Pub Date : 2025-11-19DOI: 10.1016/j.cbpc.2025.110399
Yahui Wu , Qing Huang
Astaxanthin (AST) as a natural carotenoid exhibits potent antioxidant and anti-inflammatory capacities. This work investigated AST’s protective effects against microcystin-LR (MC-LR) toxicity to zebrafish embryos. When the zebrafish embryos were exposed to a sublethal, environmentally relevant concentration of MC-LR (10 μg/L, approximately half of the LC50 value), AST (100 μg/L) could significantly reduce MC-LR-induced mortality by 39.8% and deformity rates by 60.0%. Furthermore, AST decreased ROS and MDA levels by 11.0% and 14.5%, respectively, and enhanced the activities of superoxide dismutase (SOD, 4.4-fold), catalase (CAT, 1.2-fold), and glutathione reductase (GR, 1.6-fold). It also ameliorated MC-LR-induced inflammatory responses, as evidenced by a 49.1% reduction in neutral red staining, a 42.0% to 42.9% improvement in host resistance, and a significant down-regulation of major cytokines (IL-1β, IL-6, IL-8, TNF-α) by 0.4 to 0.6-fold. Analysis of the transcriptome revealed that AST can inhibit the C-type lectin receptor signaling pathway and others to counteract the inflammatory and oxidative stress induced by MC-LR. Our findings confirm that AST neutralizes the toxicity of MC-LR through the mechanisms of antagonizing oxidative stress, exhibiting anti-inflammatory and immunomodulatory effects, which may pave the way for AST being used in aquaculture and environmental health.
{"title":"Astaxanthin mitigates the inflammatory toxicity of microcystin-LR on zebrafish embryos","authors":"Yahui Wu , Qing Huang","doi":"10.1016/j.cbpc.2025.110399","DOIUrl":"10.1016/j.cbpc.2025.110399","url":null,"abstract":"<div><div>Astaxanthin (AST) as a natural carotenoid exhibits potent antioxidant and anti-inflammatory capacities. This work investigated AST’s protective effects against microcystin-LR (MC-LR) toxicity to zebrafish embryos. When the zebrafish embryos were exposed to a sublethal, environmentally relevant concentration of MC-LR (10 μg/L, approximately half of the LC<sub>50</sub> value), AST (100 μg/L) could significantly reduce MC-LR-induced mortality by 39.8% and deformity rates by 60.0%. Furthermore, AST decreased ROS and MDA levels by 11.0% and 14.5%, respectively, and enhanced the activities of superoxide dismutase (SOD, 4.4-fold), catalase (CAT, 1.2-fold), and glutathione reductase (GR, 1.6-fold). It also ameliorated MC-LR-induced inflammatory responses, as evidenced by a 49.1% reduction in neutral red staining, a 42.0% to 42.9% improvement in host resistance, and a significant down-regulation of major cytokines (IL-1β, IL-6, IL-8, TNF-α) by 0.4 to 0.6-fold. Analysis of the transcriptome revealed that AST can inhibit the C-type lectin receptor signaling pathway and others to counteract the inflammatory and oxidative stress induced by MC-LR. Our findings confirm that AST neutralizes the toxicity of MC-LR through the mechanisms of antagonizing oxidative stress, exhibiting anti-inflammatory and immunomodulatory effects, which may pave the way for AST being used in aquaculture and environmental health.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110399"},"PeriodicalIF":4.3,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145573364","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}
Di-ethylhexyl phthalate (DEHP) is an endocrine disruptor with established neurotoxic as well as potential neurodegenerative effects. The myelin sheath plays a crucial role in maintaining the health of the nervous system, whereas demyelination contributes to the onset of brain diseases. This study investigated the effect of DEHP on the neurological development with special reference to endoplasmic reticulum (ER) stress, inflammation, and concurrently with demyelination and cellular apoptotic development in zebrafish larvae. Results indicated that DEHP exposure can lead to demyelination through ER stress and inflammation, as evident from the decreased expression of myelin basic protein (Mbp) in both the brain and spinal cord of zebrafish larvae analyzed through immunofluorescent assay. The mRNA expression of axon marker nfl significantly increased, while tuba1a was decreased with DEHP exposure. Western blotting analysis revealed that ER stress markers such as phosphorylated inositol-requiring enzyme 1 alpha (p-Ire1α), activating transcription factor 4 (Atf4), binding immunoglobulin protein (Bip), phosphorylated e-IF2 alpha (p-eIF2α), CCAAT/enhancer-binding protein homologous protein (Chop), and inflammatory markers (nuclear factor kappa B subunit p65; Nf-κb p65), ionized calcium-binding adaptor molecule 1 (Iba1), and glial fibrillary acid protein (Gfap), were significantly upregulated on exposure to DEHP. Scototaxis, a behavioral assay, showed an altered anxiety-like behaviour in DEHP-treated larvae. Oxidative stress markers, such as superoxide dismutase (SOD), catalase, and monoamine oxidase (MAO) were also elevated. Apoptotic cells were observed in DEHP-treated zebrafish larvae in acridine orange staining. Overall, the DEHP exposure to zebrafish larvae caused myelin sheath degeneration and axonal dysfunction due to the generation of ER stress and inflammation.
{"title":"Concurrent endoplasmic reticulum stress and demyelination in DEHP-exposed zebrafish larvae at the early developmental stages","authors":"Garima Jindal , Anuradha Mangla , Mehjbeen Javed , Mohd. Anas Saifi , Iqra Mazahir , Padmshree Mudgal , Shiekh Raisuddin","doi":"10.1016/j.cbpc.2025.110394","DOIUrl":"10.1016/j.cbpc.2025.110394","url":null,"abstract":"<div><div>Di-ethylhexyl phthalate (DEHP) is an endocrine disruptor with established neurotoxic as well as potential neurodegenerative effects. The myelin sheath plays a crucial role in maintaining the health of the nervous system, whereas demyelination contributes to the onset of brain diseases. This study investigated the effect of DEHP on the neurological development with special reference to endoplasmic reticulum (ER) stress, inflammation, and concurrently with demyelination and cellular apoptotic development in zebrafish larvae. Results indicated that DEHP exposure can lead to demyelination through ER stress and inflammation, as evident from the decreased expression of myelin basic protein (Mbp) in both the brain and spinal cord of zebrafish larvae analyzed through immunofluorescent assay. The mRNA expression of axon marker <em>nfl</em> significantly increased, while <em>tuba1a</em> was decreased with DEHP exposure. Western blotting analysis revealed that ER stress markers such as phosphorylated inositol-requiring enzyme 1 alpha (p-Ire1α), activating transcription factor 4 (Atf4), binding immunoglobulin protein (Bip), phosphorylated e-IF2 alpha (p-eIF2α), CCAAT/enhancer-binding protein homologous protein (Chop), and inflammatory markers (nuclear factor kappa B subunit p65; Nf-κb p65), ionized calcium-binding adaptor molecule 1 (Iba1), and glial fibrillary acid protein (Gfap), were significantly upregulated on exposure to DEHP. Scototaxis, a behavioral assay, showed an altered anxiety-like behaviour in DEHP-treated larvae. Oxidative stress markers, such as superoxide dismutase (SOD), catalase, and monoamine oxidase (MAO) were also elevated. Apoptotic cells were observed in DEHP-treated zebrafish larvae in acridine orange staining. Overall, the DEHP exposure to zebrafish larvae caused myelin sheath degeneration and axonal dysfunction due to the generation of ER stress and inflammation.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"301 ","pages":"Article 110394"},"PeriodicalIF":4.3,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145563064","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 : 2025-11-14DOI: 10.1016/j.cbpc.2025.110389
Luana Granada , Inês F.C. Morão , Marco F.L. Lemos , Peter Bossier , Sara C. Novais
The rotifer Brachionus sp. is of great importance for aquaculture, as the reproduction cycle under rearing conditions of many economically important species larvae depends on the use of rotifers as first live feed. Establishing a protocol that results in an improved tolerance of rotifers to environmental stressors will allow for a more stable rotifer production. The exposure to non-lethal heat shocks (NLHS) already proved to enhance the tolerance, not only to heat stress, but also to other stressors in several aquatic species, by activating the heat shock response and epigenetic mechanisms. This study aimed to determine the potential of a single NLHS to induce tolerance to different abiotic stressors in two strains of B. koreanus (MRS10 and IBA3) and to evaluate possible molecular mechanisms involved in the achievement of increased tolerance to hydrogen peroxide induced by NLHS. Cross-tolerance was achieved for both strains, namely to high salinity, cadmium chloride, and hydrogen peroxide. Scale-up tests resulted in increased tolerance to hydrogen peroxide only for MRS10. During the exposure to this substance, heat-shocked MRS10 rotifers showed an up-regulation of genes related to oxidative stress response and histone modifications, increased production of HSP70, and higher levels of total acetylation of histone H3. A single NLHS proved to induce epigenetic effects when rotifers were exposed to other stressor later in life. However, further studies should elucidate if the NLHS conditions used in this study can yield a persistent outcome, allowing the establishment of tolerant rotifer strain lines and, consequently, a more stable production.
{"title":"Non-lethal heat shock induces cross-tolerance to different stressors in two strains of Brachionus koreanus (Rotifera: Monogononta): Mechanisms of increased tolerance to hydrogen peroxide","authors":"Luana Granada , Inês F.C. Morão , Marco F.L. Lemos , Peter Bossier , Sara C. Novais","doi":"10.1016/j.cbpc.2025.110389","DOIUrl":"10.1016/j.cbpc.2025.110389","url":null,"abstract":"<div><div>The rotifer <em>Brachionus</em> sp. is of great importance for aquaculture, as the reproduction cycle under rearing conditions of many economically important species larvae depends on the use of rotifers as first live feed. Establishing a protocol that results in an improved tolerance of rotifers to environmental stressors will allow for a more stable rotifer production. The exposure to non-lethal heat shocks (NLHS) already proved to enhance the tolerance, not only to heat stress, but also to other stressors in several aquatic species, by activating the heat shock response and epigenetic mechanisms. This study aimed to determine the potential of a single NLHS to induce tolerance to different abiotic stressors in two strains of <em>B. koreanus</em> (MRS10 and IBA3) and to evaluate possible molecular mechanisms involved in the achievement of increased tolerance to hydrogen peroxide induced by NLHS. Cross-tolerance was achieved for both strains, namely to high salinity, cadmium chloride, and hydrogen peroxide. Scale-up tests resulted in increased tolerance to hydrogen peroxide only for MRS10. During the exposure to this substance, heat-shocked MRS10 rotifers showed an up-regulation of genes related to oxidative stress response and histone modifications, increased production of HSP70, and higher levels of total acetylation of histone H3. A single NLHS proved to induce epigenetic effects when rotifers were exposed to other stressor later in life. However, further studies should elucidate if the NLHS conditions used in this study can yield a persistent outcome, allowing the establishment of tolerant rotifer strain lines and, consequently, a more stable production.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110389"},"PeriodicalIF":4.3,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534408","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 : 2025-11-13DOI: 10.1016/j.cbpc.2025.110390
Anqi Liu , Kun Chen , Xuchun Qiu , Yuki Takai , Yohei Shimasaki , Yuji Oshima
Amitriptyline (AMI), a commonly used tricyclic antidepressant, has been identified as a significant pharmaceutical contaminant in aquatic environments. Although parental exposure of zebrafish to AMI has been found to induce changes in the development, behavior, and gene expression of their F1 offspring, it is unclear whether such adverse effects will be further extended to subsequent generations. In the current study, we explored the effects of ancestral exposure to AMI at environmentally relevant concentrations (0 and 0.8 μg/L) on the early life stages of zebrafish F2 offspring. The results showed that ancestral exposure to AMI had no significant effect on the survival and development of the zebrafish F2 offspring. However, significant hyperactivity was observed in the F2 larvae in the ancestral AMI exposure group during the dark periods of a light-dark locomotion assay. Transcription analysis revealed that ancestral exposure to AMI significantly disrupted pathways associated with xenobiotic biodegradation and metabolism, as well as the metabolism of cofactors and vitamins. Furthermore, ancestral exposure to AMI significantly decreased the level of cytochrome P450 and the activity of glutathione S-transferase within the F2 larvae, which are critical enzymes involved in xenobiotic metabolism. These findings provide valuable insights into the multigenerational effects of AMI exposure in zebrafish, emphasizing the importance of assessing the risks posed by such pollutants to fish populations.
{"title":"Ancestral exposure to amitriptyline disrupts the behavior and gene expression in zebrafish F2 offspring","authors":"Anqi Liu , Kun Chen , Xuchun Qiu , Yuki Takai , Yohei Shimasaki , Yuji Oshima","doi":"10.1016/j.cbpc.2025.110390","DOIUrl":"10.1016/j.cbpc.2025.110390","url":null,"abstract":"<div><div>Amitriptyline (AMI), a commonly used tricyclic antidepressant, has been identified as a significant pharmaceutical contaminant in aquatic environments. Although parental exposure of zebrafish to AMI has been found to induce changes in the development, behavior, and gene expression of their F1 offspring, it is unclear whether such adverse effects will be further extended to subsequent generations. In the current study, we explored the effects of ancestral exposure to AMI at environmentally relevant concentrations (0 and 0.8 μg/L) on the early life stages of zebrafish F2 offspring. The results showed that ancestral exposure to AMI had no significant effect on the survival and development of the zebrafish F2 offspring. However, significant hyperactivity was observed in the F2 larvae in the ancestral AMI exposure group during the dark periods of a light-dark locomotion assay. Transcription analysis revealed that ancestral exposure to AMI significantly disrupted pathways associated with xenobiotic biodegradation and metabolism, as well as the metabolism of cofactors and vitamins. Furthermore, ancestral exposure to AMI significantly decreased the level of cytochrome P450 and the activity of glutathione S-transferase within the F2 larvae, which are critical enzymes involved in xenobiotic metabolism. These findings provide valuable insights into the multigenerational effects of AMI exposure in zebrafish, emphasizing the importance of assessing the risks posed by such pollutants to fish populations.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110390"},"PeriodicalIF":4.3,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530475","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 : 2025-11-13DOI: 10.1016/j.cbpc.2025.110392
Davide Asnicar , Benjamin de Jourdan
Azamethiphos and hydrogen peroxide are active ingredients (AI) of formulations used as water-bath pesticides in Atlantic salmon aquaculture to remove ectoparasitic copepods. Despite their long-term use, unknowns and concerns are still present, particularly regarding the toxicity towards non-target commercially and ecologically important species in Atlantic Canada, and potential differences in toxicity between the AI and the formulated product.
Here, we tested the acute effects of azamethiphos and hydrogen peroxide on five marine species. Hazard data (half maximal effective and lethal concentrations, respectively EC50 and LC50) were determined for 10 endpoints, assessed at various timepoints, during the exposure of Stage I larval American lobster Homarus americanus, green sea urchin Strongylocentrotus droebachiensis gametes, haemocytes and adults of blue mussel Mytilus edulis, common periwinkle snail Littorina littorea, and copepod Acartia tonsa.
To investigate whether formulations had the same effect as the AI, for azamethiphos, both the AI and the formulation (Salmosan® Vet) were tested. For hydrogen peroxide, potential differences in the toxicity of three formulations (purchased solutions 50 %, 35 %, and 3 %) were compared.
Results suggest no differences between the azamethiphos and Salmosan® Vet, with similar L/EC50 values. Little differences were found among the three hydrogen peroxide formulations. For azamethiphos, the most sensitive species was the American lobster, followed by sea urchin, whereas for hydrogen peroxide, sea urchin was the most sensitive, followed by A. tonsa. L. littorea was the least sensitive species tested. Overall, results showed that all the endpoints were greater than the Environmental Quality Standard previously determined for the two compounds.
{"title":"Anti-sea lice products azamethiphos and hydrogen peroxide effects on five coastal marine organisms","authors":"Davide Asnicar , Benjamin de Jourdan","doi":"10.1016/j.cbpc.2025.110392","DOIUrl":"10.1016/j.cbpc.2025.110392","url":null,"abstract":"<div><div>Azamethiphos and hydrogen peroxide are active ingredients (AI) of formulations used as water-bath pesticides in Atlantic salmon aquaculture to remove ectoparasitic copepods. Despite their long-term use, unknowns and concerns are still present, particularly regarding the toxicity towards non-target commercially and ecologically important species in Atlantic Canada, and potential differences in toxicity between the AI and the formulated product.</div><div>Here, we tested the acute effects of azamethiphos and hydrogen peroxide on five marine species. Hazard data (half maximal effective and lethal concentrations, respectively EC50 and LC50) were determined for 10 endpoints, assessed at various timepoints, during the exposure of Stage I larval American lobster <em>Homarus americanus</em>, green sea urchin <em>Strongylocentrotus droebachiensis</em> gametes, haemocytes and adults of blue mussel <em>Mytilus edulis</em>, common periwinkle snail <em>Littorina littorea</em>, and copepod <em>Acartia tonsa</em>.</div><div>To investigate whether formulations had the same effect as the AI, for azamethiphos, both the AI and the formulation (Salmosan® Vet) were tested. For hydrogen peroxide, potential differences in the toxicity of three formulations (purchased solutions 50 %, 35 %, and 3 %) were compared.</div><div>Results suggest no differences between the azamethiphos and Salmosan® Vet, with similar L/EC50 values. Little differences were found among the three hydrogen peroxide formulations. For azamethiphos, the most sensitive species was the American lobster, followed by sea urchin, whereas for hydrogen peroxide, sea urchin was the most sensitive, followed by <em>A. tonsa</em>. <em>L. littorea</em> was the least sensitive species tested. Overall, results showed that all the endpoints were greater than the Environmental Quality Standard previously determined for the two compounds.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110392"},"PeriodicalIF":4.3,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530464","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}
Cyanotoxins are one of the major threats to aquatic ecosystems due to their diverse toxic effects on aquatic organisms. Cylindrospermopsin is a globally reported freshwater cyanotoxin that exhibits hepatotoxic, cytotoxic, immunotoxic, and neurotoxic effects in teleosts; however, its harmful effects on reproductive health remain less explored. This study investigates the impacts of cylindrospermopsin on the reproductive endocrine and paracrine system, emphasising the HPGL axis of female zebrafish. Following 14 days of in-vivo cylindrospermopsin exposure, decreased gonadosomatic and hepatosomatic indices were observed. The number of fully grown (vitellogenic and post-vitellogenic) oocytes was decreased in treated groups, signifying oocyte growth impairments. Disruption of serum gonadotropin levels (FSH and LH) and steroid (17β-estradiol/testosterone) ratio was also observed, indicating the endocrine-disrupting effects of cylindrospermopsin. Following in-vitro cylindrospermopsin exposure for 8 h, increased GVBD was observed, representing early oocyte maturation. Besides endocrine regulation, stress-induced immune-activation of paracrine factors also regulates oocyte maturation. Subsequently, elevated lipid peroxidation and antioxidant activity were observed in the ovary of exposed groups, which disrupts the expression of different steroidogenesis and antioxidant marker genes. This is followed by upregulated expression of paracrine factors: nf-κb, tnf-α and il-1β genes in the ovary, which further activates the apoptotic cascade in the CYN-treated oocytes by upregulating p53, bax, casp3 and suppressing bcl2 gene expression. This revealed that cylindrospermopsin is an effective endocrine disruptor that induces reproductive toxicity by promoting oxidative stress and inducing early oocyte maturation by immune-activation of the NF-κB/TNF-α pathway, emphasising the importance of deciphering its ecotoxicological risk.
{"title":"Chronic cylindrospermopsin exposure impairs oocyte growth and maturation by stress-induced endocrine disruption and immune activation of NF-κB/TNF-α pathway in female zebrafish","authors":"Chayan Biswas, Madhuchhanda Adhikari, Kousik Pramanick","doi":"10.1016/j.cbpc.2025.110387","DOIUrl":"10.1016/j.cbpc.2025.110387","url":null,"abstract":"<div><div>Cyanotoxins are one of the major threats to aquatic ecosystems due to their diverse toxic effects on aquatic organisms. Cylindrospermopsin is a globally reported freshwater cyanotoxin that exhibits hepatotoxic, cytotoxic, immunotoxic, and neurotoxic effects in teleosts; however, its harmful effects on reproductive health remain less explored. This study investigates the impacts of cylindrospermopsin on the reproductive endocrine and paracrine system, emphasising the HPGL axis of female zebrafish. Following 14 days of <em>in-vivo</em> cylindrospermopsin exposure, decreased gonadosomatic and hepatosomatic indices were observed. The number of fully grown (vitellogenic and post-vitellogenic) oocytes was decreased in treated groups, signifying oocyte growth impairments. Disruption of serum gonadotropin levels (FSH and LH) and steroid (17β-estradiol/testosterone) ratio was also observed, indicating the endocrine-disrupting effects of cylindrospermopsin. Following <em>in-vitro</em> cylindrospermopsin exposure for 8 h, increased GVBD was observed, representing early oocyte maturation. Besides endocrine regulation, stress-induced immune-activation of paracrine factors also regulates oocyte maturation. Subsequently, elevated lipid peroxidation and antioxidant activity were observed in the ovary of exposed groups, which disrupts the expression of different steroidogenesis and antioxidant marker genes. This is followed by upregulated expression of paracrine factors: <em>nf-κb</em>, <em>tnf-α</em> and <em>il-1β</em> genes in the ovary, which further activates the apoptotic cascade in the CYN-treated oocytes by upregulating <em>p53, bax, casp3</em> and suppressing <em>bcl2</em> gene expression. This revealed that cylindrospermopsin is an effective endocrine disruptor that induces reproductive toxicity by promoting oxidative stress and inducing early oocyte maturation by immune-activation of the NF-κB/TNF-α pathway, emphasising the importance of deciphering its ecotoxicological risk.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"300 ","pages":"Article 110387"},"PeriodicalIF":4.3,"publicationDate":"2025-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145480561","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 : 2025-11-07DOI: 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}
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