration following parental PHE treatment in F1 larvae. Collectively, this study established that PHE can transfer to the F1 generation from adult zebrafish, causing thyroid disruption and developmental toxicity.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"301 ","pages":"Article 110439"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827114","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":"Immunotoxicity and mechanism analysis of zebrafish embryos exposure to benzothiazole and its derivatives","authors":"Wan-Ting Huang ,&nbsp;Run-Fan Wu ,&nbsp;Zhong-Qian Xuan ,&nbsp;Jia-Qi Wu ,&nbsp;Ming-Fang He","doi":"10.1016/j.cbpc.2025.110427","DOIUrl":"10.1016/j.cbpc.2025.110427","url":null,"abstract":"<div><div>Benzothiazole derivatives (BTHs), including benzothiazole (BTH), 2-hydroxybenzothiazole (OBT), 2-aminobenzothiazole (NTH), and 2-(methylthio)benzothiazole (MTBT), pose significant exposure risks to organisms. Despite their recognized toxicity, the immunotoxic effects of BTHs remain poorly understood. This study systematically evaluated the immunotoxicity of four BTHs (BTH: 50 μM, 100 μM, and 200 μM; OBT: 50 μM, 100 μM, and 200 μM; NTH: 25 μM, 50 μM, and 100 μM; and MTBT: 3.125 μM, 6.25 μM, and 12.5 μM) in zebrafish embryos, including developmental toxicity, innate immune cell responses, oxidative stress levels, and bacterial challenge experiments were conducted to determine the impact of BTHs on pathogen resistance. RNA-seq and qRT-PCR assay were used to determine the mechanisms underlying BTHs-induced immunotoxicity. Results showed that BTH, OBT, NTH, and MTBT exposure caused developmental abnormalities, reduced macrophage and neutrophils numbers, and induced oxidative stress, including superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), and reactive oxygen species (ROS). Bacterial challenge assay revealed that BTH, OBT, NTH, and MTBT significantly impaired zebrafish resistance to bacterial infection. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis identified key differentially expressed genes (DEGs) in the TLR/NLR-NF-κB signaling pathway following BTH-exposure, which were further validated by qRT-PCR. In summary, BTHs not only exhibit developmental toxicity but also induce immunotoxicity by disrupting the Toll-like Receptors - Nucleotide-binding Oligomerization Domain-like Receptors - Nuclear Factor kappa-B (TLR/NLR-NF-κB) signaling pathway. These findings provide critical insights into the ecological risks of BTHs exposure in aquatic environments.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"301 ","pages":"Article 110427"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145699990","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":"Phosphorus-potassium fertilizer exposure induces oxidative stress and riboflavin metabolism disruption in juvenile turbot (Scophthalmus maximus)","authors":"Ying Tao ,&nbsp;Xin Li ,&nbsp;Lele Wu ,&nbsp;Ting Qi ,&nbsp;Xinlu Yue ,&nbsp;Xian Li","doi":"10.1016/j.cbpc.2025.110430","DOIUrl":"10.1016/j.cbpc.2025.110430","url":null,"abstract":"<div><div>Intensive agriculture's excessive fertilizer use significantly contributes to coastal nutrient pollution. While phosphorus's ecological impacts are recognized, the toxicity of combined phosphorus nutrients on marine life remains unclear. This study examined phosphorus-potassium fertilizer's (P-K fertilizer) effects on juvenile turbot (<em>Scophthalmus maximus</em>) via a 96-hour acute exposure experiment. Exposure solutions were prepared at environmentally relevant concentrations, resulting in elevated seawater phosphorus and potassium levels by 117.25 mg/L and 152.94 mg/L, respectively. Compound fertilizer aggravated multi-tissue damage, such as gill epithelial cell proliferation. Untargeted metabolomics identified that P-K fertilizer disrupts riboflavin metabolism, leading to reduced riboflavin levels. This deficiency impaired the production of flavin mononucleotide and flavin adenine dinucleotide. Meanwhile, excess potassium ions triggered Na⁺/K⁺ ATPase pump and gene of the renal outer medullary K⁺ channel to maintain ionic balance. Following riboflavin metabolism disruption, juvenile turbot exhibited impaired antioxidant capacity, with significantly decreased activities of glutathione peroxidase (by 54.5 %) and superoxide dismutase (by 12.6 %), a significant increase in catalase activity, obvious accumulation of malondialdehyde, and a reduction in total antioxidant capacity. The changes in related gene expression measured by real-time qPCR were consistent with the observed alterations in enzyme activities. Overall, compared to exposure to PO₄³⁻-P alone, the combined P-K fertilizer exposure resulted in more severe disruption of riboflavin metabolism and exacerbated oxidative damage in marine fish, indicating that K⁺ potentiated the adverse effects through synergistic interactions. This work provides critical insights for managing nutrient pollution in marine ecosystems and safeguarding coastal biodiversity and ecosystem services.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"301 ","pages":"Article 110430"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145707583","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}