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}
Pub Date : 2025-10-20DOI: 10.1016/j.cbpc.2025.110376
Juan Wang , Yingying Lu , Xinyi Wu , Xinru Zhang , Qu Cai , Chenbo Huang , Zhi Wang
This study investigated the compound stresses of cadmium (Cd) and antibiotics on the immune defense system of wolf spiders, Pardosa pseudoannulata, which is a vital predator for pest control in the paddy ecosystem. Overall, the synergistic effect of Cd and antibiotics on the inhibition of immune response was identified in spiderlings, which manifested by decreased resistance to a pathogen, reduced concentration of immune effectors, and altered concentrations of antioxidants. Similarly, changes in the relative abundances of several antimicrobial peptides, such as lycosins, lycotoxins, and pardosins, were consistent with the change of immune effectors. Specific responsive genes of compound stresses suggested a broader disturbance in the immune system, like the antioxidase system, phenoloxidase, and lysosome, as well as changes in the developmental events like the biosynthesis of molting and juvenile hormones in spiderlings, which were acknowledged as potential contributors to the combined exposure toxicity. Another group of genes involved in ribosome, energy metabolism, and phagosome can act as co-damage markers in response to alone or combined exposures of Cd and antibiotics. These results expanded the insights into the ecotoxicology assessment of combined pollutants in the paddy field.
{"title":"Combined effects of cadmium and antibiotics on the immune defense system of the wolf spider Pardosa pseudoannulata","authors":"Juan Wang , Yingying Lu , Xinyi Wu , Xinru Zhang , Qu Cai , Chenbo Huang , Zhi Wang","doi":"10.1016/j.cbpc.2025.110376","DOIUrl":"10.1016/j.cbpc.2025.110376","url":null,"abstract":"<div><div>This study investigated the compound stresses of cadmium (Cd) and antibiotics on the immune defense system of wolf spiders, <em>Pardosa pseudoannulata</em>, which is a vital predator for pest control in the paddy ecosystem. Overall, the synergistic effect of Cd and antibiotics on the inhibition of immune response was identified in spiderlings, which manifested by decreased resistance to a pathogen, reduced concentration of immune effectors, and altered concentrations of antioxidants. Similarly, changes in the relative abundances of several antimicrobial peptides, such as lycosins, lycotoxins, and pardosins, were consistent with the change of immune effectors. Specific responsive genes of compound stresses suggested a broader disturbance in the immune system, like the antioxidase system, phenoloxidase, and lysosome, as well as changes in the developmental events like the biosynthesis of molting and juvenile hormones in spiderlings, which were acknowledged as potential contributors to the combined exposure toxicity. Another group of genes involved in ribosome, energy metabolism, and phagosome can act as co-damage markers in response to alone or combined exposures of Cd and antibiotics. These results expanded the insights into the ecotoxicology assessment of combined pollutants in the paddy field.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110376"},"PeriodicalIF":4.3,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343953","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 : 2025-10-19DOI: 10.1016/j.cbpc.2025.110377
Xiaoyu Mao , Dashuang Mo , Mengzhu Lv
Disinfection by-products are widespread contaminants formed during water disinfection processes, with bromoacetic acids (BAAs), including bromoacetic acid (BAA) and dibromoacetic acid (DBAA), frequently detected in swimming pools, spas, and tap water. Although their environmental occurrence is well documented, the in vivo organ-specific toxicity of BAAs remains poorly understood. In this study, zebrafish (Danio rerio) were employed to investigate the developmental and cardiotoxic effects of BAA and DBAA, individually and in combination. Exposure to BAA or combined BAA/DBAA significantly increased mortality and reduced hatching rates, whereas DBAA alone showed no significant effect on hatching. Both compounds induced morphological abnormalities, including reduced body length, swim bladder defects, and pericardial edema. Cardiac assessments revealed enlarged pericardial areas, decreased heart rates, and downregulation of key cardiac developmental genes. BAAs also elevated reactive oxygen species (ROS) levels in the heart, upregulated ROS-generating genes, and suppressed antioxidant genes. Furthermore, BAAs reduced cardiomyocyte proliferation, increased γH2AX-positive cells, and upregulated apoptosis-related genes, indicating DNA damage and apoptosis. Co-treatment with the antioxidant N-acetylcysteine mitigated pericardial edema and reduced γH2AX-positive cells, confirming a central role of oxidative stress in BAAs-induced cardiotoxicity. These findings demonstrate that BAA and DBAA impair zebrafish heart development through oxidative stress–mediated disruption of cell proliferation and promotion of apoptosis. This study highlights the need for further evaluation of BAA and DBAA toxicity to better understand their potential health risks in humans.
{"title":"Bromoacetic acid and dibromoacetic acid induce cardiotoxicity in larval zebrafish by triggering oxidative stress","authors":"Xiaoyu Mao , Dashuang Mo , Mengzhu Lv","doi":"10.1016/j.cbpc.2025.110377","DOIUrl":"10.1016/j.cbpc.2025.110377","url":null,"abstract":"<div><div>Disinfection by-products are widespread contaminants formed during water disinfection processes, with bromoacetic acids (BAAs), including bromoacetic acid (BAA) and dibromoacetic acid (DBAA), frequently detected in swimming pools, spas, and tap water. Although their environmental occurrence is well documented, the <em>in vivo</em> organ-specific toxicity of BAAs remains poorly understood. In this study, zebrafish (<em>Danio rerio</em>) were employed to investigate the developmental and cardiotoxic effects of BAA and DBAA, individually and in combination. Exposure to BAA or combined BAA/DBAA significantly increased mortality and reduced hatching rates, whereas DBAA alone showed no significant effect on hatching. Both compounds induced morphological abnormalities, including reduced body length, swim bladder defects, and pericardial edema. Cardiac assessments revealed enlarged pericardial areas, decreased heart rates, and downregulation of key cardiac developmental genes. BAAs also elevated reactive oxygen species (ROS) levels in the heart, upregulated ROS-generating genes, and suppressed antioxidant genes. Furthermore, BAAs reduced cardiomyocyte proliferation, increased γH2AX-positive cells, and upregulated apoptosis-related genes, indicating DNA damage and apoptosis. Co-treatment with the antioxidant <em>N</em>-acetylcysteine mitigated pericardial edema and reduced γH2AX-positive cells, confirming a central role of oxidative stress in BAAs-induced cardiotoxicity. These findings demonstrate that BAA and DBAA impair zebrafish heart development through oxidative stress–mediated disruption of cell proliferation and promotion of apoptosis. This study highlights the need for further evaluation of BAA and DBAA toxicity to better understand their potential health risks in humans.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110377"},"PeriodicalIF":4.3,"publicationDate":"2025-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343952","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 : 2025-10-18DOI: 10.1016/j.cbpc.2025.110375
Ariana Pérez-Pereira , Ana R. Carvalho , Pedro A. Costa , Bruno B. Castro , João S. Carrola , Virgínia M.F. Gonçalves , Ana R.L. Ribeiro , Ana Sofia Almeida , Carla Fernandes , Maria E. Tiritan , Cláudia Ribeiro
The enantioselective toxicity of 3,4-methylenedioxypyrovalerone (MDPV) remains unexplored in freshwater organisms. This study investigated the effects of MDPV racemate and its enantiomers in Daphnia magna using two approaches: (i) an 8-day sub-chronic assay focused on early development stages; and (ii) the standard 21-day reproduction assay. The sub-chronic assay tested two environmental concentrations (0.10 and 1.0 μg L−1), for both racemate or individual enantiomers, and a higher sublethal concentration of 10 μg L−1 for the racemate. Survival, morphophysiological, behavioural, reproductive, and biochemical responses were evaluated. The reproduction assay tested concentrations from 0.10 to 1.79 μg L−1, and evaluated survival, body size, and reproductive effects.
Sub-chronic exposure to 10 μg L−1 (R,S)-MDPV decreased survival. MDPV racemate and its enantiomers changed morphophysiological parameters, except for body growth. In juveniles, the heart area increased with 0.10 μg L−1 of (R)-MDPV whereas the heart size decreased with 0.10 and 1.0 μg L−1 of (S)-MDPV. Enantioselective effects were observed in swimming behaviour: (S)-MDPV increased speed and (R)-MDPV increased active time. No effects were observed in biochemical (except in reactive oxygen species for (S)-MDPV) and early reproductive parameters. The reproduction assay revealed enhanced growth in all MDPV forms (except at 0.56 μg L−1). A nonsignificant reduction in survival to the higher concentrations of (R)-MDPV was accompanied by reduced reproductive output (at 1.00 and 1.79 μg L−1) and intrinsic rate of population increase (at 1.79 μg L−1). Our findings suggest that, in general, (S)-MDPV triggers more severe sub-chronic effects, whereas (R)-MDPV is associated with harmful effects for longer time exposure.
{"title":"Enantioselective toxicity of 3,4-methylenedioxypyrovalerone in Daphnia magna: Assessment of morphophysiological, behavioural, biochemical and reproductive responses","authors":"Ariana Pérez-Pereira , Ana R. Carvalho , Pedro A. Costa , Bruno B. Castro , João S. Carrola , Virgínia M.F. Gonçalves , Ana R.L. Ribeiro , Ana Sofia Almeida , Carla Fernandes , Maria E. Tiritan , Cláudia Ribeiro","doi":"10.1016/j.cbpc.2025.110375","DOIUrl":"10.1016/j.cbpc.2025.110375","url":null,"abstract":"<div><div>The enantioselective toxicity of 3,4-methylenedioxypyrovalerone (MDPV) remains unexplored in freshwater organisms. This study investigated the effects of MDPV racemate and its enantiomers in <em>Daphnia magna</em> using two approaches: (<em>i</em>) an 8-day sub-chronic assay focused on early development stages; and (<em>ii</em>) the standard 21-day reproduction assay. The sub-chronic assay tested two environmental concentrations (0.10 and 1.0 μg L<sup>−1</sup>), for both racemate or individual enantiomers, and a higher sublethal concentration of 10 μg L<sup>−1</sup> for the racemate. Survival, morphophysiological, behavioural, reproductive, and biochemical responses were evaluated. The reproduction assay tested concentrations from 0.10 to 1.79 μg L<sup>−1</sup>, and evaluated survival, body size, and reproductive effects.</div><div>Sub-chronic exposure to 10 μg L<sup>−1</sup> (<em>R</em>,<em>S</em>)-MDPV decreased survival. MDPV racemate and its enantiomers changed morphophysiological parameters, except for body growth. In juveniles, the heart area increased with 0.10 μg L<sup>−1</sup> of (<em>R</em>)-MDPV whereas the heart size decreased with 0.10 and 1.0 μg L<sup>−1</sup> of (<em>S</em>)-MDPV. Enantioselective effects were observed in swimming behaviour: (<em>S</em>)-MDPV increased speed and (<em>R</em>)-MDPV increased active time. No effects were observed in biochemical (except in reactive oxygen species for (<em>S</em>)-MDPV) and early reproductive parameters. The reproduction assay revealed enhanced growth in all MDPV forms (except at 0.56 μg L<sup>−1</sup>). A nonsignificant reduction in survival to the higher concentrations of (<em>R</em>)-MDPV was accompanied by reduced reproductive output (at 1.00 and 1.79 μg L<sup>−1</sup>) and intrinsic rate of population increase (at 1.79 μg L<sup>−1</sup>). Our findings suggest that, in general, (<em>S</em>)-MDPV triggers more severe sub-chronic effects, whereas (<em>R</em>)-MDPV is associated with harmful effects for longer time exposure.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110375"},"PeriodicalIF":4.3,"publicationDate":"2025-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336519","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 : 2025-10-14DOI: 10.1016/j.cbpc.2025.110372
Bi-Xia Huang , Tao Zhang , Qing-Bin Dong , Peng-Xing Lin , Yi Zhou , Xin-Shuo Chen
Iron oxide nanoparticles (IONPs) are widely applied in biomedicine and industry, yet their impact on early nervous system formation is poorly understood. Here, we assessed IONP toxicity using cultured chick embryo fibroblasts, fertilized chicken eggs, and zebrafish embryos. In vitro exposure reduced fibroblast viability, elevated lipid peroxidation, and boosted reactive oxygen species levels. The injection of IONPs in chick embryo caused growth delays, smaller brain size, neuroepithelial thickening, and marked loss of neural stem and progenitor cells. At the molecular level, IONPs reduced PI3K and mTOR activity, increased apoptotic markers, and induced ferroptosis hallmarks, including mitochondrial membrane potential loss, ATP depletion, elevated mitochondrial ROS, and downregulation of xCT and GPX4. In zebrafish, IONPs triggered early developmental defects, microcephaly, and yolk malabsorption, alongside redox imbalance and dysregulation of ferroptosis-related genes. Together, these data show that IONPs impair neural proliferation, promote multiple forms of cell death, and disrupt redox equilibrium through ferroptotic mechanisms, highlighting the need for careful safety evaluation before their widespread use.
{"title":"Neurodevelopmental toxicity induced by iron oxide nanoparticles: Insights from chick and zebrafish embryonic models","authors":"Bi-Xia Huang , Tao Zhang , Qing-Bin Dong , Peng-Xing Lin , Yi Zhou , Xin-Shuo Chen","doi":"10.1016/j.cbpc.2025.110372","DOIUrl":"10.1016/j.cbpc.2025.110372","url":null,"abstract":"<div><div>Iron oxide nanoparticles (IONPs) are widely applied in biomedicine and industry, yet their impact on early nervous system formation is poorly understood. Here, we assessed IONP toxicity using cultured chick embryo fibroblasts, fertilized chicken eggs, and zebrafish embryos. In vitro exposure reduced fibroblast viability, elevated lipid peroxidation, and boosted reactive oxygen species levels. The injection of IONPs in chick embryo caused growth delays, smaller brain size, neuroepithelial thickening, and marked loss of neural stem and progenitor cells. At the molecular level, IONPs reduced PI3K and mTOR activity, increased apoptotic markers, and induced ferroptosis hallmarks, including mitochondrial membrane potential loss, ATP depletion, elevated mitochondrial ROS, and downregulation of xCT and GPX4. In zebrafish, IONPs triggered early developmental defects, microcephaly, and yolk malabsorption, alongside redox imbalance and dysregulation of ferroptosis-related genes. Together, these data show that IONPs impair neural proliferation, promote multiple forms of cell death, and disrupt redox equilibrium through ferroptotic mechanisms, highlighting the need for careful safety evaluation before their widespread use.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"299 ","pages":"Article 110372"},"PeriodicalIF":4.3,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298873","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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