Pub Date : 2025-11-07DOI: 10.1016/j.cbpc.2025.110388
Seong Chan Yun , Haksoo Jeong , Jin-Sol Lee , Jin-Hyoung Kim , Il-Chan Kim , Piotr Maszczyk , Zhou Yang , Atsushi Hagiwara , Jae-Seong Lee
Ammonia (NH3) is a widespread environmental pollutant with significant ecological and physiological impacts on aquatic organisms. While ammonia plays a key role in nitrogen cycling, excessive amounts disrupt homeostasis and cause toxic effects in various species. Its toxicity is influenced by environmental conditions such as pH, temperature, and salinity, with un-ionized ammonia being especially harmful due to its high membrane permeability. High ammonia levels impair ion balance, disturb nitrogen metabolism, trigger oxidative stress, affect neurophysiological functions at the intracellular level. Furthermore, ammonia can damage vital tissues, eliciting species-specific differential responses (fish, invertebrates, and amphibians), and impair survival, development, reproductive ability, and even movement. In addition, ammonia can alter the microorganisms' composition and metabolic functions. These findings highlight a complex relationship between microbial changes and host health conditions. Therefore, this review can aid in understanding the profound toxicity of ammonia, which affects both organisms and microorganisms, while emphasizing the need for monitoring and management strategies. As climate change intensifies environmental variability, a more profound understanding of ammonia toxicity is essential for protecting aquatic biodiversity and maintaining ecosystem stability.
{"title":"A review of ammonia toxicity on aquatic organisms: Species-specific responses, microbial shifts, and environmental interactions","authors":"Seong Chan Yun , Haksoo Jeong , Jin-Sol Lee , Jin-Hyoung Kim , Il-Chan Kim , Piotr Maszczyk , Zhou Yang , Atsushi Hagiwara , Jae-Seong Lee","doi":"10.1016/j.cbpc.2025.110388","DOIUrl":"10.1016/j.cbpc.2025.110388","url":null,"abstract":"<div><div>Ammonia (NH<sub>3</sub>) is a widespread environmental pollutant with significant ecological and physiological impacts on aquatic organisms. While ammonia plays a key role in nitrogen cycling, excessive amounts disrupt homeostasis and cause toxic effects in various species. Its toxicity is influenced by environmental conditions such as pH, temperature, and salinity, with un-ionized ammonia being especially harmful due to its high membrane permeability. High ammonia levels impair ion balance, disturb nitrogen metabolism, trigger oxidative stress, affect neurophysiological functions at the intracellular level. Furthermore, ammonia can damage vital tissues, eliciting species-specific differential responses (fish, invertebrates, and amphibians), and impair survival, development, reproductive ability, and even movement. In addition, ammonia can alter the microorganisms' composition and metabolic functions. These findings highlight a complex relationship between microbial changes and host health conditions. Therefore, this review can aid in understanding the profound toxicity of ammonia, which affects both organisms and microorganisms, while emphasizing the need for monitoring and management strategies. As climate change intensifies environmental variability, a more profound understanding of ammonia toxicity is essential for protecting aquatic biodiversity and maintaining ecosystem stability.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110388"},"PeriodicalIF":4.3,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145480296","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}
Pub Date : 2025-11-04DOI: 10.1016/j.cbpc.2025.110383
Marta Cunha , Alessio Lenzi , Constança Figueiredo , Lucia De Marchi , Carla Leite , Tania Russo , Gianfranca Monni , Valentina Meucci , Amadeu M.V.M. Soares , Gianluca Polese , Eduarda Pereira , Carlo Pretti , Rosa Freitas
Environmental salinity shifts, intensified by climate change, can influence the toxicity of pollutants such as antibiotics in marine organisms. In this study, specimens of the mussel Mytilus galloprovincialis were exposed for 28 days to three salinity levels (20, 30, and 40) in the presence or absence of tetracycline (TC) (1 mg/L). At the end of the exposure period, the effects were evaluated using an integrated metabolomic, biochemical, and histopathological approach. Tetracycline bioaccumulation did not differ significantly across salinities, indicating that biological effects were driven by stressor interactions rather than uptake. Metabolomic profiling showed that salinity and salinity-TC combinations had stronger impacts than TC alone. At salinity 20, mussels exhibited early oxidative stress and metabolic adjustments, along with tissue atrophy and lipofuscin buildup. Mussels at salinity 30 displayed relative physiological stability despite moderate histological changes under TC. In contrast, salinity 40 caused severe cellular damage, including membrane remodeling, lipid peroxidation, depleted antioxidants, and neurotoxic responses. The integrated multi-level analysis revealed coordinated stress responses involving oxidative stress, altered energy metabolism, and detoxification. Overall, these findings highlight salinity 30 as the optimal condition for M. galloprovincialis and emphasize the synergistic effects of climate-driven salinity changes and antibiotic pollution, underscoring the need to account for abiotic stressors in ecotoxicological assessments.
{"title":"From metabolites to tissues: A comprehensive analysis of salinity-driven modulation of tetracycline effects in Mytilus galloprovincialis","authors":"Marta Cunha , Alessio Lenzi , Constança Figueiredo , Lucia De Marchi , Carla Leite , Tania Russo , Gianfranca Monni , Valentina Meucci , Amadeu M.V.M. Soares , Gianluca Polese , Eduarda Pereira , Carlo Pretti , Rosa Freitas","doi":"10.1016/j.cbpc.2025.110383","DOIUrl":"10.1016/j.cbpc.2025.110383","url":null,"abstract":"<div><div>Environmental salinity shifts, intensified by climate change, can influence the toxicity of pollutants such as antibiotics in marine organisms. In this study, specimens of the mussel <em>Mytilus galloprovincialis</em> were exposed for 28 days to three salinity levels (20, 30, and 40) in the presence or absence of tetracycline (TC) (1 mg/L). At the end of the exposure period, the effects were evaluated using an integrated metabolomic, biochemical, and histopathological approach. Tetracycline bioaccumulation did not differ significantly across salinities, indicating that biological effects were driven by stressor interactions rather than uptake. Metabolomic profiling showed that salinity and salinity-TC combinations had stronger impacts than TC alone. At salinity 20, mussels exhibited early oxidative stress and metabolic adjustments, along with tissue atrophy and lipofuscin buildup. Mussels at salinity 30 displayed relative physiological stability despite moderate histological changes under TC. In contrast, salinity 40 caused severe cellular damage, including membrane remodeling, lipid peroxidation, depleted antioxidants, and neurotoxic responses. The integrated multi-level analysis revealed coordinated stress responses involving oxidative stress, altered energy metabolism, and detoxification. Overall, these findings highlight salinity 30 as the optimal condition for <em>M. galloprovincialis</em> and emphasize the synergistic effects of climate-driven salinity changes and antibiotic pollution, underscoring the need to account for abiotic stressors in ecotoxicological assessments.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110383"},"PeriodicalIF":4.3,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457878","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}
Pub Date : 2025-11-01DOI: 10.1016/j.cbpc.2025.110384
Jaehee Kim , Seong Duk Do , Jae-Sung Rhee
Despite being persistent pollutants of global concern and frequently detected in aquatic environments, the detrimental effects of short-chain chlorinated paraffins (SCCPs) on aquatic crustaceans remain limited. Here, we analyzed the acute and chronic effects of SCCPs on the freshwater flea Moina macrocopa. The no observed effect concentration (NOEC) value of SCCPs for 48 h was determined to be 0.24 μg L−1, while the 10 % (LC10) and 50 % (LC50) lethality values were measured as 3.7 and 36 μg L−1, respectively. In the acute exposure experiment, exposure to the LC10 value of SCCPs reduced feeding performance, acetylcholinesterase activity, and thoracic limb movement. In response to the LC10 value, reactive oxygen species levels increased, accompanied by elevated concentrations of malondialdehyde and glutathione. Enzymatic activities of glutathione S-transferase, catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase were significantly elevated at the LC10 value, indicating active involvement of the antioxidant defense system in mitigating oxidative stress. Long-term exposure to the 1/10 NOEC and NOEC values across three generations showed multigenerational detrimental impacts of SCCPs, including reductions in survival, growth, and reproduction in the second and/or third generations. Taken together, our results suggest that even sublethal concentrations of SCCPs can acutely induce cholinergic impairment and oxidative stress, while chronically impairing population maintenance in M. macrocopa.
{"title":"Effects of short-chain chlorinated paraffins on feeding, oxidative status, and multigenerational parameters in the water flea Moina macrocopa","authors":"Jaehee Kim , Seong Duk Do , Jae-Sung Rhee","doi":"10.1016/j.cbpc.2025.110384","DOIUrl":"10.1016/j.cbpc.2025.110384","url":null,"abstract":"<div><div>Despite being persistent pollutants of global concern and frequently detected in aquatic environments, the detrimental effects of short-chain chlorinated paraffins (SCCPs) on aquatic crustaceans remain limited. Here, we analyzed the acute and chronic effects of SCCPs on the freshwater flea <em>Moina macrocopa</em>. The no observed effect concentration (NOEC) value of SCCPs for 48 h was determined to be 0.24 μg L<sup>−1</sup>, while the 10 % (LC10) and 50 % (LC50) lethality values were measured as 3.7 and 36 μg L<sup>−1</sup>, respectively. In the acute exposure experiment, exposure to the LC10 value of SCCPs reduced feeding performance, acetylcholinesterase activity, and thoracic limb movement. In response to the LC10 value, reactive oxygen species levels increased, accompanied by elevated concentrations of malondialdehyde and glutathione. Enzymatic activities of glutathione <em>S</em>-transferase, catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase were significantly elevated at the LC10 value, indicating active involvement of the antioxidant defense system in mitigating oxidative stress. Long-term exposure to the 1/10 NOEC and NOEC values across three generations showed multigenerational detrimental impacts of SCCPs, including reductions in survival, growth, and reproduction in the second and/or third generations. Taken together, our results suggest that even sublethal concentrations of SCCPs can acutely induce cholinergic impairment and oxidative stress, while chronically impairing population maintenance in <em>M. macrocopa</em>.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110384"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145437270","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}
Pub Date : 2025-10-31DOI: 10.1016/j.cbpc.2025.110379
Fan Wang, Yiran Liu, Huiwen Yang, Ying Zhang, Fei Liu
Triclosan (TCS), a widely used antimicrobial agent, has been identified as a reproductive endocrine disruptor. However, the mechanisms underlying TCS-induced gonadal damage remain incompletely understood. In this study, zebrafish were chronically exposed to TCS from 4 h post-fertilization (hpf) to 120 days post-fertilization (dpf). A comprehensive analysis was conducted, including assessment of testicular cell apoptosis in adult fish, evaluation of apoptosis-related genes and proteins in both adult testes and 50-day-old juveniles, and transcriptome sequencing. The results showed that TCS exposure downregulated mRNA expression of oxidative stress-related and anti-apoptotic genes, while upregulating pro-apoptotic gene expression along with P53 and Caspase 3 protein levels, ultimately leading to a significant increase in testicular apoptotic cells. Transcriptome sequencing analysis revealed enrichment of the P53 signaling pathway, apoptosis pathway, response to oxidative stress biological process. These findings indicate that postembryonic exposure to TCS causes gonadal damage primarily by inducing oxidative stress, which increases P53 expression, subsequently regulating pro-apoptotic gene expression and suppressing anti-apoptotic proteins, thereby activating the mitochondrial apoptosis pathway and death receptor pathway, potentially affecting growth, development, and reproductive toxicity. This study systematically elucidates the molecular mechanism by which TCS induces reproductive toxicity through the oxidative stress-P53 axis, which triggers both the mitochondrial and death receptor apoptotic pathways. Our findings provide important experimental evidence and a theoretical reference for the scientific assessment of TCS-related reproductive health risks.
三氯生（TCS）是一种广泛使用的抗菌剂，已被确定为生殖内分泌干扰物。然而，tcs诱导性腺损伤的机制仍不完全清楚。在本研究中，斑马鱼从受精后4 h （hpf）到受精后120 d （dpf）长期暴露于TCS。我们进行了全面的分析，包括评估成鱼睾丸细胞凋亡，评估成鱼睾丸和50日龄幼鱼中凋亡相关基因和蛋白，以及转录组测序。结果表明，TCS暴露可下调氧化应激相关基因和抗凋亡基因的mRNA表达，上调促凋亡基因的表达以及P53和Caspase 3蛋白水平，最终导致睾丸凋亡细胞显著增加。转录组测序分析显示P53信号通路、凋亡通路富集，响应氧化应激的生物过程。这些研究结果表明，胚胎后暴露于TCS主要通过诱导氧化应激导致性腺损伤，氧化应激增加P53表达，随后调节促凋亡基因表达，抑制抗凋亡蛋白，从而激活线粒体凋亡途径和死亡受体途径，可能影响生长发育和生殖毒性。本研究系统阐明了TCS通过氧化应激- p53轴诱导生殖毒性的分子机制，该轴触发线粒体和死亡受体凋亡途径。本研究结果为科学评估tcs相关生殖健康风险提供了重要的实验依据和理论参考。
{"title":"Triclosan induces spermatogenic damage via the oxidative stress-P53-apoptosis pathway in zebrafish","authors":"Fan Wang, Yiran Liu, Huiwen Yang, Ying Zhang, Fei Liu","doi":"10.1016/j.cbpc.2025.110379","DOIUrl":"10.1016/j.cbpc.2025.110379","url":null,"abstract":"<div><div>Triclosan (TCS), a widely used antimicrobial agent, has been identified as a reproductive endocrine disruptor. However, the mechanisms underlying TCS-induced gonadal damage remain incompletely understood. In this study, zebrafish were chronically exposed to TCS from 4 h post-fertilization (hpf) to 120 days post-fertilization (dpf). A comprehensive analysis was conducted, including assessment of testicular cell apoptosis in adult fish, evaluation of apoptosis-related genes and proteins in both adult testes and 50-day-old juveniles, and transcriptome sequencing. The results showed that TCS exposure downregulated mRNA expression of oxidative stress-related and anti-apoptotic genes, while upregulating pro-apoptotic gene expression along with P53 and Caspase 3 protein levels, ultimately leading to a significant increase in testicular apoptotic cells. Transcriptome sequencing analysis revealed enrichment of the P53 signaling pathway, apoptosis pathway, response to oxidative stress biological process. These findings indicate that postembryonic exposure to TCS causes gonadal damage primarily by inducing oxidative stress, which increases P53 expression, subsequently regulating pro-apoptotic gene expression and suppressing anti-apoptotic proteins, thereby activating the mitochondrial apoptosis pathway and death receptor pathway, potentially affecting growth, development, and reproductive toxicity. This study systematically elucidates the molecular mechanism by which TCS induces reproductive toxicity through the oxidative stress-P53 axis, which triggers both the mitochondrial and death receptor apoptotic pathways. Our findings provide important experimental evidence and a theoretical reference for the scientific assessment of TCS-related reproductive health risks.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110379"},"PeriodicalIF":4.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145430368","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}
Pub Date : 2025-10-31DOI: 10.1016/j.cbpc.2025.110386
Jéssica Ferreira de Souza , Mayara Moura Silveira , Ana Luisa Pires Moreira , Juliana Alves Costa Ribeiro Souza , Rafael Xavier Martins , Davi Farias , Francisco Carlos da Silva Junior , Ana Carolina Luchiari
Oxybenzone (also known as benzophenone-3 or BP-3) is an organic ultraviolet (UV) filter commonly used in personal care products. BP-3 has been detected in various aquatic environments and is a major concern in reef areas due to their biological richness and vital role in marine ecosystems. This research focused on investigating the effects of BP-3 exposure in dusky damselfish Stegastes fuscus, an endemic species of the Brazilian coast, analyzing behavioral responses, enzymatic biomarkers on encephalon and liver (catalase (CAT), glutathione S-transferase (GST), acetylcholinesterase (AChE), and lactate dehydrogenase (LDH)), and general health indicators (growth rate and hepatosomatic index). Adults of S. fuscus were fed a diet containing BP-3 at concentrations of 10 μg/g food and 20 μg/g food for 44 days, with behavioral tests starting after 30 days of exposure. Light-dark preference, novel tank and aggressiveness tests were conducted. Our results showed that BP-3 exposure decreased health indicators and altered fish behavior, decreasing risk-perception and locomotion, although agonistic behavior remained unaffected. Enzymatic assays revealed changes that varied depending on the tissue analyzed. These findings highlight the potential of BP-3 to impair behavioral and physiological processes in reef fish, emphasizing the need for regulations on UV filters to protect marine ecosystems and reef life.
{"title":"Behavioral and biochemical effects of benzophenone-3 ingestion in dusky damselfish Stegastes fuscus","authors":"Jéssica Ferreira de Souza , Mayara Moura Silveira , Ana Luisa Pires Moreira , Juliana Alves Costa Ribeiro Souza , Rafael Xavier Martins , Davi Farias , Francisco Carlos da Silva Junior , Ana Carolina Luchiari","doi":"10.1016/j.cbpc.2025.110386","DOIUrl":"10.1016/j.cbpc.2025.110386","url":null,"abstract":"<div><div>Oxybenzone (also known as benzophenone-3 or BP-3) is an organic ultraviolet (UV) filter commonly used in personal care products. BP-3 has been detected in various aquatic environments and is a major concern in reef areas due to their biological richness and vital role in marine ecosystems. This research focused on investigating the effects of BP-3 exposure in dusky damselfish <em>Stegastes fuscus</em>, an endemic species of the Brazilian coast, analyzing behavioral responses, enzymatic biomarkers on encephalon and liver (catalase (CAT), glutathione S-transferase (GST), acetylcholinesterase (AChE), and lactate dehydrogenase (LDH)), and general health indicators (growth rate and hepatosomatic index). Adults of <em>S. fuscus</em> were fed a diet containing BP-3 at concentrations of 10 μg/g food and 20 μg/g food for 44 days, with behavioral tests starting after 30 days of exposure. Light-dark preference, novel tank and aggressiveness tests were conducted. Our results showed that BP-3 exposure decreased health indicators and altered fish behavior, decreasing risk-perception and locomotion, although agonistic behavior remained unaffected. Enzymatic assays revealed changes that varied depending on the tissue analyzed. These findings highlight the potential of BP-3 to impair behavioral and physiological processes in reef fish, emphasizing the need for regulations on UV filters to protect marine ecosystems and reef life.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110386"},"PeriodicalIF":4.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145430158","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}
Pub Date : 2025-10-31DOI: 10.1016/j.cbpc.2025.110381
Deok-Seo Yoon , Jin-Hyoung Kim , Il-Chan Kim , Youji Wang , Zhou Yang , Min-Chul Lee , Jae-Seong Lee
Aquatic environments are dynamic systems where multiple factors influence the intricate interactions between hosts and their gut microbiomes. This review explores how various stressors alter the gut microbiota of fish and aquatic invertebrates, by examining factors that include water characteristics, photoperiod, external pollutants such as heavy metals and microplastics, food availability, and practical aquaculture feed additives, for example, ethoxyquin. Across these diverse factors, common patterns emerge, including disruptions to microbial diversity, compromised gut barrier integrity, and the induction of oxidative stress. Conversely, beneficial additives like probiotics and astaxanthin are shown to mitigate these negative effects by reinforcing gut structure and modulating the microbial community. Collectively, these findings underscore the critical role of the gut microbiota in mediating host responses to environmental changes. Future research should therefore focus on elucidating specific toxicological pathways like the gut-organ axis, investigating the transgenerational effects of pollutants, and developing probiotic-based strategies to enhance the resilience and sustainability of aquaculture.
{"title":"Effects of environmental factors on host-microbiota interactions in the guts of aquatic organisms: A review","authors":"Deok-Seo Yoon , Jin-Hyoung Kim , Il-Chan Kim , Youji Wang , Zhou Yang , Min-Chul Lee , Jae-Seong Lee","doi":"10.1016/j.cbpc.2025.110381","DOIUrl":"10.1016/j.cbpc.2025.110381","url":null,"abstract":"<div><div>Aquatic environments are dynamic systems where multiple factors influence the intricate interactions between hosts and their gut microbiomes. This review explores how various stressors alter the gut microbiota of fish and aquatic invertebrates, by examining factors that include water characteristics, photoperiod, external pollutants such as heavy metals and microplastics, food availability, and practical aquaculture feed additives, for example, ethoxyquin. Across these diverse factors, common patterns emerge, including disruptions to microbial diversity, compromised gut barrier integrity, and the induction of oxidative stress. Conversely, beneficial additives like probiotics and astaxanthin are shown to mitigate these negative effects by reinforcing gut structure and modulating the microbial community. Collectively, these findings underscore the critical role of the gut microbiota in mediating host responses to environmental changes. Future research should therefore focus on elucidating specific toxicological pathways like the gut-organ axis, investigating the transgenerational effects of pollutants, and developing probiotic-based strategies to enhance the resilience and sustainability of aquaculture.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110381"},"PeriodicalIF":4.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145430110","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}
Pub Date : 2025-10-31DOI: 10.1016/j.cbpc.2025.110380
Jinhao Bian , Hanshuang Zhao , Wenping Xu , Zhong Li , Yang Zhang
The widespread use of prothioconazole (PTCZ), a globally applied triazole fungicide, raises concerns regarding ecological risks from environmental residues and highlights the critical gap in pesticide safety assessment concerning enantiomeric differences in toxicity. This study investigated the stereoselective toxicity and molecular mechanisms of PTCZ enantiomers in an aquatic model using a zebrafish embryo exposure system. The toxic effects were systematically analyzed through multidimensional endpoint assessments, which examined developmental malformations, liver histopathology, lipid metabolism indicators, and lipid peroxidation. The underlying molecular mechanisms were explored through GPX4 immunofluorescence, as well as qPCR and Western blot analyses of ferroptosis-related genes. A ferroptosis inhibitor rescue experiment utilizing Ferrostatin-1 was conducted to investigate the role of ferroptosis in the observed toxicity. Our findings demonstrate that the S-(+)-PTCZ enantiomer induced significantly more severe developmental toxicity and liver injury compared to its counterpart. Mechanistically, S-(+)-PTCZ triggered hepatic damage by activating the lipid peroxidation-ferroptosis axis, as evidenced by inhibition of GPX4 protein expression and an upregulation of the pro-ferroptotic gene acsl4. Crucially, Ferrostatin-1 significantly reversed these effects, reducing lipid peroxidation. Our results confirm that traditional risk assessments based on the racemate (Rac-PTCZ) would substantially underestimate the actual environmental risk posed by the highly non-target bioactive S-(+)-enantiomer. This work provides a critical theoretical basis for the precise regulation and low-toxicity design of chiral pesticides.
{"title":"Prothioconazole induced stereoselective developmental toxicity and liver injury in zebrafish embryos via ferroptosis","authors":"Jinhao Bian , Hanshuang Zhao , Wenping Xu , Zhong Li , Yang Zhang","doi":"10.1016/j.cbpc.2025.110380","DOIUrl":"10.1016/j.cbpc.2025.110380","url":null,"abstract":"<div><div>The widespread use of prothioconazole (PTCZ), a globally applied triazole fungicide, raises concerns regarding ecological risks from environmental residues and highlights the critical gap in pesticide safety assessment concerning enantiomeric differences in toxicity. This study investigated the stereoselective toxicity and molecular mechanisms of PTCZ enantiomers in an aquatic model using a zebrafish embryo exposure system. The toxic effects were systematically analyzed through multidimensional endpoint assessments, which examined developmental malformations, liver histopathology, lipid metabolism indicators, and lipid peroxidation. The underlying molecular mechanisms were explored through GPX4 immunofluorescence, as well as qPCR and Western blot analyses of ferroptosis-related genes. A ferroptosis inhibitor rescue experiment utilizing Ferrostatin-1 was conducted to investigate the role of ferroptosis in the observed toxicity. Our findings demonstrate that the S-(+)-PTCZ enantiomer induced significantly more severe developmental toxicity and liver injury compared to its counterpart. Mechanistically, S-(+)-PTCZ triggered hepatic damage by activating the lipid peroxidation-ferroptosis axis, as evidenced by inhibition of GPX4 protein expression and an upregulation of the pro-ferroptotic gene <em>acsl4</em>. Crucially, Ferrostatin-1 significantly reversed these effects, reducing lipid peroxidation. Our results confirm that traditional risk assessments based on the racemate (Rac-PTCZ) would substantially underestimate the actual environmental risk posed by the highly non-target bioactive S-(+)-enantiomer. This work provides a critical theoretical basis for the precise regulation and low-toxicity design of chiral pesticides.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110380"},"PeriodicalIF":4.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145430344","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}
Pub Date : 2025-10-31DOI: 10.1016/j.cbpc.2025.110385
Gil Martins , Sunil Poudel , Ana Portela , Gonçalo Pinto , Tamára F. Santos , Francisco A. Guardiola , Ana Marreiros , Paulo J. Gavaia
Zebrafish is a relevant model in skeletal research, enabling insights into bone development and regeneration. Inflammation supports tissue regeneration; however, excessive or chronic inflammation can delay the healing process and contribute to the development of skeletal disorders. Bacterial infections or LPS exposure exacerbate inflammation, hindering bone regeneration. Here, we tested the effects of LPS (1 and 10 μg/mL) as an inducer of an inflammatory response and evaluated its impact on the bone using zebrafish regenerating scales as a model. Results showed that exposure to LPS leads to an inflammatory process that affects scale regenerative ability. Exposure to LPS (10 μg/mL) led to a reduction in scale area, increased scale aspect ratio, osteoclast activity with scale demineralization, as well as overexpression of osteoclastic markers (acp5 and oc-stamp) and downregulation of the osteoblastic marker sp7. Our data suggest that zebrafish regenerating scales exposed to LPS can be further developed as an in vivo screening method to elucidate the mechanisms involved in the increased bone resorption associated with inflammatory processes, to evaluate the effects on osteoblast-osteoclast interaction in fish, and to search for novel therapeutic compounds for skeletal disorders and diseases.
{"title":"Lipopolysaccharides increase the resorption levels and affect zebrafish scales de novo bone formation","authors":"Gil Martins , Sunil Poudel , Ana Portela , Gonçalo Pinto , Tamára F. Santos , Francisco A. Guardiola , Ana Marreiros , Paulo J. Gavaia","doi":"10.1016/j.cbpc.2025.110385","DOIUrl":"10.1016/j.cbpc.2025.110385","url":null,"abstract":"<div><div>Zebrafish is a relevant model in skeletal research, enabling insights into bone development and regeneration. Inflammation supports tissue regeneration; however, excessive or chronic inflammation can delay the healing process and contribute to the development of skeletal disorders. Bacterial infections or LPS exposure exacerbate inflammation, hindering bone regeneration. Here, we tested the effects of LPS (1 and 10 μg/mL) as an inducer of an inflammatory response and evaluated its impact on the bone using zebrafish regenerating scales as a model. Results showed that exposure to LPS leads to an inflammatory process that affects scale regenerative ability. Exposure to LPS (10 μg/mL) led to a reduction in scale area, increased scale aspect ratio, osteoclast activity with scale demineralization, as well as overexpression of osteoclastic markers (<em>acp5</em> and <em>oc-stamp</em>) and downregulation of the osteoblastic marker <em>sp7</em>. Our data suggest that zebrafish regenerating scales exposed to LPS can be further developed as an <em>in vivo</em> screening method to elucidate the mechanisms involved in the increased bone resorption associated with inflammatory processes, to evaluate the effects on osteoblast-osteoclast interaction in fish, and to search for novel therapeutic compounds for skeletal disorders and diseases.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110385"},"PeriodicalIF":4.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145430118","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}
Pub Date : 2025-10-31DOI: 10.1016/j.cbpc.2025.110382
Helei Cai , Qizhuan Lin , Changyong Gong , Fan Yu , Libo Jin , Renyi Peng
Per-and polyfluoroalkyl substances (PFAS) are widely distributed across freshwater systems in mainland China, with concentrations showing marked spatial heterogeneity—particularly in eastern regions with intensive industrial activity. Fish not only play a vital ecological role but also serve as an important source of protein for humans. Due to the biomagnification factors (BMF > 1) of PFAS in the food chain, the risk of exposure increases for high-trophic-level fish, other predators, and ultimately humans. Co-exposure with other environmental pollutants further amplifies PFAS-induced immunotoxic effects. The immunotoxicity of PFAS is influenced by carbon chain length and functional groups, with long-chain PFAS and sulfonic acid groups generally exhibiting stronger immunotoxic effects in fish. These compounds significantly suppress both innate and adaptive immune responses by interfering with Toll-like receptor signaling pathways, inducing oxidative stress, and impairing immune cell function. Although current technologies are available for PFAS removal, they still face considerable limitations and challenges. This review summarizes the characteristics and spatial distribution of PFAS contamination in mainland China's aquatic environments and focuses on the mechanisms of PFAS-induced immunotoxicity in fish. It offers valuable insights for future research into the synergistic/antagonistic and time-dependent effects of combined PFAS and multi-pollutant exposure. Moreover, it provides important references for the development of mitigation technologies targeting PFAS-related ecotoxicity in aquatic food chains and for informing relevant policy formulation.
{"title":"PFAS-induced immunotoxicity in freshwater fish of inland China: mechanisms and ecological risks","authors":"Helei Cai , Qizhuan Lin , Changyong Gong , Fan Yu , Libo Jin , Renyi Peng","doi":"10.1016/j.cbpc.2025.110382","DOIUrl":"10.1016/j.cbpc.2025.110382","url":null,"abstract":"<div><div><em>Per</em>-and polyfluoroalkyl substances (PFAS) are widely distributed across freshwater systems in mainland China, with concentrations showing marked spatial heterogeneity—particularly in eastern regions with intensive industrial activity. Fish not only play a vital ecological role but also serve as an important source of protein for humans. Due to the biomagnification factors (BMF > 1) of PFAS in the food chain, the risk of exposure increases for high-trophic-level fish, other predators, and ultimately humans. Co-exposure with other environmental pollutants further amplifies PFAS-induced immunotoxic effects. The immunotoxicity of PFAS is influenced by carbon chain length and functional groups, with long-chain PFAS and sulfonic acid groups generally exhibiting stronger immunotoxic effects in fish. These compounds significantly suppress both innate and adaptive immune responses by interfering with Toll-like receptor signaling pathways, inducing oxidative stress, and impairing immune cell function. Although current technologies are available for PFAS removal, they still face considerable limitations and challenges. This review summarizes the characteristics and spatial distribution of PFAS contamination in mainland China's aquatic environments and focuses on the mechanisms of PFAS-induced immunotoxicity in fish. It offers valuable insights for future research into the synergistic/antagonistic and time-dependent effects of combined PFAS and multi-pollutant exposure. Moreover, it provides important references for the development of mitigation technologies targeting PFAS-related ecotoxicity in aquatic food chains and for informing relevant policy formulation.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110382"},"PeriodicalIF":4.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145430167","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}
The liver is a major organ of digestion and detoxification metabolism in animals, and the occurrence of most liver diseases is closely associated with environmental pollution. Besides, liver is a non-reproductive primary target organ regulated by sex steroid hormone signaling. In this study, we elucidated the detoxification metabolism pathways of B[a]P in the clam Ruditapes philippinarum and identified the hepatotoxicity mechanism of B[a]P using technical approaches such as transcriptomics, computer simulation and experimental validation. We found that the AhR signaling pathway and CYP450 family (CYP1A1, CYP2B1, CYP3A4) and FMO in the digestive gland of clam play important roles in the detoxification metabolism of B[a]P, but the performance varied between male and female clams. SOD1 and CAT, GPX, PRDX play antioxidant function but PRDX pathway did not function in females. The level of detoxification metabolism in reproductive clams under B[a]P stress was female < male, oxidative stress was female > male, and oxidative damage was female < male. Cell death (apoptosis, pyroptosis and ferroptosis) was aggravated in the digestive gland of both males and females, with a reduced level of hepatic function health and an increase in the level of inflammatory factors, but males presented a more pronounced tendency toward hepatic fibrosis. In summary, the results of this study enrich the research perspectives on the metabolic pathways of POPs in aquatic invertebrates and lay the foundation for the study of POPs-induced hepatotoxicity, which is of great significance for the conservation of marine biological resources and the monitoring of POPs pollution.
{"title":"Detoxification metabolic pathways and hepatotoxicity mechanisms of B[a]P in reproductive clam Ruditapes philippinarum","authors":"Yueyao Zhou, Zhiheng He, Qiuhong Xu, Songhui Xie, Pengfei Li, Qiaoqiao Wang, Jingjing Miao, Luqing Pan","doi":"10.1016/j.cbpc.2025.110378","DOIUrl":"10.1016/j.cbpc.2025.110378","url":null,"abstract":"<div><div>The liver is a major organ of digestion and detoxification metabolism in animals, and the occurrence of most liver diseases is closely associated with environmental pollution. Besides, liver is a non-reproductive primary target organ regulated by sex steroid hormone signaling. In this study, we elucidated the detoxification metabolism pathways of B[<em>a</em>]P in the clam <em>Ruditapes philippinarum</em> and identified the hepatotoxicity mechanism of B[<em>a</em>]P using technical approaches such as transcriptomics, computer simulation and experimental validation. We found that the <em>AhR</em> signaling pathway and <em>CYP450</em> family (<em>CYP1A1</em>, <em>CYP2B1</em>, <em>CYP3A4</em>) and <em>FMO</em> in the digestive gland of clam play important roles in the detoxification metabolism of B[<em>a</em>]P, but the performance varied between male and female clams. <em>SOD1</em> and CAT, GPX, PRDX play antioxidant function but PRDX pathway did not function in females. The level of detoxification metabolism in reproductive clams under B[<em>a</em>]P stress was female < male, oxidative stress was female > male, and oxidative damage was female < male. Cell death (apoptosis, pyroptosis and ferroptosis) was aggravated in the digestive gland of both males and females, with a reduced level of hepatic function health and an increase in the level of inflammatory factors, but males presented a more pronounced tendency toward hepatic fibrosis. In summary, the results of this study enrich the research perspectives on the metabolic pathways of POPs in aquatic invertebrates and lay the foundation for the study of POPs-induced hepatotoxicity, which is of great significance for the conservation of marine biological resources and the monitoring of POPs pollution.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110378"},"PeriodicalIF":4.3,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367745","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}
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