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

Structure, transduction pathway, behavior and toxicity of fish olfactory in aquatic environments

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 : 2025-03-17 DOI: 10.1016/j.cbpc.2025.110195

Ning Yue , Dan Li , Yanling Pan , Liting Chen , Sisi Liu , Meifang Hou , Yongju Luo

The olfactory system in teleost fish plays a vital role as chemosensory organ that directly interacts with the aquatic environment, exhibiting high sensitivity to chemical alteration in aquatic environments. However, despite its importance, there has been a lack of systematic reviews in the past decade on fish olfactory structure, transduction mechanisms, and the impact of environmental pollutants on olfactory toxicity. This study analyzed 272 relevant studies, focusing on the role of the olfactory system and the disruption of olfactory function by contaminants. Fish processes odors through olfactory receptor neurons, olfactory nerves, mitral/ruffed cells, glomeruli, and neurotransmitters, mediated by membrane potentials resulting from ion channels in the olfactory epithelium and olfactory bulb, which are then relayed to higher brain regions via the medial olfactory tracts and lateral olfactory tracts for further integration and modulation. This process minimizes the overlap between complex odor sets, ensuring distinct representation of each odor and eliciting appropriate olfactory-mediated behaviors, such as feeding, migration, alarm responses, and reproduction. Current research identifies four main types of contaminants affecting the fish olfactory system: heavy metals (51.60 %), organic contaminants (33.79 %), acidification (12.33 %), and salinity (5.94 %). The main mechanisms of impact are: morphological changes (21.19 %), alterations in olfactory receptors (29.24 %), damage to olfactory receptor neurons and neurotransmitters disruption (26.69 %), plasticity (2.97 %), and defense mechanisms (19.92 %). We also identify uncertainties and proposes future research directions on the effects of contaminants on fish olfactory. Overall, this review provides valuable insights into the toxicity of contaminants on fish olfactory.

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引用次数: 0

Zearalenone (ZEN) impairs motor function and induces neurotoxicity via inflammatory pathways: Evidence from zebrafish models and molecular docking studies

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 : 2025-03-15 DOI: 10.1016/j.cbpc.2025.110194

Ting Xu , Yuanfeng Xiong , Mi Zhou , Mingyang Wang , Dianxia Xing , Jiyin Zhang , Bo Wang , Yu Xu

ZEN is a low-molecular-weight food contaminant that is frequently detected in various crops and regions due to its high thermal stability and persistence. It poses a significant threat to the biological nervous system. However, the molecular mechanisms underlying ZEN-induced neurotoxicity remain incompletely understood. To further explore this issue, this study focused on the effects of ZEN on the nervous system, particularly its key targets and related molecular mechanisms. The study combined network toxicology and molecular docking methods and performed behavioral analysis of zebrafish larvae exposed to ZEN.

Firstly, motor capacity tests revealed that ZEN exposure significantly reduced the overall movement speed of zebrafish larvae during both photoperiod and dark cycles. We then identified 141 potential targets associated with ZEN-induced neurotoxicity from the GeneCards, OMIM, and DrugBank databases. Further screening using STRING and Cytoscape software extracted 25 key nodes, including TP53, AKT1, CASP3, MAPK3, and NFKB1. Analysis of GO and KEGG pathways suggested 20 of the most relevant signaling pathways and indicated that the core targets of ZEN-induced neurotoxicity were primarily involved in inflammatory pathways. Molecular docking using AutoDock further confirmed the strong binding affinity between ZEN and the targets. All six core target proteins exhibited strong binding affinity with ZEN, with binding energies of less than −7.

In summary, the results of this study suggest that ZEN may impact cognitive dysfunction and neuropathy by activating neuroinflammatory signaling pathways, ultimately leading to neuronal death. This study provides important insights into the molecular mechanisms of ZEN-induced neurotoxicity and highlights the potential for prevention and treatment of diseases associated with exposure to ZEN and similar food contaminants.

{"title":"Zearalenone (ZEN) impairs motor function and induces neurotoxicity via inflammatory pathways: Evidence from zebrafish models and molecular docking studies","authors":"Ting Xu , Yuanfeng Xiong , Mi Zhou , Mingyang Wang , Dianxia Xing , Jiyin Zhang , Bo Wang , Yu Xu","doi":"10.1016/j.cbpc.2025.110194","DOIUrl":"10.1016/j.cbpc.2025.110194","url":null,"abstract":"<div><div>ZEN is a low-molecular-weight food contaminant that is frequently detected in various crops and regions due to its high thermal stability and persistence. It poses a significant threat to the biological nervous system. However, the molecular mechanisms underlying ZEN-induced neurotoxicity remain incompletely understood. To further explore this issue, this study focused on the effects of ZEN on the nervous system, particularly its key targets and related molecular mechanisms. The study combined network toxicology and molecular docking methods and performed behavioral analysis of zebrafish larvae exposed to ZEN.</div><div>Firstly, motor capacity tests revealed that ZEN exposure significantly reduced the overall movement speed of zebrafish larvae during both photoperiod and dark cycles. We then identified 141 potential targets associated with ZEN-induced neurotoxicity from the GeneCards, OMIM, and DrugBank databases. Further screening using STRING and Cytoscape software extracted 25 key nodes, including TP53, AKT1, CASP3, MAPK3, and NFKB1. Analysis of GO and KEGG pathways suggested 20 of the most relevant signaling pathways and indicated that the core targets of ZEN-induced neurotoxicity were primarily involved in inflammatory pathways. Molecular docking using AutoDock further confirmed the strong binding affinity between ZEN and the targets. All six core target proteins exhibited strong binding affinity with ZEN, with binding energies of less than −7.</div><div>In summary, the results of this study suggest that ZEN may impact cognitive dysfunction and neuropathy by activating neuroinflammatory signaling pathways, ultimately leading to neuronal death. This study provides important insights into the molecular mechanisms of ZEN-induced neurotoxicity and highlights the potential for prevention and treatment of diseases associated with exposure to ZEN and similar food contaminants.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110194"},"PeriodicalIF":3.9,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143643164","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

D-tetramethrin induces cardiac looping failure in zebrafish during embryonic development

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 : 2025-03-12 DOI: 10.1016/j.cbpc.2025.110193

Xinhao Ye , Mijia Li , YunLong Meng , Shiyi Duan , Sijie Zhang , Keyuan Zhong

Cardiac looping is a crucial process during embryonic development. Abnormalities or failures in cardiac looping can lead to congenital heart defects, thereby affecting normal physiological function. Environmental pollutant exposure is one of the major causes of cardiac looping failure. D-tetramethrin is a hygienic insecticide widely used in households and public places, that can enter the human body through contact, insect transmission, and the food chain, thereby impacting human health. In this study, zebrafish embryos were exposed to different concentrations of D-tetramethrin to analyze its effects on heart development, and oxidative stress levels within the embryos. Additionally, qPCR was employed to analyze the transcription and the expression levels of genes related to heart development and function. The results showed that (1) D-tetramethrin exposure significantly reduced heart rate and increased the distance between the sinus venosus and the bulbus arteriosus (SV-BA), which suggested that D-tetramethrin induced cardiac looping failure and led to abnormal heart function. (2) D-tetramethrin exposure elevated the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in zebrafish embryos while decreasing the enzyme activities of key antioxidant stress enzymes, such as catalase (CAT) and superoxide dismutase (SOD). (3) D-tetramethrin exposure resulted in a significant downregulation of the transcription of cardiac looping-related genes (Myh6, Nkx2.5, Tbx2b, Tbx5a, Tnnt2c and Hand2) and heart function-related genes (Gata4, Vmhc and Nppa). Our findings indicate that D-tetramethrin causes the accumulation of ROS, which in turn alters the transcription levels of genes related to cardiac looping, ultimately resulting in cardiac looping failure.

{"title":"D-tetramethrin induces cardiac looping failure in zebrafish during embryonic development","authors":"Xinhao Ye , Mijia Li , YunLong Meng , Shiyi Duan , Sijie Zhang , Keyuan Zhong","doi":"10.1016/j.cbpc.2025.110193","DOIUrl":"10.1016/j.cbpc.2025.110193","url":null,"abstract":"<div><div>Cardiac looping is a crucial process during embryonic development. Abnormalities or failures in cardiac looping can lead to congenital heart defects, thereby affecting normal physiological function. Environmental pollutant exposure is one of the major causes of cardiac looping failure. D-tetramethrin is a hygienic insecticide widely used in households and public places, that can enter the human body through contact, insect transmission, and the food chain, thereby impacting human health. In this study, zebrafish embryos were exposed to different concentrations of D-tetramethrin to analyze its effects on heart development, and oxidative stress levels within the embryos. Additionally, qPCR was employed to analyze the transcription and the expression levels of genes related to heart development and function. The results showed that (1) D-tetramethrin exposure significantly reduced heart rate and increased the distance between the sinus venosus and the bulbus arteriosus (SV-BA), which suggested that D-tetramethrin induced cardiac looping failure and led to abnormal heart function. (2) D-tetramethrin exposure elevated the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in zebrafish embryos while decreasing the enzyme activities of key antioxidant stress enzymes, such as catalase (CAT) and superoxide dismutase (SOD). (3) D-tetramethrin exposure resulted in a significant downregulation of the transcription of cardiac looping-related genes (<em>Myh6</em>, <em>Nkx2.5</em>, <em>Tbx2b</em>, <em>Tbx5a, Tnnt2c and Hand2</em>) and heart function-related genes (<em>Gata4, Vmhc</em> and <em>Nppa</em>). Our findings indicate that D-tetramethrin causes the accumulation of ROS, which in turn alters the transcription levels of genes related to cardiac looping, ultimately resulting in cardiac looping failure.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110193"},"PeriodicalIF":3.9,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143629417","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

Toxic effects of combined exposure to carbamazepine and triclosan on adult zebrafish (Danio rerio): Insights into acute mortality, neurotransmitters, biochemical response, and histopathology.

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 : 2025-03-12 DOI: 10.1016/j.cbpc.2025.110190

Jiangong Jiang, Shuxin Zhao, Xinjie Guo, Wenzhen Liu, Huixue Duan, Xinyuan Zhou, Rongyu Li, Yanhong Chang, Haiyang Yu, Xinxin Du, Xing Hu

As two representative pharmaceuticals and personal care products (PCPPs), carbamazepine (CBZ) and triclosan (TCS) are frequently detected in aquatic ecosystems worldwide, but their toxicological interactions remain unclear. This work evaluated the combined toxicity of CBZ and TCS to zebrafish (Danio rerio) in terms of acute mortality, biochemical response, and histopathology. The results showed that the 96-h acute toxicity interaction of CBZ and TCS fitted well to the concentration addition (CA) model, suggesting an additive effect. Compared with exposure to either CBZ or TCS alone, co-exposure to CBZ and TCS at equivalent toxic concentrations can lead to a profound increase in gamma-aminobutyric acid (GABA) and a reduction in acetylcholine (ACh) and acetylcholinesterase (AChE) levels. Compared with CBZ or TCS alone, the 21-day co-exposure to CBZ and TCS at the 2 % LC₅₀ aggravated oxidative stress and histopathological damage to the gills, brain, and liver. Overall, these findings provide a reference for the rational and complete assessment of the combined toxicity of the PPCPs to aquatic organisms.

{"title":"Toxic effects of combined exposure to carbamazepine and triclosan on adult zebrafish (Danio rerio): Insights into acute mortality, neurotransmitters, biochemical response, and histopathology.","authors":"Jiangong Jiang, Shuxin Zhao, Xinjie Guo, Wenzhen Liu, Huixue Duan, Xinyuan Zhou, Rongyu Li, Yanhong Chang, Haiyang Yu, Xinxin Du, Xing Hu","doi":"10.1016/j.cbpc.2025.110190","DOIUrl":"10.1016/j.cbpc.2025.110190","url":null,"abstract":"<p><p>As two representative pharmaceuticals and personal care products (PCPPs), carbamazepine (CBZ) and triclosan (TCS) are frequently detected in aquatic ecosystems worldwide, but their toxicological interactions remain unclear. This work evaluated the combined toxicity of CBZ and TCS to zebrafish (Danio rerio) in terms of acute mortality, biochemical response, and histopathology. The results showed that the 96-h acute toxicity interaction of CBZ and TCS fitted well to the concentration addition (CA) model, suggesting an additive effect. Compared with exposure to either CBZ or TCS alone, co-exposure to CBZ and TCS at equivalent toxic concentrations can lead to a profound increase in gamma-aminobutyric acid (GABA) and a reduction in acetylcholine (ACh) and acetylcholinesterase (AChE) levels. Compared with CBZ or TCS alone, the 21-day co-exposure to CBZ and TCS at the 2 % LC<sub>50</sub> aggravated oxidative stress and histopathological damage to the gills, brain, and liver. Overall, these findings provide a reference for the rational and complete assessment of the combined toxicity of the PPCPs to aquatic organisms.</p>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":" ","pages":"110190"},"PeriodicalIF":3.9,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630033","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 hypoxia induces sleep disorders via sima/HIF-1α regulation of circadian rhythms in adult Drosophila

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 : 2025-03-12 DOI: 10.1016/j.cbpc.2025.110192

Shuwei Wang , Shihong Zhou , Xiaolin Jiang , Dan Yang , Jianzheng He , Minghui Xiu

The atmospheric oxygen concentration is significantly reduced in highland regions compared to lowland areas. The first entering the plateau can induce sleep disorders in individuals, primarily attributed to insufficient oxygen supply. This study used Drosophila melanogaster as a model organism to better understand the molecular mechanism of acute hypoxia-induced sleep disorders. The Drosophila activity monitoring system (DAMS) was employed to observe the sleep-wake in adult (w¹¹¹⁸, sima^KG07607, and clock^jrk) female flies. Quantifying the relative mRNA expression levels of sima and circadian clock genes in the head of flies was accomplished by utilizing qRT-PCR. Acute hypoxia caused sleep disorders in w¹¹¹⁸ flies, such as shortened sleep duration and length, and prolonged sleep latency. PCR results showed that sima and clock genes were up-regulated in ZT6 and ZT12 and down-regulated in ZT0 and ZT18 in acute hypoxic w¹¹¹⁸ flies compared to normoxic w¹¹¹⁸ flies. Under normoxic conditions, sleep indexes in sima^KG07607 flies were not substantially different from w¹¹¹⁸ flies. However, clock^jrk flies demonstrated a reduced sleep duration, decreased sleep bout length, and increased sleep latency and activities. Sleep and gene expression in sima^KG07607 flies under acute hypoxic conditions were not significantly different from those under normoxic conditions. Surprisingly, sleep and gene expression in clock^jrk flies showed opposite trends to w¹¹¹⁸ flies. The present study indicates that acute hypoxia disrupt circadian rhythms through the activation of sima/HIF-1α, leading to the onset of sleep disorders, with Clock signaling potentially serving as a contributing factor.

{"title":"Acute hypoxia induces sleep disorders via sima/HIF-1α regulation of circadian rhythms in adult Drosophila","authors":"Shuwei Wang , Shihong Zhou , Xiaolin Jiang , Dan Yang , Jianzheng He , Minghui Xiu","doi":"10.1016/j.cbpc.2025.110192","DOIUrl":"10.1016/j.cbpc.2025.110192","url":null,"abstract":"<div><div>The atmospheric oxygen concentration is significantly reduced in highland regions compared to lowland areas. The first entering the plateau can induce sleep disorders in individuals, primarily attributed to insufficient oxygen supply. This study used <em>Drosophila melanogaster</em> as a model organism to better understand the molecular mechanism of acute hypoxia-induced sleep disorders. The <em>Drosophila</em> activity monitoring system (DAMS) was employed to observe the sleep-wake in adult (<em>w</em><sup><em>1118</em></sup>, <em>sima</em><sup><em>KG07607</em></sup>, and <em>clock</em><sup><em>jrk</em></sup>) female flies. Quantifying the relative mRNA expression levels of <em>sima</em> and circadian clock genes in the head of flies was accomplished by utilizing qRT-PCR. Acute hypoxia caused sleep disorders in <em>w</em><sup><em>1118</em></sup> flies, such as shortened sleep duration and length, and prolonged sleep latency. PCR results showed that <em>sima</em> and clock genes were up-regulated in ZT6 and ZT12 and down-regulated in ZT0 and ZT18 in acute hypoxic <em>w</em><sup><em>1118</em></sup> flies compared to normoxic <em>w</em><sup><em>1118</em></sup> flies. Under normoxic conditions, sleep indexes in <em>sima</em><sup><em>KG07607</em></sup> flies were not substantially different from <em>w</em><sup><em>1118</em></sup> flies. However, <em>clock</em><sup><em>jrk</em></sup> flies demonstrated a reduced sleep duration, decreased sleep bout length, and increased sleep latency and activities. Sleep and gene expression in <em>sima</em><sup><em>KG07607</em></sup> flies under acute hypoxic conditions were not significantly different from those under normoxic conditions. Surprisingly, sleep and gene expression in <em>clock</em><sup><em>jrk</em></sup> flies showed opposite trends to <em>w</em><sup><em>1118</em></sup> flies. The present study indicates that acute hypoxia disrupt circadian rhythms through the activation of <em>sima</em>/<em>HIF-1α</em>, leading to the onset of sleep disorders, with <em>Clock</em> signaling potentially serving as a contributing factor.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110192"},"PeriodicalIF":3.9,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143620098","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

Selenium-enriched Bacillus subtilis attenuates emamectin benzoate-induced liver injury in grass carp through inhibiting inflammation and ferroptosis via activating Nrf2 signaling pathway

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 : 2025-03-12 DOI: 10.1016/j.cbpc.2025.110191

Fengyan Zhang , Xinhui Zhang , Musen Li , Qingsong Sun , Yuehong Li , Yunhe Fu , Yue Zhang

The widespread use of emamectin benzoate (EMB) has caused many pests to develop resistance to it, and there have been reports of toxic effects of methomyl on marine animals. We tested whether Se-rich B. subtilis exerted protective effects against EMB-induced liver injury in grass carp. The carps were cultured in an aquatic environment containing 2.4 μg/L of EMB for 30 days. Se-rich B. subtilis (10⁵, 10⁶, 10⁷ Colony Forming Unit (CFU)/g) was given daily for 10 days. According to the results, Se-rich B. subtilis alleviated liver pathological injury, aspartate aminotransferase (AST), alanine aminotransferase (ALT), TNF-α and IL-1β production. Meanwhile, EMB-induced ferroptosis was attenuated by Se-rich B. subtilis. The subsequent experiment revealed that Se-rich B. subtilis inhibited EMB-induced nuclear factor kappa-B (NF-κB) activation. Further research demonstrated that nuclear factor erythroid-2 related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) expression was increased by Se-rich B. subtilis. Taken together, Se-rich B. subtilis attenuated EMB-induced liver injury by alleviating inflammation and ferroptosis via Nrf2 signaling.

{"title":"Selenium-enriched Bacillus subtilis attenuates emamectin benzoate-induced liver injury in grass carp through inhibiting inflammation and ferroptosis via activating Nrf2 signaling pathway","authors":"Fengyan Zhang , Xinhui Zhang , Musen Li , Qingsong Sun , Yuehong Li , Yunhe Fu , Yue Zhang","doi":"10.1016/j.cbpc.2025.110191","DOIUrl":"10.1016/j.cbpc.2025.110191","url":null,"abstract":"<div><div>The widespread use of emamectin benzoate (EMB) has caused many pests to develop resistance to it, and there have been reports of toxic effects of methomyl on marine animals. We tested whether Se-rich <em>B. subtilis</em> exerted protective effects against EMB-induced liver injury in grass carp. The carps were cultured in an aquatic environment containing 2.4 μg/L of EMB for 30 days. Se-rich <em>B. subtilis</em> (10<sup>5</sup>, 10<sup>6</sup>, 10<sup>7</sup> Colony Forming Unit (CFU)/g) was given daily for 10 days. According to the results, Se-rich <em>B. subtilis</em> alleviated liver pathological injury, aspartate aminotransferase (AST), alanine aminotransferase (ALT), TNF-α and IL-1β production. Meanwhile, EMB-induced ferroptosis was attenuated by Se-rich <em>B. subtilis</em>. The subsequent experiment revealed that Se-rich <em>B. subtilis</em> inhibited EMB-induced nuclear factor kappa-B (NF-κB) activation. Further research demonstrated that nuclear factor erythroid-2 related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) expression was increased by Se-rich <em>B. subtilis</em>. Taken together, Se-rich <em>B. subtilis</em> attenuated EMB-induced liver injury by alleviating inflammation and ferroptosis via Nrf2 signaling.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110191"},"PeriodicalIF":3.9,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143629305","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

AMP1-1 derived from Atractylodes macrocephala Koidz prevents bone aging triggered by lead and cadmium

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 : 2025-03-11 DOI: 10.1016/j.cbpc.2025.110189

Jinpeng Wang , Yu Jiang , Xiaoyu Hou , Tahir Raza , Yiping He , Xinyue Liu , Defeng Xing , Lijun Wei

As the major pollutants of industrial wastewater, lead (Pb) and cadmium (Cd) contaminate the environment and lead to bone aging when combined. To elucidate the potential mechanism by which Pb and Cd accelerate bone aging and to screen effective protective agents, we determined the optimum concentrations of Pb and Cd to establish the aging models in vitro and in vivo. The successful establishment of aging models was confirmed through β-galactosidase (β-gal) staining, the detection of aging markers, and the evaluation of biomechanical parameters. Subsequently, the polysaccharides were extracted separately from seven plants and Atractylodes macrocephala polysaccharide (AMP) was confirmed to have the strongest effect on osteoblast proliferation. Therefore, we purified AMP to obtain a small molecular fragment called AMP1-1 and investigated its effect. It has been revealed that AMP1-1 could resist oxidative stress and promote the proliferation and differentiation of osteoblasts, thereby slowing apoptosis and alleviating cell senescence through the results of the β-gal staining and the analyses of the osteoblastic, antioxidant, apoptotic, and senescence indexes. The results in vivo suggested that AMP1-1 exerted a protective role in bone aging by inhibiting the above pathways. Consequently, AMP1-1 has theoretical significance for further development of biological protective agents against heavy metal pollution.

{"title":"AMP1-1 derived from Atractylodes macrocephala Koidz prevents bone aging triggered by lead and cadmium","authors":"Jinpeng Wang , Yu Jiang , Xiaoyu Hou , Tahir Raza , Yiping He , Xinyue Liu , Defeng Xing , Lijun Wei","doi":"10.1016/j.cbpc.2025.110189","DOIUrl":"10.1016/j.cbpc.2025.110189","url":null,"abstract":"<div><div>As the major pollutants of industrial wastewater, lead (Pb) and cadmium (Cd) contaminate the environment and lead to bone aging when combined. To elucidate the potential mechanism by which Pb and Cd accelerate bone aging and to screen effective protective agents, we determined the optimum concentrations of Pb and Cd to establish the aging models <em>in vitro</em> and <em>in vivo</em>. The successful establishment of aging models was confirmed through β-galactosidase (β-gal) staining, the detection of aging markers, and the evaluation of biomechanical parameters. Subsequently, the polysaccharides were extracted separately from seven plants and <em>Atractylodes macrocephala</em> polysaccharide (AMP) was confirmed to have the strongest effect on osteoblast proliferation. Therefore, we purified AMP to obtain a small molecular fragment called AMP1-1 and investigated its effect. It has been revealed that AMP1-1 could resist oxidative stress and promote the proliferation and differentiation of osteoblasts, thereby slowing apoptosis and alleviating cell senescence through the results of the β-gal staining and the analyses of the osteoblastic, antioxidant, apoptotic, and senescence indexes. The results <em>in vivo</em> suggested that AMP1-1 exerted a protective role in bone aging by inhibiting the above pathways. Consequently, AMP1-1 has theoretical significance for further development of biological protective agents against heavy metal pollution.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110189"},"PeriodicalIF":3.9,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143610347","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

Nitric oxide-mediated induction of superoxide dismutase and catalase genes, and altered expression of glutathione-dependent genes to defend against the TiO2 NP-induced oxidative stress in primary hepatocytes of air-breathing catfish, Clarias magur

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 : 2025-03-09 DOI: 10.1016/j.cbpc.2025.110188

Elvis Khongmawloh , Debaprasad Koner , Revelbornstar Snaitang, Nirmalendu Saha

The main objectives of the present investigation were to elucidate the possible induction of antioxidant genes under the TiO₂ NP-induced oxidative stress and the potential involvement of endogenously produced nitric oxide (NO) in its antioxidant strategies in primary hepatocytes of air-breathing magur catfish (Clarias magur). As expected, exposure to TiO₂ NPs led to (1) more ROS production as evidenced by a sharp rise of hydrogen peroxide (H₂O₂) and malonaldehyde (MDA) associated with cellular damage as evidenced by the increase of lactate dehydrogenase (LDH) leakage from hepatocytes, (2) induction of superoxide dismutase (SOD), catalase (CAT), followed by induction of different glutathione-related genes such as glutathione peroxidase (GPx), glutathione-S-transferase (GST), and thioredoxin glutathione reductase (TGR) with the induction of activities of corresponding enzymes, and (3) more production of NO associated with induction of inducible nitric oxide synthase (iNOS) activity and its corresponding gene. However, inhibition of NO production in primary hepatocytes using certain inhibitors in the presence of TiO₂ NPs, resulted in (1) more generation of H₂O₂ and MDA, (2) inhibition of SOD and CAT genes expression in primary hepatocytes with more leakage of LDH leakage into the culture media. Thus, it can be contemplated that stimulation NO production plays a vital role in inducing the SOD-CAT system to handle the problems associated with enhanced TiO₂ NP-induced ROS production and subsequent oxidative stress in magur catfish as a unique adaptational strategy. However, the NO-mediated induction of glutathione-related antioxidant genes under TiO₂ NP-induced oxidative stress is yet to be established.

{"title":"Nitric oxide-mediated induction of superoxide dismutase and catalase genes, and altered expression of glutathione-dependent genes to defend against the TiO2 NP-induced oxidative stress in primary hepatocytes of air-breathing catfish, Clarias magur","authors":"Elvis Khongmawloh , Debaprasad Koner , Revelbornstar Snaitang, Nirmalendu Saha","doi":"10.1016/j.cbpc.2025.110188","DOIUrl":"10.1016/j.cbpc.2025.110188","url":null,"abstract":"<div><div>The main objectives of the present investigation were to elucidate the possible induction of antioxidant genes under the TiO<sub>2</sub> NP-induced oxidative stress and the potential involvement of endogenously produced nitric oxide (NO) in its antioxidant strategies in primary hepatocytes of air-breathing magur catfish (<em>Clarias magur</em>). As expected, exposure to TiO<sub>2</sub> NPs led to (1) more ROS production as evidenced by a sharp rise of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and malonaldehyde (MDA) associated with cellular damage as evidenced by the increase of lactate dehydrogenase (LDH) leakage from hepatocytes, (2) induction of superoxide dismutase (SOD), catalase (CAT), followed by induction of different glutathione-related genes such as glutathione peroxidase (GPx), glutathione-S-transferase (GST), and thioredoxin glutathione reductase (TGR) with the induction of activities of corresponding enzymes, and (3) more production of NO associated with induction of inducible nitric oxide synthase (iNOS) activity and its corresponding gene. However, inhibition of NO production in primary hepatocytes using certain inhibitors in the presence of TiO<sub>2</sub> NPs, resulted in (1) more generation of H<sub>2</sub>O<sub>2</sub> and MDA, (2) inhibition of SOD and CAT genes expression in primary hepatocytes with more leakage of LDH leakage into the culture media. Thus, it can be contemplated that stimulation NO production plays a vital role in inducing the SOD-CAT system to handle the problems associated with enhanced TiO<sub>2</sub> NP-induced ROS production and subsequent oxidative stress in magur catfish as a unique adaptational strategy. However, the NO-mediated induction of glutathione-related antioxidant genes under TiO<sub>2</sub> NP-induced oxidative stress is yet to be established.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110188"},"PeriodicalIF":3.9,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591939","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

Sublethal 6PPD-quinone exposure impairs swimming performance and aerobic metabolism in juvenile lake trout (Salvelinus namaycush)

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 : 2025-03-04 DOI: 10.1016/j.cbpc.2025.110166

Summer Selinger , Blake Hunnie , Catherine Roberts , Mawuli Amekor , Natacha Hogan , Steve Wiseman , Markus Hecker , Lynn Weber , David Janz , Markus Brinkmann

6PPD-quinone, an environmental oxidation product of the rubber tire antioxidant 6PPD, has recently gained recognition as a chemical of concern. Frequently detected in road runoff and surface waters, studies have reported this compound to cause acute lethality in several salmonid species at extremely low concentrations, including lake trout (Salvelinus namaycush; 24-h LC₅₀ = 0.51 μg/L). Following exposure, species experiencing acute lethality show characteristic symptoms such as gasping, spiraling, increased ventilation, loss of equilibrium, erratic movements, and tumbling. However, there is a deficit of research targeted at understanding sublethal toxicities of 6PPD-quinone exposure, particularly concerning swimming capability and metabolic function. To evaluate these effects, juvenile lake trout were exposed for 20 h to a measured concentration of 0.46 μg/L 6PPD-quinone in a swim tunnel respirometer to assess temporal changes in standard metabolic rate (SMR) compared to controls. Following exposure, fish underwent a swim trial to determine critical swimming speed (U_crit), oxygen consumption rate (MO₂), active metabolic rate (AMR), aerobic scope (AS) and energetic cost of transport (CoT), followed by analysis of muscle triglyceride and glycogen concentrations. Results showed that 6PPD-quinone exposure impaired swimming performance, evident by a decrease in U_crit. Additionally, exposure resulted in decreased AMR, although alterations in SMR were not observed. Decreased concentrations of muscle triglycerides of swam fish were also observed. These findings suggest that environmentally relevant concentrations of 6PPD-quinone disrupt aerobic metabolic capacity in juvenile lake trout, producing adverse effects that diminish endurance and maximum swim speeds, which may affect survival of fish populations.

{"title":"Sublethal 6PPD-quinone exposure impairs swimming performance and aerobic metabolism in juvenile lake trout (Salvelinus namaycush)","authors":"Summer Selinger , Blake Hunnie , Catherine Roberts , Mawuli Amekor , Natacha Hogan , Steve Wiseman , Markus Hecker , Lynn Weber , David Janz , Markus Brinkmann","doi":"10.1016/j.cbpc.2025.110166","DOIUrl":"10.1016/j.cbpc.2025.110166","url":null,"abstract":"<div><div>6PPD-quinone, an environmental oxidation product of the rubber tire antioxidant 6PPD, has recently gained recognition as a chemical of concern. Frequently detected in road runoff and surface waters, studies have reported this compound to cause acute lethality in several salmonid species at extremely low concentrations, including lake trout (<em>Salvelinus namaycush</em>; 24-h LC<sub>50</sub> = 0.51 μg/L). Following exposure, species experiencing acute lethality show characteristic symptoms such as gasping, spiraling, increased ventilation, loss of equilibrium, erratic movements, and tumbling. However, there is a deficit of research targeted at understanding sublethal toxicities of 6PPD-quinone exposure, particularly concerning swimming capability and metabolic function. To evaluate these effects, juvenile lake trout were exposed for 20 h to a measured concentration of 0.46 μg/L 6PPD-quinone in a swim tunnel respirometer to assess temporal changes in standard metabolic rate (SMR) compared to controls. Following exposure, fish underwent a swim trial to determine critical swimming speed (U<sub>crit</sub>), oxygen consumption rate (MO<sub>2</sub>), active metabolic rate (AMR), aerobic scope (AS) and energetic cost of transport (CoT), followed by analysis of muscle triglyceride and glycogen concentrations. Results showed that 6PPD-quinone exposure impaired swimming performance, evident by a decrease in U<sub>crit</sub>. Additionally, exposure resulted in decreased AMR, although alterations in SMR were not observed. Decreased concentrations of muscle triglycerides of swam fish were also observed. These findings suggest that environmentally relevant concentrations of 6PPD-quinone disrupt aerobic metabolic capacity in juvenile lake trout, producing adverse effects that diminish endurance and maximum swim speeds, which may affect survival of fish populations.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"294 ","pages":"Article 110166"},"PeriodicalIF":3.9,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572258","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 essential oils on enzymes activity, reserve products, biomarkers, and gene expression of Tribolium castaneum

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 : 2025-03-02 DOI: 10.1016/j.cbpc.2025.110167

Houssam Annaz , Francesco Cacciola , Ayoub Kounnoun , Noureddin Bouayad , Kacem Rharrabe

Essential oils (EOs) are concentrated volatiles renowned for their strong fumigant, contact, feeding deterrence, and repellent effects. These oils can disrupt vital functions and the activity of essential enzymes in major stored product pests like Tribolium castaneum. Hence, the study of the physiological effects of these EOs can provide a better understanding of the impact of EOs and propose new strategies for the control of this pest. Therefore, this review aims to review available data regarding the potential impact of EOs on T. castaneum enzyme activities, biomarkers, gene expression, and transcriptomic profile. Articles retrieved provide interesting findings regarding the activity of digestive enzymes (α-amylase, alanine aminotransferase, and aspartate aminotransferase) detoxification enzymes (cytochrome P450 monooxygenase, esterase, glutathione S-transferase), antioxidant enzymes (catalase, superoxide dismutase) and acetylcholinesterase, ATPase, in adults and larvae exposed to different EOs. Moreover, some articles evaluated the content reserve products (proteins, lipids, carbohydrates) and biomarkers linked to stress (reactive oxygen species), lipid peroxidation (conjugated diene, malondialdehyde), and antioxidant system (reduced and oxidized glutathione). Other molecular aspects were also evaluated, including transcriptomics and gene expression, to assess the physiological interactions after exposure to EOs.

{"title":"Impact of essential oils on enzymes activity, reserve products, biomarkers, and gene expression of Tribolium castaneum","authors":"Houssam Annaz , Francesco Cacciola , Ayoub Kounnoun , Noureddin Bouayad , Kacem Rharrabe","doi":"10.1016/j.cbpc.2025.110167","DOIUrl":"10.1016/j.cbpc.2025.110167","url":null,"abstract":"<div><div>Essential oils (EOs) are concentrated volatiles renowned for their strong fumigant, contact, feeding deterrence, and repellent effects. These oils can disrupt vital functions and the activity of essential enzymes in major stored product pests like <em>Tribolium castaneum</em>. Hence, the study of the physiological effects of these EOs can provide a better understanding of the impact of EOs and propose new strategies for the control of this pest. Therefore, this review aims to review available data regarding the potential impact of EOs on <em>T. castaneum</em> enzyme activities, biomarkers, gene expression, and transcriptomic profile. Articles retrieved provide interesting findings regarding the activity of digestive enzymes (α-amylase, alanine aminotransferase, and aspartate aminotransferase) detoxification enzymes (cytochrome P450 monooxygenase, esterase, glutathione S-transferase), antioxidant enzymes (catalase, superoxide dismutase) and acetylcholinesterase, ATPase, in adults and larvae exposed to different EOs. Moreover, some articles evaluated the content reserve products (proteins, lipids, carbohydrates) and biomarkers linked to stress (reactive oxygen species), lipid peroxidation (conjugated diene, malondialdehyde), and antioxidant system (reduced and oxidized glutathione). Other molecular aspects were also evaluated, including transcriptomics and gene expression, to assess the physiological interactions after exposure to EOs.</div></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":"293 ","pages":"Article 110167"},"PeriodicalIF":3.9,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0