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

Mechanistic understanding of the toxic effects of tri-n-butyl phosphate (TnBP) and tricresyl phosphate (TCP) to Escherichia coli: Evidence from alterations in biomarker expression and perturbations of the metabolic network

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-04-24 DOI: 10.1016/j.cbpc.2025.110211

Xiaolong Yu , Runlin Yao , Ruipu Yao , Xu Jin , Jiahui Huang , Qianwei Liang , Ling N. Jin , Jianteng Sun

Tri-n-butyl phosphate (TnBP) and tricresyl phosphate (TCP), emerging flame retardants and plasticizers, have garnered increasing attention due to their potential risks to ecosystem. A few researches regarding the toxicological mechanisms of TnBP and TCP had been performed, while molecular-level toxic effects of them and metabolic response using microbial models are the lack of relevant investigation. Thus, we investigated the cytotoxicity, oxidative stress response, and metabolic response in E. coli exposed to TnBP and TCP. Exposure to them significantly increased the activities of antioxidant enzymes, indicating activation of the antioxidant defense system. Excessive accumulation of reactive oxygen species (ROS) triggered various biological events, including a reduction in membrane potential (MP), decrease of adenosine triphosphatase (ATPase) activity, and increased malondialdehyde (MDA) content. These findings suggested that oxidative damage compromised membrane proteins function, membrane stability, and intracellular homeostasis. GC–MS and LC-MS-based metabolomics analyses revealed that TnBP and TCP strongly disrupted multiple metabolic pathways, including carbohydrate metabolism, nucleotide metabolism, lipid metabolism, beta-alanine metabolism, pyruvate metabolism and oxidative phosphorylation. These disruptions highlighted the inhibitory effects on molecular functions and metabolic processes. Notably, lipids biomarkers e.g., PC(11:0/16:0), PA(17:1(9Z)/18:2(9Z,12Z)), PE(17:0/14:1(9Z)), and LysoPE(0:0/18:1(11Z)) were significantly altered, verifying that the regulation of lipid-associated metabolite synthesis plays a protective role in maintaining cellular membrane function. In summary, this study enhances our understanding of TnBP and TCP toxicity in E. coli, providing novel insights into their toxicological mechanisms at molecular and network levels. These findings underscore the ecological risks posed by organophosphate flame retardants in aquatic ecosystem.

{"title":"Mechanistic understanding of the toxic effects of tri-n-butyl phosphate (TnBP) and tricresyl phosphate (TCP) to Escherichia coli: Evidence from alterations in biomarker expression and perturbations of the metabolic network","authors":"Xiaolong Yu , Runlin Yao , Ruipu Yao , Xu Jin , Jiahui Huang , Qianwei Liang , Ling N. Jin , Jianteng Sun","doi":"10.1016/j.cbpc.2025.110211","DOIUrl":"10.1016/j.cbpc.2025.110211","url":null,"abstract":"<div><div>Tri-n-butyl phosphate (TnBP) and tricresyl phosphate (TCP), emerging flame retardants and plasticizers, have garnered increasing attention due to their potential risks to ecosystem. A few researches regarding the toxicological mechanisms of TnBP and TCP had been performed, while molecular-level toxic effects of them and metabolic response using microbial models are the lack of relevant investigation. Thus, we investigated the cytotoxicity, oxidative stress response, and metabolic response in <em>E. coli</em> exposed to TnBP and TCP. Exposure to them significantly increased the activities of antioxidant enzymes, indicating activation of the antioxidant defense system. Excessive accumulation of reactive oxygen species (ROS) triggered various biological events, including a reduction in membrane potential (MP), decrease of adenosine triphosphatase (ATPase) activity, and increased malondialdehyde (MDA) content. These findings suggested that oxidative damage compromised membrane proteins function, membrane stability, and intracellular homeostasis. GC–MS and LC-MS-based metabolomics analyses revealed that TnBP and TCP strongly disrupted multiple metabolic pathways, including carbohydrate metabolism, nucleotide metabolism, lipid metabolism, beta-alanine metabolism, pyruvate metabolism and oxidative phosphorylation. These disruptions highlighted the inhibitory effects on molecular functions and metabolic processes. Notably, lipids biomarkers e.g., PC(11:0/16:0), PA(17:1(9Z)/18:2(9Z,12Z)), PE(17:0/14:1(9Z)), and LysoPE(0:0/18:1(11Z)) were significantly altered, verifying that the regulation of lipid-associated metabolite synthesis plays a protective role in maintaining cellular membrane function. In summary, this study enhances our understanding of TnBP and TCP toxicity in <em>E. coli</em>, providing novel insights into their toxicological mechanisms at molecular and network levels. These findings underscore the ecological risks posed by organophosphate flame retardants in aquatic ecosystem.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"295 ","pages":"Article 110211"},"PeriodicalIF":3.9,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143873779","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}

引用次数: 0

Morphological, biochemical, and histological alterations in juvenile giant freshwater prawns (Macrobrachium rosenbergii) exposed to sub-lethal concentrations of 2,4-D dimethylammonium

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-04-23 DOI: 10.1016/j.cbpc.2025.110212

Sugunya Kumla , Boonthiwa Chartchumni , Phochit Nanthanawat , Jakkaphun Nanuam , Sawipa Ruttanakorn , Panomsak Meemon , Chutima Thanomsit

The widespread use of herbicides, such as 2,4-D dimethylammonium, poses significant risks to aquatic ecosystems. This study assessed the toxicological effects of 2,4-D dimethylammonium on juvenile giant freshwater prawns (Macrobrachium rosenbergii) by assessing mortality, total hemocyte count (THC), acetylcholinesterase (AChE) expression, and tissue integrity using optical coherence tomography (OCT) and histological analysis. Prawns were exposed to 0, 250, 300, 350, 400, and 450 μL/L of 2,4-D dimethylammonium for 24, 48, 72, and 96 h, and both LC₅₀ values and sub-lethal effects were examined. Acute toxicity tests revealed dose- and time-dependent mortality, with declining LC₅₀ values over 24 to 96 h. THC levels significantly decreased (p < 0.05) at higher concentrations, with prawns exposed to 450 μL/L showing a 35 % reduction at 96 h. Western blot analysis revealed AChE suppression, with expression becoming faintly detectable at 72 h and undetectable at 96 h at 450 μL/L. OCT analysis showed tissue disorganization, increased light scattering, and structural degradation, aligning with histological findings of hepatopancreas and muscle deterioration in high-exposure groups. The study highlights the environmental risks of 2,4-D dimethylammonium contamination and supports OCT as a non-invasive tool for assessing pesticide toxicity in aquatic organisms.

{"title":"Morphological, biochemical, and histological alterations in juvenile giant freshwater prawns (Macrobrachium rosenbergii) exposed to sub-lethal concentrations of 2,4-D dimethylammonium","authors":"Sugunya Kumla , Boonthiwa Chartchumni , Phochit Nanthanawat , Jakkaphun Nanuam , Sawipa Ruttanakorn , Panomsak Meemon , Chutima Thanomsit","doi":"10.1016/j.cbpc.2025.110212","DOIUrl":"10.1016/j.cbpc.2025.110212","url":null,"abstract":"<div><div>The widespread use of herbicides, such as 2,4-D dimethylammonium, poses significant risks to aquatic ecosystems. This study assessed the toxicological effects of 2,4-D dimethylammonium on juvenile giant freshwater prawns (<em>Macrobrachium rosenbergii</em>) by assessing mortality, total hemocyte count (THC), acetylcholinesterase (AChE) expression, and tissue integrity using optical coherence tomography (OCT) and histological analysis. Prawns were exposed to 0, 250, 300, 350, 400, and 450 μL/L of 2,4-D dimethylammonium for 24, 48, 72, and 96 h, and both LC<sub>50</sub> values and sub-lethal effects were examined. Acute toxicity tests revealed dose- and time-dependent mortality, with declining LC<sub>50</sub> values over 24 to 96 h. THC levels significantly decreased (<em>p</em> < 0.05) at higher concentrations, with prawns exposed to 450 μL/L showing a 35 % reduction at 96 h. Western blot analysis revealed AChE suppression, with expression becoming faintly detectable at 72 h and undetectable at 96 h at 450 μL/L. OCT analysis showed tissue disorganization, increased light scattering, and structural degradation, aligning with histological findings of hepatopancreas and muscle deterioration in high-exposure groups. The study highlights the environmental risks of 2,4-D dimethylammonium contamination and supports OCT as a non-invasive tool for assessing pesticide toxicity in aquatic organisms.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"295 ","pages":"Article 110212"},"PeriodicalIF":3.9,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143868866","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}

引用次数: 0

Neurotoxicity induced by difenoconazole in zebrafish larvae via activating oxidative stress and the protective role of resveratrol

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-04-15 DOI: 10.1016/j.cbpc.2025.110208

Chunlan Liu , Jiansheng Zhu , Renfei Zhu , Yifei Yin

Difenoconazole (DIF) is a typical triazole fungicide detected in the aquatic ecosystem and organisms. However, the neurotoxic effects of DIF remain largely unknown. This study aimed to investigate the neurotoxicity of DIF in zebrafish and the underlying neuroprotective properties of resveratrol (RES, an antioxidant polyphenol). Zebrafish embryos/larvae were treated with 0.6 and 1.2 mg/L DIF from 4 to 96 h post fertilization (hpf) and neurodevelopment was systematically assessed. DIF induced developmental toxicity and aberrant neurobehaviors, including decreased movement time, swimming distance and clockwise rotation times. DIF suppressed the neurogenesis of the central nervous system (CNS) in HuC:egfp transgenic zebrafish and the length of motor neuron axon in hb9:egfp transgenic zebrafish. DIF inhibited cholinesterase activities and downregulated neurodevelopment related genes. DIF also increased oxidative stress via excessive production of reactive oxygen species and decreased activities of antioxidant enzymes, subsequently triggering neuronal apoptosis in the brain. RES partially reinstated DIF-induced neurotoxicity and developmental toxicity by inhibiting excessive oxidative stress and apoptosis, suggesting the involvement of oxidative stress in DIF-induced neurotoxicity. Overall, this study identified the potential mechanisms underlying DIF-induced neurotoxicity and suggested RES as a promising therapeutic strategy.

{"title":"Neurotoxicity induced by difenoconazole in zebrafish larvae via activating oxidative stress and the protective role of resveratrol","authors":"Chunlan Liu , Jiansheng Zhu , Renfei Zhu , Yifei Yin","doi":"10.1016/j.cbpc.2025.110208","DOIUrl":"10.1016/j.cbpc.2025.110208","url":null,"abstract":"<div><div>Difenoconazole (DIF) is a typical triazole fungicide detected in the aquatic ecosystem and organisms. However, the neurotoxic effects of DIF remain largely unknown. This study aimed to investigate the neurotoxicity of DIF in zebrafish and the underlying neuroprotective properties of resveratrol (RES, an antioxidant polyphenol). Zebrafish embryos/larvae were treated with 0.6 and 1.2 mg/L DIF from 4 to 96 h post fertilization (hpf) and neurodevelopment was systematically assessed. DIF induced developmental toxicity and aberrant neurobehaviors, including decreased movement time, swimming distance and clockwise rotation times. DIF suppressed the neurogenesis of the central nervous system (CNS) in <em>HuC:egfp</em> transgenic zebrafish and the length of motor neuron axon in <em>hb9:egfp</em> transgenic zebrafish. DIF inhibited cholinesterase activities and downregulated neurodevelopment related genes. DIF also increased oxidative stress via excessive production of reactive oxygen species and decreased activities of antioxidant enzymes, subsequently triggering neuronal apoptosis in the brain. RES partially reinstated DIF-induced neurotoxicity and developmental toxicity by inhibiting excessive oxidative stress and apoptosis, suggesting the involvement of oxidative stress in DIF-induced neurotoxicity. Overall, this study identified the potential mechanisms underlying DIF-induced neurotoxicity and suggested RES as a promising therapeutic strategy.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"295 ","pages":"Article 110208"},"PeriodicalIF":3.9,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860280","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}

引用次数: 0

Assessing neonicotinoid pollution in aquatic ecosystems: A systematic review and bibliometric-content analysis 评估水生生态系统中的新烟碱污染：系统综述和文献计量学内容分析

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-04-15 DOI: 10.1016/j.cbpc.2025.110207

Qinglin Yang , Xiaoqi Tang , Yuzhuo He , Xianyun Wu , Xiaobo Yu , Yanhong Li , Zhengli Wu

The widespread use and distribution of neonicotinoids (NNIs) have led to their significant accumulation in aquatic ecosystems, posing serious ecological risks to non-target species and the human food chain. This review employed bibliometric analysis to examine global research from 2013 to 2023, highlighting key trends, advancements, and research priorities. Moreover, we summarized the global distribution of NNIs in various aquatic environments through content analysis and assessed their ecotoxicological effects under controlled laboratory conditions. Our findings indicate a growing global concern about NNIs in aquatic systems, with research efforts primarily concentrated in regions most affected by their use. The presence of NNIs across different water bodies highlights widespread contamination, with China facing particularly severe pollution. However, research on the safety of NNIs in aquatic environments remains insufficient. Future studies should focus on monitoring chronic NNIs exposure and its long-term ecological impacts through field research. Moreover, developing microbial formulations, integrating phytoremediation, and combining multiple technologies for synergy are crucial for developing sustainable strategies to mitigate NNIs pollution, protect human health, and preserve aquatic ecosystems.

{"title":"Assessing neonicotinoid pollution in aquatic ecosystems: A systematic review and bibliometric-content analysis","authors":"Qinglin Yang , Xiaoqi Tang , Yuzhuo He , Xianyun Wu , Xiaobo Yu , Yanhong Li , Zhengli Wu","doi":"10.1016/j.cbpc.2025.110207","DOIUrl":"10.1016/j.cbpc.2025.110207","url":null,"abstract":"<div><div>The widespread use and distribution of neonicotinoids (NNIs) have led to their significant accumulation in aquatic ecosystems, posing serious ecological risks to non-target species and the human food chain. This review employed bibliometric analysis to examine global research from 2013 to 2023, highlighting key trends, advancements, and research priorities. Moreover, we summarized the global distribution of NNIs in various aquatic environments through content analysis and assessed their ecotoxicological effects under controlled laboratory conditions. Our findings indicate a growing global concern about NNIs in aquatic systems, with research efforts primarily concentrated in regions most affected by their use. The presence of NNIs across different water bodies highlights widespread contamination, with China facing particularly severe pollution. However, research on the safety of NNIs in aquatic environments remains insufficient. Future studies should focus on monitoring chronic NNIs exposure and its long-term ecological impacts through field research. Moreover, developing microbial formulations, integrating phytoremediation, and combining multiple technologies for synergy are crucial for developing sustainable strategies to mitigate NNIs pollution, protect human health, and preserve aquatic ecosystems.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110207"},"PeriodicalIF":3.9,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848336","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}

引用次数: 0

Dinotefuran exposure induces immunotoxicity in zebrafish embryos 接触克百威可诱导斑马鱼胚胎产生免疫毒性

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-04-11 DOI: 10.1016/j.cbpc.2025.110206

Yunshuo Chen , Yacan Gong , Dan Li , Weiwei Feng , Yao Chen , Ting Zhao , Liuqing Yang , Guanghua Mao , Xiangyang Wu

As a typical neonicotinoid insecticide, dinotefuran (DIN) has immunotoxicity, but its immunotoxicity effects on aquatic organisms and its molecular mechanisms are not known. In this study, zebrafish embryos were used as model to reveal its immunotoxicity and its mechanism from the perspective of inflammatory response. Zebrafish larvae were exposed to DIN at environmentally relevant concentrations (0, 2, 200, and 2000 mg/L) for 120 h, followed by comprehensive analyses of immune cell populations, immune marker activities, oxidative stress levels, and gene expression profiles. The results showed that the number of neutrophils and macrophages, two types of innate immune cells, was significantly reduced, and the activities of the immune markers, lysozyme (LYS), immunoglobulin M (IgM), and complement protein C3, were significantly inhibited. The level of oxidative stress in zebrafish larvae was significantly elevated and antioxidant enzyme activities were markedly inhibited in a dose-dependent manner after exposure to DIN. In this case, pro-inflammatory cytokines such as TNF-α, IL-6 and IL-1β were also abnormally expressed, and the expression levels of the genes related to the NF-κB pathway and the JNK-STAT pathway, tlr4a, myd88, nf-κb p65, jak1, jak2, and stat3, were elevated. The expression levels of genes related to the antioxidant signaling pathway Nrf2-keap1 signaling pathway were suppressed. Taken together, our results suggest that DIN exposure causes damage to the immune system of zebrafish embryos-larvae, generating oxidative stress and inflammatory responses that lead to immunotoxicity.

{"title":"Dinotefuran exposure induces immunotoxicity in zebrafish embryos","authors":"Yunshuo Chen , Yacan Gong , Dan Li , Weiwei Feng , Yao Chen , Ting Zhao , Liuqing Yang , Guanghua Mao , Xiangyang Wu","doi":"10.1016/j.cbpc.2025.110206","DOIUrl":"10.1016/j.cbpc.2025.110206","url":null,"abstract":"<div><div>As a typical neonicotinoid insecticide, dinotefuran (DIN) has immunotoxicity, but its immunotoxicity effects on aquatic organisms and its molecular mechanisms are not known. In this study, zebrafish embryos were used as model to reveal its immunotoxicity and its mechanism from the perspective of inflammatory response. Zebrafish larvae were exposed to DIN at environmentally relevant concentrations (0, 2, 200, and 2000 mg/L) for 120 h, followed by comprehensive analyses of immune cell populations, immune marker activities, oxidative stress levels, and gene expression profiles. The results showed that the number of neutrophils and macrophages, two types of innate immune cells, was significantly reduced, and the activities of the immune markers, lysozyme (LYS), immunoglobulin M (IgM), and complement protein C3, were significantly inhibited. The level of oxidative stress in zebrafish larvae was significantly elevated and antioxidant enzyme activities were markedly inhibited in a dose-dependent manner after exposure to DIN. In this case, pro-inflammatory cytokines such as TNF-α, IL-6 and IL-1β were also abnormally expressed, and the expression levels of the genes related to the NF-κB pathway and the JNK-STAT pathway, <em>tlr4a, myd88, nf-κb p65, jak1, jak2</em>, and <em>stat3</em>, were elevated. The expression levels of genes related to the antioxidant signaling pathway Nrf2-keap1 signaling pathway were suppressed. Taken together, our results suggest that DIN exposure causes damage to the immune system of zebrafish embryos-larvae, generating oxidative stress and inflammatory responses that lead to immunotoxicity.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"295 ","pages":"Article 110206"},"PeriodicalIF":3.9,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855945","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}

引用次数: 0

Oxidative and metabolic responses in Crassostrea gasar under combined stressors of elevated temperature and microplastic exposure

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-04-11 DOI: 10.1016/j.cbpc.2025.110204

Júlia Ferreiro , Maidana da Silva Idiarte , Júlia Oliveira , Suamy Cruz , Gabriela Soares Correa , Larissa Müller , Juliane Ventura-Lima

This study investigates two critical threats to species such as the oyster Crassostrea gasar: elevated temperatures and microplastic (MP) contamination. To assess the combined effects of MP and temperature, oysters were exposed to different temperatures (20 °C, 26 °C, and 28 °C, with 20 °C considered the control group) and to a nominal concentration of 100 μg/L of MP (spherical polystyrene, 1.1 μm) at the same temperatures for 7 days. Oxidative stress parameters were analyzed, including the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST), as well as glutathione (GSH) levels and lipid peroxidation. Additionally, energy metabolism indicators, such as glucose and lactate levels and lactate dehydrogenase activity, were evaluated, along with the accumulation of MP in the gills and digestive glands of oysters. The results showed that regardless of temperature both gills and digestive gland accumulated MP. Besides, the thermal stress increased GST activity in both tissues and altered GSH levels. At the highest temperature, MP exposure led to increased SOD activity in the gills and decreased CAT activity in the digestive gland. GST activity was elevated in oysters exposed to MP at 20 °C, alongside higher GSH levels. At 26 °C, glucose and lactate levels, as well as lactate dehydrogenase activity, were significantly elevated. Co-exposure to MP notably affected oysters at 26 °C, reducing glucose levels in the gills while increasing them in the digestive gland. The Integrated Biomarker Response (IBR) index revealed that co-exposure had a more pronounced impact on the gills than on the digestive gland. Overall, this study underscores how a commercially important oyster species could be adversely affected by the combined impacts of global warming and MP contamination.

{"title":"Oxidative and metabolic responses in Crassostrea gasar under combined stressors of elevated temperature and microplastic exposure","authors":"Júlia Ferreiro , Maidana da Silva Idiarte , Júlia Oliveira , Suamy Cruz , Gabriela Soares Correa , Larissa Müller , Juliane Ventura-Lima","doi":"10.1016/j.cbpc.2025.110204","DOIUrl":"10.1016/j.cbpc.2025.110204","url":null,"abstract":"<div><div>This study investigates two critical threats to species such as the oyster <em>Crassostrea gasar</em>: elevated temperatures and microplastic (MP) contamination. To assess the combined effects of MP and temperature, oysters were exposed to different temperatures (20 °C, 26 °C, and 28 °C, with 20 °C considered the control group) and to a nominal concentration of 100 μg/L of MP (spherical polystyrene, 1.1 μm) at the same temperatures for 7 days. Oxidative stress parameters were analyzed, including the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST), as well as glutathione (GSH) levels and lipid peroxidation. Additionally, energy metabolism indicators, such as glucose and lactate levels and lactate dehydrogenase activity, were evaluated, along with the accumulation of MP in the gills and digestive glands of oysters. The results showed that regardless of temperature both gills and digestive gland accumulated MP. Besides, the thermal stress increased GST activity in both tissues and altered GSH levels. At the highest temperature, MP exposure led to increased SOD activity in the gills and decreased CAT activity in the digestive gland. GST activity was elevated in oysters exposed to MP at 20 °C, alongside higher GSH levels. At 26 °C, glucose and lactate levels, as well as lactate dehydrogenase activity, were significantly elevated. Co-exposure to MP notably affected oysters at 26 °C, reducing glucose levels in the gills while increasing them in the digestive gland. The Integrated Biomarker Response (IBR) index revealed that co-exposure had a more pronounced impact on the gills than on the digestive gland. Overall, this study underscores how a commercially important oyster species could be adversely affected by the combined impacts of global warming and MP contamination.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110204"},"PeriodicalIF":3.9,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143844484","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}

引用次数: 0

The crosstalk between autophagy and apoptosis mechanism of hemocytes in Chlamys farreri under B[a]P exposure in vitro

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-04-07 DOI: 10.1016/j.cbpc.2025.110202

Ning Zhang, Luqing Pan, Qilong Liao, Fengjun Lei, Ruixue Tong, Yaobing Li

The impact of polycyclic aromatic hydrocarbons (PAHs) on the immune function of marine animals has garnered significant attention. C. farrei is frequently exposed to pollutants and has only innate immunity. To delve more deeply into the immunotoxicity mechanism of PAHs in C. farrei, its hemocytes were cultured in vitro as they were the primary drivers of immune activities. The autophagy and apoptosis of hemocytes are essential components of the immune response. The exposure of pollutant, autophagy and apoptosis of immune cells are often disrupted, leading to immunodeficiency. In aquatic animals, the mechanism of autophagy and apoptosis in hemocytes remains unclear, and the crosstalk between the two needs to be further investigated. To evaluate the mechanism of autophagy and apoptosis of hemocytes in vitro, 0 μM, 1 μM, 2.5 μM or 5 μM Benzopyrene (B[a]p) was chosen. Experimental results demonstrated that B[a]P triggered autophagosome formation, but also caused significant damage to lysosomes, resulting in a compromised autophagic flux. B[a]P causes an increase in apoptosis levels in hemocytes of C. farreri by affecting the transcriptional level of AIF. To further explore the crosstalk mechanism between the two, activator and inhibitor of autophagy were used. After adding autophagy activator or inhibitor, the present results indicated that Lysosomal function determined the patency of autophagic flux. When massive autophagosomes accumulate, it leads to a much higher rate of apoptosis through caspase-dependent apoptotic pathway. Lysosomal damage further leads to apoptosis and inhibit autophagy. In the B[a]P-treated group, immunological parameters were markedly decreased due to autophagy and apoptosis of hemocytes. The immunotoxicity mechanism of B[a]P in C. farreri hemocytes was investigated in present study, which enriched the immunotoxicity network.

{"title":"The crosstalk between autophagy and apoptosis mechanism of hemocytes in Chlamys farreri under B[a]P exposure in vitro","authors":"Ning Zhang, Luqing Pan, Qilong Liao, Fengjun Lei, Ruixue Tong, Yaobing Li","doi":"10.1016/j.cbpc.2025.110202","DOIUrl":"10.1016/j.cbpc.2025.110202","url":null,"abstract":"<div><div>The impact of polycyclic aromatic hydrocarbons (PAHs) on the immune function of marine animals has garnered significant attention. <em>C. farrei</em> is frequently exposed to pollutants and has only innate immunity. To delve more deeply into the immunotoxicity mechanism of PAHs in <em>C. farrei</em>, its hemocytes were cultured <em>in vitro</em> as they were the primary drivers of immune activities. The autophagy and apoptosis of hemocytes are essential components of the immune response. The exposure of pollutant, autophagy and apoptosis of immune cells are often disrupted, leading to immunodeficiency. In aquatic animals, the mechanism of autophagy and apoptosis in hemocytes remains unclear, and the crosstalk between the two needs to be further investigated. To evaluate the mechanism of autophagy and apoptosis of hemocytes <em>in vitro</em>, 0 μM, 1 μM, 2.5 μM or 5 μM Benzopyrene (B[<em>a</em>]p) was chosen. Experimental results demonstrated that B[<em>a</em>]P triggered autophagosome formation, but also caused significant damage to lysosomes, resulting in a compromised autophagic flux. B[<em>a</em>]P causes an increase in apoptosis levels in hemocytes of <em>C. farreri</em> by affecting the transcriptional level of AIF. To further explore the crosstalk mechanism between the two, activator and inhibitor of autophagy were used. After adding autophagy activator or inhibitor, the present results indicated that Lysosomal function determined the patency of autophagic flux. When massive autophagosomes accumulate, it leads to a much higher rate of apoptosis through caspase-dependent apoptotic pathway. Lysosomal damage further leads to apoptosis and inhibit autophagy. In the B[<em>a</em>]P-treated group, immunological parameters were markedly decreased due to autophagy and apoptosis of hemocytes. The immunotoxicity mechanism of B[<em>a</em>]P in <em>C. farreri</em> hemocytes was investigated in present study, which enriched the immunotoxicity network.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110202"},"PeriodicalIF":3.9,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823958","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}

引用次数: 0

Involvement of the weak metabolic function in cardiovascular toxicity induced by idebenone in zebrafish

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-04-07 DOI: 10.1016/j.cbpc.2025.110203

Jiashuo Zhou , Yanan Yang , Jingcheng Zhao, Te Zheng, Yun Zhang

Idebenone (IDE) is a commonly used psychotropic drug in the clinic. However, the cardiovascular toxicity of IDE has not been reported previously. Therefore, we evaluated the safety of IDE and preliminarily elucidated the mechanism of cardiovascular toxicity induced by IDE using zebrafish as the model organism. In this study, wild-type AB zebrafish, and transgenic zebrafish Tg(cmcl2:EGFP) with green fluorescence-labelled cardiomyocytes were used as the research objects. We evaluated the effects of IDE on the sinus venosus-bulbus arteriosus (SV-BA) distance, ejection fraction, ventricular short-axis shortening rate, blood flow rate, and the staining area and intensity of cardiac erythrocytes. The toxic mechanism of IDE was elucidated using transcriptomics and Quantitative real-time PCR (qRT-PCR). We found that high concentrations of IDE could cause acute poisoning of some zebrafish within a short period (6 h), mainly characterized by severe cardiac venous stasis. IDE decreased the blood flow and reduced the red blood cell stained area in the heart region of some zebrafish. The results of transcriptome analysis and qRT-PCR showed that the expression of genes related to drug metabolism and lipid metabolism was significantly down-regulated in zebrafish with IDE-induced cardiovascular toxicity. We believe that IDE may be more likely to cause acute cardiovascular toxicity in organisms with weak metabolic enzyme function. The present study investigated the mechanism of the toxic effects of IDE using a zebrafish model and laid the foundation for a more comprehensive understanding of the cardiovascular toxicity of IDE.

艾地苯醌（IDE）是一种临床常用的精神药物。然而，IDE 的心血管毒性此前尚未见报道。因此，我们以斑马鱼为模型生物，评估了IDE的安全性，并初步阐明了IDE诱导心血管毒性的机制。本研究以野生型AB斑马鱼和带有绿色荧光标记心肌细胞的转基因斑马鱼Tg（cmcl2:EGFP）为研究对象。我们评估了IDE对静脉窦-大动脉（SV-BA）距离、射血分数、心室短轴缩短率、血流速度以及心脏红细胞染色面积和强度的影响。利用转录组学和定量实时 PCR（qRT-PCR）阐明了 IDE 的毒性机制。我们发现，高浓度的IDE可在短时间（6小时）内导致部分斑马鱼急性中毒，主要表现为严重的心脏静脉淤血。一些斑马鱼心脏区域的血流量减少，红细胞染色面积缩小。转录组分析和qRT-PCR结果显示，在IDE诱导的心血管毒性斑马鱼中，与药物代谢和脂质代谢相关的基因表达显著下调。我们认为，在代谢酶功能较弱的生物体内，IDE可能更容易引起急性心血管毒性。本研究利用斑马鱼模型研究了IDE的毒性作用机制，为更全面地了解IDE的心血管毒性奠定了基础。

{"title":"Involvement of the weak metabolic function in cardiovascular toxicity induced by idebenone in zebrafish","authors":"Jiashuo Zhou , Yanan Yang , Jingcheng Zhao, Te Zheng, Yun Zhang","doi":"10.1016/j.cbpc.2025.110203","DOIUrl":"10.1016/j.cbpc.2025.110203","url":null,"abstract":"<div><div>Idebenone (IDE) is a commonly used psychotropic drug in the clinic. However, the cardiovascular toxicity of IDE has not been reported previously. Therefore, we evaluated the safety of IDE and preliminarily elucidated the mechanism of cardiovascular toxicity induced by IDE using zebrafish as the model organism. In this study, wild-type AB zebrafish, and transgenic zebrafish <em>Tg(cmcl2:EGFP)</em> with green fluorescence-labelled cardiomyocytes were used as the research objects. We evaluated the effects of IDE on the sinus venosus-bulbus arteriosus (SV-BA) distance, ejection fraction, ventricular short-axis shortening rate, blood flow rate, and the staining area and intensity of cardiac erythrocytes. The toxic mechanism of IDE was elucidated using transcriptomics and Quantitative real-time PCR (qRT-PCR). We found that high concentrations of IDE could cause acute poisoning of some zebrafish within a short period (6 h), mainly characterized by severe cardiac venous stasis. IDE decreased the blood flow and reduced the red blood cell stained area in the heart region of some zebrafish. The results of transcriptome analysis and qRT-PCR showed that the expression of genes related to drug metabolism and lipid metabolism was significantly down-regulated in zebrafish with IDE-induced cardiovascular toxicity. We believe that IDE may be more likely to cause acute cardiovascular toxicity in organisms with weak metabolic enzyme function. The present study investigated the mechanism of the toxic effects of IDE using a zebrafish model and laid the foundation for a more comprehensive understanding of the cardiovascular toxicity of IDE.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110203"},"PeriodicalIF":3.9,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823959","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}

引用次数: 0

Impact of environmental salinity on the MAPK-NFAT5 pathway in Trachemys scripta elegans and its role in osmoregulaton

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-03-31 DOI: 10.1016/j.cbpc.2025.110201

Xin Niu , Yingnan Lu , Yue Yuan, Jiao Li, Yunjuan Xiao, Haitao Shi, Meiling Hong, Li Ding

Globally, sea level rise (SLR) leads to salinization of coastal freshwater, in where organisms might be affected and in turn promote osmoregulation and adaptation in response to freshwater salinization. Trachemys scripta elegans a freshwater turtle species, exhibits remarkable tolerance to varying salinity environments, yet the underlying regulatory mechanisms remain poorly understood. This study aimed to elucidate the molecular mechanisms of osmoregulation in this species based on previous RNA-seq data. Our findings revealed that when exposed to 5 PSU (5 ‰) and 15 PSU (15 ‰) salinities, the turtles exhibited increased concentrations of ions (Na⁺, K⁺) and urea in urine, along with elevated osmotic pressures in both plasma and urine. Additionally, the protein levels of aquaporins (AQPs) and transporters of ions and organic osmolytes in the kidney were upregulated in saline water. Notably, the transcriptional level of the hypertonic regulator NFAT5 was significantly elevated, accompanied by an increase in phosphorylated NFAT5 levels in the nucleus of renal tubular epithelial cells. Furthermore, we observed upregulated phosphorylated levels of MAPKs in saline water. The use of MAPK inhibitors effectively blocked the transcription of NFAT5 and osmoregulatory target genes. Collectively, these results suggest that T. scripta elegans activates the MAPK-NFAT5 signaling pathway to modulate osmotic pressure in adaptation to saline water environments. Our study provides valuable insights into the osmoregulatory responses of aquatic organisms to saline environments and aids in understanding the adaptability of organisms inhabiting coastal areas facing rising sea levels.

{"title":"Impact of environmental salinity on the MAPK-NFAT5 pathway in Trachemys scripta elegans and its role in osmoregulaton","authors":"Xin Niu , Yingnan Lu , Yue Yuan, Jiao Li, Yunjuan Xiao, Haitao Shi, Meiling Hong, Li Ding","doi":"10.1016/j.cbpc.2025.110201","DOIUrl":"10.1016/j.cbpc.2025.110201","url":null,"abstract":"<div><div>Globally, sea level rise (SLR) leads to salinization of coastal freshwater, in where organisms might be affected and in turn promote osmoregulation and adaptation in response to freshwater salinization. <em>Trachemys scripta elegans</em> a freshwater turtle species, exhibits remarkable tolerance to varying salinity environments, yet the underlying regulatory mechanisms remain poorly understood. This study aimed to elucidate the molecular mechanisms of osmoregulation in this species based on previous RNA-seq data. Our findings revealed that when exposed to 5 PSU (5 ‰) and 15 PSU (15 ‰) salinities, the turtles exhibited increased concentrations of ions (Na<sup>+</sup>, K<sup>+</sup>) and urea in urine, along with elevated osmotic pressures in both plasma and urine. Additionally, the protein levels of aquaporins (AQPs) and transporters of ions and organic osmolytes in the kidney were upregulated in saline water. Notably, the transcriptional level of the hypertonic regulator NFAT5 was significantly elevated, accompanied by an increase in phosphorylated NFAT5 levels in the nucleus of renal tubular epithelial cells. Furthermore, we observed upregulated phosphorylated levels of MAPKs in saline water. The use of MAPK inhibitors effectively blocked the transcription of NFAT5 and osmoregulatory target genes. Collectively, these results suggest that <em>T. scripta elegans</em> activates the MAPK-NFAT5 signaling pathway to modulate osmotic pressure in adaptation to saline water environments. Our study provides valuable insights into the osmoregulatory responses of aquatic organisms to saline environments and aids in understanding the adaptability of organisms inhabiting coastal areas facing rising sea levels.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110201"},"PeriodicalIF":3.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771545","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}

引用次数: 0

Acute exposure to antimony elicits endocrine disturbances, leading to PCOS and ovarian fibrosis in female zebrafish

IF 3.9 3区环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Comparative Biochemistry and Physiology C-toxicology & Pharmacology

Pub Date : 2025-03-31 DOI: 10.1016/j.cbpc.2025.110198

Zhongqian Cen , Shenghan Lv , Qing Li , Jingyun Zhang , ShiXue Mei , Xia Hu , Aijiang Yang

Antimony (Sb) is an estrogenic metal. Exogenous exposure to Sb can affect estrogen levels and their receptor expression in organisms, exerting estrogen-disrupting effects and even inducing polycystic ovary syndrome (PCOS), which is accompanied by the progression of ovarian fibrosis. To investigate the pathological mechanism of this reproductive damage caused by Sb exposure, we exposed female zebrafish to Sb solution for 18 days for acute toxicity experiments. The results showed that Sb exposure affected the changes of GnRH, FSH, LH, E2 and T levels on the HPG axis, which disrupted the balance of sex steroid hormones in the internal environment of zebrafish and progression of PCOS. Furthermore, Sirius red staining revealed significant fibrosis in the ovarian tissues of Sb-exposed female zebrafish. This study adopted transcriptome sequencing and Western Blotting to explore the mechanisms of action. The biological processes and signaling pathways potentially associated with Sb-induced ovarian fibrosis were predicted by using GO annotation and KEGG pathway enrichment analysis, such as ECM receptors, TGF-β/Smad and WNT/β-catenin. The experiment results showed that Sb induced up-regulation of the transcription levels of the pro-fibrotic factors tgf-β3, wnt10a, ctnnb1, and β-catenin protein expression, suggesting the activation of the WNT/β-catenin pathways and TGF-β/Smad. Sb exposure led to up-regulation of ECM-related genes col2a1a, itgb1b.2, lamc1, fn1a and up-regulation of fibrosis markers α-SMA, Fn1a, col4a2 protein expression, Therefore, we hypothesized that Sb exposure activates the TGF-β/Smad and WNT/β-catenin pathways, leading to abnormal ECM deposition and promoting the progression of ovarian fibrosis in zebrafish.

{"title":"Acute exposure to antimony elicits endocrine disturbances, leading to PCOS and ovarian fibrosis in female zebrafish","authors":"Zhongqian Cen , Shenghan Lv , Qing Li , Jingyun Zhang , ShiXue Mei , Xia Hu , Aijiang Yang","doi":"10.1016/j.cbpc.2025.110198","DOIUrl":"10.1016/j.cbpc.2025.110198","url":null,"abstract":"<div><div>Antimony (Sb) is an estrogenic metal. Exogenous exposure to Sb can affect estrogen levels and their receptor expression in organisms, exerting estrogen-disrupting effects and even inducing polycystic ovary syndrome (PCOS), which is accompanied by the progression of ovarian fibrosis. To investigate the pathological mechanism of this reproductive damage caused by Sb exposure, we exposed female zebrafish to Sb solution for 18 days for acute toxicity experiments. The results showed that Sb exposure affected the changes of GnRH, FSH, LH, E2 and T levels on the HPG axis, which disrupted the balance of sex steroid hormones in the internal environment of zebrafish and progression of PCOS. Furthermore, Sirius red staining revealed significant fibrosis in the ovarian tissues of Sb-exposed female zebrafish. This study adopted transcriptome sequencing and Western Blotting to explore the mechanisms of action. The biological processes and signaling pathways potentially associated with Sb-induced ovarian fibrosis were predicted by using GO annotation and KEGG pathway enrichment analysis, such as ECM receptors, TGF-β/Smad and WNT/β-catenin. The experiment results showed that Sb induced up-regulation of the transcription levels of the pro-fibrotic factors <em>tgf-β3</em>, <em>wnt10a</em>, <em>ctnnb1</em>, and β-catenin protein expression, suggesting the activation of the WNT/β-catenin pathways and TGF-β/Smad. Sb exposure led to up-regulation of ECM-related genes <em>col2a1a</em>, <em>itgb1b.2</em>, <em>lamc1</em>, <em>fn1a</em> and up-regulation of fibrosis markers α-SMA, Fn1a, col4a2 protein expression, Therefore, we hypothesized that Sb exposure activates the TGF-β/Smad and WNT/β-catenin pathways, leading to abnormal ECM deposition and promoting the progression of ovarian fibrosis in zebrafish.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110198"},"PeriodicalIF":3.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771533","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}

引用次数: 0