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Article: Ferulic acid attenuates difenoconazole exposure induced liver injury in carp by modulating oxidative damage, inflammation and apoptosis.

Sun, Ying / Jin, Xiaohui / Yang, Zuwang / Hu, Zunhan / Li, Qiulu / Dong, Jingquan / Fu, Mian

Comparative biochemistry and physiology. Toxicology & pharmacology : CBP

2024 Volume 280, Page(s) 109885

Abstract: Difenoconazole (DFZ) is a widely used triazole fungicide in agricultural production. However, the presence of DFZ residue in the environment poses a significant risk to non-target organisms. Ferulic acid (FA) is a phenolic compound known for its ... ...

Abstract	Difenoconazole (DFZ) is a widely used triazole fungicide in agricultural production. However, the presence of DFZ residue in the environment poses a significant risk to non-target organisms. Ferulic acid (FA) is a phenolic compound known for its antioxidant and anti-inflammatory properties. This study aims to investigate the hepatic damage caused by DFZ in carp and explore the mechanism through which FA alleviates this damage. The findings revealed that FA enhanced the antioxidant capability of the carp's liver and reduced the accumulation of reactive oxygen species (ROS) in the liver tissue. Moreover, FA regulated the transcriptional levels of inflammation-related factors, effectively preventing the inflammatory response triggered by the NF-κB signaling pathway. Additionally, TUNEL results demonstrated that DFZ initiated apoptosis, while dietary supplementation with FA decreased the protein expression levels of Bax and Cytochrome C (Cyt c) and the transcriptional levels of bax, caspase3, caspase9, p53 genes. Furthermore, FA increased the protein expression and transcriptional levels of Bcl-2. In conclusion, FA protects against liver injury induced by DFZ exposure in carp by modulating oxidative damage, inflammation, and apoptosis.
MeSH term(s)	Animals ; Antioxidants/pharmacology ; Carps ; bcl-2-Associated X Protein ; Chemical and Drug Induced Liver Injury, Chronic ; Oxidative Stress ; Inflammation/chemically induced ; Triazoles/toxicity ; Apoptosis ; Coumaric Acids ; Dioxolanes
Chemical Substances	Antioxidants ; ferulic acid (AVM951ZWST) ; difenoconazole (D9612XCH4P) ; bcl-2-Associated X Protein ; Triazoles ; Coumaric Acids ; Dioxolanes
Language	English
Publishing date	2024-03-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	189285-x
ISSN	1532-0456 ; 0306-4492 ; 0742-8413
ISSN	1532-0456 ; 0306-4492 ; 0742-8413
DOI	10.1016/j.cbpc.2024.109885
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Article ; Online: Abamectin causes cardiac dysfunction in carp via inhibiting redox equilibrium and resulting in immune inflammatory response and programmed cell death

Zhao, Panpan / Wang, Yan / Yang, Qiankun / Yu, Guili / Ma, Fenfen / Dong, Jingquan

Environ Sci Pollut Res. 2023 Mar., v. 30, no. 11 p.29494-29509

2023

Abstract: This study aims to investigate the effects of environmentally relevant concentrations of abamectin on the cardiac function of carp and the potential mechanisms. Here, male carp were exposed to abamectin, and cardiac function-related enzymatic markers ... ...

Abstract	This study aims to investigate the effects of environmentally relevant concentrations of abamectin on the cardiac function of carp and the potential mechanisms. Here, male carp were exposed to abamectin, and cardiac function-related enzymatic markers were examined. Cardiac histopathology, redox equilibrium, inflammation, and cell death were evaluated. Abamectin exposure caused cardiac dysfunction by upregulating lactate dehydrogenase (LDH), aspartate aminotransferase (AST), creatine kinase (CK), creatine Kinase MB isoenzyme (CK-MB) and white blood cells (WBCs), and decreasing red blood cells (RBCs) and hemoglobin (Hb). DHE staining and biochemical assays revealed that abamectin caused ROS release and oxidative stress by inhibiting Nrf2-ARE pathway. Histopathological and real-time fluorescence quantitative PCR (RT-qPCR) assays revealed that abamectin caused myocardial fiber swelling and inflammatory cell infiltration, enhanced pro-inflammatory cytokines tumor necrosis factor-α (Tnf-α), interleukin-1 beta (Il-1β), and Il-6 levels and attenuated anti-inflammatory cytokines Il-10 and transforming growth factor beta 1 (Tgf-β1) through activating NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome and nuclear factor kappa-B (NF-κB) pathway. Tunel staining showed that abamectin triggered cardiac apoptosis via activating p53-mediated mitochondrial apoptosis with elevated bcl2-associated X (Bax), reduced B-cell lymphoma-2 (Bcl-2), and activated Caspase-9 and Caspase-3. Immunoblot analysis revealed that abamectin activated autophagic flow by inhibiting mammalian target of rapamycin (mTOR), resulting in the conversion of LC3B from LC3-I to LC3-II, elevation of autophagy protein 5 (Atg5), and reduction of p62. Overall, abamectin caused cardiac dysfunction in carp via inhibiting redox equilibrium and resulting in immune inflammatory response and programmed cell death.
Keywords	B-lymphocytes ; abamectin ; apoptosis ; aspartate transaminase ; autophagy ; cardiac output ; carp ; caspase-3 ; caspase-9 ; creatine kinase ; fluorescence ; hemoglobin ; histopathology ; inflammasomes ; inflammation ; interleukin-10 ; interleukin-1beta ; interleukin-6 ; isozymes ; lactate dehydrogenase ; males ; mammals ; mitochondria ; necrosis ; neoplasms ; oxidative stress ; quantitative polymerase chain reaction ; rapamycin
Language	English
Dates of publication	2023-03
Size	p. 29494-29509.
Publishing place	Springer Berlin Heidelberg
Document type	Article ; Online
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-022-24004-6
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Article ; Online: Pesticide avermectin-induced hepatotoxicity and growth inhibition in carp: Ameliorative capacity and potential mechanisms of quercetin as a dietary additive.

Xin, Yue / Li, Xueqing / Ping, Kaixin / Xiang, Yannan / Li, Mengxin / Li, Xing / Yang, Haitao / Dong, Jingquan

Aquatic toxicology (Amsterdam, Netherlands)

2024 Volume 268, Page(s) 106859

Abstract: Flavonoid quercetin (QUE) has biological activities of anti-oxidation, anti-inflammation and anti-apoptosis, however, its protective effects against avermectin (AVM) induced liver toxicity in carp remains unclear. The objective of this research is to ... ...

Abstract	Flavonoid quercetin (QUE) has biological activities of anti-oxidation, anti-inflammation and anti-apoptosis, however, its protective effects against avermectin (AVM) induced liver toxicity in carp remains unclear. The objective of this research is to explore the biologically potent effects of QUE in AVM-induced hepatotoxicity in carp and its underlying mechanism. Therefore, we established a liver injury model in carp induced by AVM to evaluate QUE against AVM induced liver toxicity in carp. In this investigation, AVM dosage was determined as 2.404 μg/L for both groups, and an experimentation of 30 days duration was carried out. Various methods including hematoxylin and eosin (H&E) staining, biochemical kits, real-time quantitative PCR (qRT-PCR), western blotting, TUNEL, reactive oxygen species (ROS) staining, immunofluorescence (Hoseinifar, et al.,), and oil red O staining were used in this study. Results showed that the growth inhibition of carp was relieved in the QUE treatment group comparing to the AVM group. In the QUE treatment group, there was a significant decrease in the levels of ALT and AST in carp liver tissue. Additionally, the histopathological damage and lipid accumulation were alleviated compared to the AVM group. Moreover, QUE prevented AVM induced decrease in the activities of antioxidant enzymes of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), glutathione (GSH), catalase (CAT) and the accumulation of reactive oxygen species (ROS), but reduced accumulation of malondialdehyde (MDA). In addition, the mRNA levels of liver pro-inflammatory factors of tumor necrosis factor-α (TNF-α), interleukin-1β (iL-1β), interleukin-6 (iL-6), interleukin-10 (iL-10) and the protein levels of NOD-like receptor protein 3 (NLRP3) inflammasome were significantly down-regulated in the QUE treatment group in comparison to the AVM group. We also found that QUE could affect the expression of Bcl2-associated x (Bax), B-cell lymphoma-2 (Bcl-2), cleaved-cysteinyl aspartate specific proteinase (CCaspase3) key apoptotic proteins and TUNEL-labeled apoptotic hepatocytes by regulating SIRT1/FOXO3a signal pathway. In summary, QUE alleviated the growth inhibition, liver oxidative damage, lipid accumulation, inflammatory response, and apoptosis of carp induced by AVM. QUE is a potential protective agent against liver injury induced by AVM in carp.
MeSH term(s)	Animals ; Quercetin/pharmacology ; Reactive Oxygen Species/metabolism ; Carps/metabolism ; Water Pollutants, Chemical/toxicity ; Antioxidants/pharmacology ; Antioxidants/metabolism ; Oxidative Stress ; Glutathione/metabolism ; Apoptosis ; Chemical and Drug Induced Liver Injury/prevention & control ; Lipids ; Ivermectin/analogs & derivatives
Chemical Substances	Quercetin (9IKM0I5T1E) ; Reactive Oxygen Species ; avermectin (73989-17-0) ; Water Pollutants, Chemical ; Antioxidants ; Glutathione (GAN16C9B8O) ; Lipids ; Ivermectin (70288-86-7)
Language	English
Publishing date	2024-02-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	782699-0
ISSN	1879-1514 ; 0166-445X
ISSN (online)	1879-1514
ISSN	0166-445X
DOI	10.1016/j.aquatox.2024.106859
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Article ; Online: Immunoprotective effect of silybin through blocking p53-driven caspase-9-Apaf-1-Cyt c complex formation and immune dysfunction after difenoconazole exposure in carp spleen.

Pan, Enzhuang / Xin, Yue / Li, Xueqing / Ping, Kaixin / Li, Xing / Sun, Ying / Xu, Xuhui / Dong, Jingquan

Environmental science and pollution research international

2024 Volume 31, Issue 13, Page(s) 19396–19408

Abstract: As a broad-spectrum and efficient triazole fungicide, difenoconazole is widely used, which not only pollutes the environment but also exerts toxic effects on non-target organisms. The spleen plays an important role in immune protection as an important ... ...

Abstract	As a broad-spectrum and efficient triazole fungicide, difenoconazole is widely used, which not only pollutes the environment but also exerts toxic effects on non-target organisms. The spleen plays an important role in immune protection as an important secondary lymphoid organ in carp. In this study, we assessed the protective impact of silybin as a dietary additive on spleen tissues of carp during exposure to difenoconazole. Sixty carp were separated into four groups for this investigation including control group, difenoconazole group, silybin group, and silybin and difenoconazole group. By hematoxylin-eosin staining, dihydroethidium staining, immunohistochemical staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, quantitative real-time PCR assay, Western blot analysis, biochemical assays, and immune function indicator assays, we found that silybin could prevent difenoconazole-induced spleen tissue damage, oxidative stress, and immune dysfunction, and inhibited apoptosis of carp spleen tissue cells by suppressing the formation of p53-driven caspase-9-apoptotic protease activating factor-1-cytochrome C complex. The results suggested that silybin as a dietary additive could improve spleen tissue damage and immune dysfunction induced by difenoconazole in aquaculture carp.
MeSH term(s)	Animals ; Spleen/metabolism ; Caspase 9/pharmacology ; Tumor Suppressor Protein p53 ; Silybin/pharmacology ; Carps/metabolism ; Cytochromes c/metabolism ; Apoptosis ; Triazoles/pharmacology ; Dioxolanes
Chemical Substances	Caspase 9 (EC 3.4.22.-) ; Tumor Suppressor Protein p53 ; difenoconazole (D9612XCH4P) ; Silybin (4RKY41TBTF) ; Cytochromes c (9007-43-6) ; Triazoles ; Dioxolanes
Language	English
Publishing date	2024-02-15
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-024-32392-0
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Article ; Online: Gypenoside XLIX Activates the Sirt1/Nrf2 Signaling Pathway to Inhibit NLRP3 Inflammasome Activation to Alleviate Septic Acute Lung Injury.

Ping, Kaixin / Yang, Rongrong / Chen, Huizhen / Xie, Shaocheng / Xiang, Yannan / Li, Mengxin / Lu, Yingzhi / Dong, Jingquan

Inflammation

2024

Abstract: Currently, treatment options for acute lung injury (ALI) are limited. Gypenoside XLIX (Gyp-XLIX) is known for its anti-inflammatory properties, but there is a lack of extensive research on its effects against ALI. This study induced ALI in mice through ... ...

Abstract	Currently, treatment options for acute lung injury (ALI) are limited. Gypenoside XLIX (Gyp-XLIX) is known for its anti-inflammatory properties, but there is a lack of extensive research on its effects against ALI. This study induced ALI in mice through cecal ligation and puncture surgery and investigated the biological activity and potential mechanisms of Gypenoside XLIX (40 mg/kg) by intraperitoneal injection. The in vitro ALI model was established using mouse lung epithelial (MLE-12) cells stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). Various methods, including Hematoxylin and Eosin (H&E) staining, biochemical assay kits, Quantitative Polymerase Chain Reaction (qPCR) analysis, Western blotting, Terminal deoxynucleotidyl transferase dUTP Nick End Labeling (TUNEL) assay, immunofluorescence, and flow cytometry, were employed for this research. The results indicated that pretreatment with Gypenoside XLIX significantly alleviated pathological damage in mouse lung tissues and reduced the expression levels of inflammatory factors. Additionally, Gypenoside XLIX inhibited ROS levels and NLRP3 inflammasome, possibly mediated by the Sirt1/Nrf2 signaling pathway. Moreover, Gypenoside XLIX significantly inhibited sepsis-induced lung cell apoptosis and excessive autophagy of mitochondria. Specifically, it suppressed mitochondrial pathway apoptosis and the Pink1/Parkin pathway of mitochondrial autophagy. These findings reveal the multifaceted effects of Gypenoside XLIX in anti-inflammatory, antioxidative, and inhibition of cell apoptosis and autophagy. This provides strong support for its therapeutic potential in sepsis-related lung injuries.
Language	English
Publishing date	2024-05-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	434408-x
ISSN	1573-2576 ; 0360-3997
ISSN (online)	1573-2576
ISSN	0360-3997
DOI	10.1007/s10753-024-02041-2
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Article ; Online: Malvidin alleviates LPS-induced septic intestinal injury through the nuclear factor erythroid 2-related factor 2/reactive oxygen species/NLRP3 inflammasome pathway.

Wang, Guanglu / Ma, Fenfen / Zhang, Wei / Xin, Yue / Ping, Kaixin / Wang, Yan / Dong, Jingquan

Inflammopharmacology

2023 Volume 32, Issue 1, Page(s) 893–901

Abstract: Emerging evidence suggests that the gastrointestinal tract plays a crucial role in the pathophysiology of sepsis, a leading cause of mortality among patients admitted to the intensive care unit (ICU). Malvidin, belonging to the flavonoid family of ... ...

Abstract	Emerging evidence suggests that the gastrointestinal tract plays a crucial role in the pathophysiology of sepsis, a leading cause of mortality among patients admitted to the intensive care unit (ICU). Malvidin, belonging to the flavonoid family of compounds, exhibits a range of capabilities including anti-inflammatory and antioxidant properties. Studies have demonstrated that Malvidin exhibits a dose-dependent effect in mitigating sepsis-induced intestinal injury. The advantageous impact of Malvidin in safeguarding against sepsis-induced intestinal injury is associated with its capacity to counteract oxidative stress, inhibit cellular apoptosis, diminish the secretion of pro-inflammatory cytokines, and regulate the synthesis of inflammasomes. The findings indicate that Malvidin, a natural compound, exhibits protective effects on the gut by activating the nuclear factor erythroid 2-related factor 2/reactive oxygen species/NLRP3 inflammasome pathway. These results have significant implications for potential clinical applications and offer valuable insights into the treatment of sepsis-induced intestinal injury.
MeSH term(s)	Humans ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Reactive Oxygen Species ; Lipopolysaccharides ; Sepsis/drug therapy ; Anthocyanins
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; malvidin (10463-84-0) ; Reactive Oxygen Species ; Lipopolysaccharides ; Anthocyanins
Language	English
Publishing date	2023-12-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1080058-x
ISSN	1568-5608 ; 0925-4692
ISSN (online)	1568-5608
ISSN	0925-4692
DOI	10.1007/s10787-023-01378-8
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Article ; Online: Abamectin causes toxicity to the carp respiratory system by triggering oxidative stress, inflammation, and apoptosis and inhibiting autophagy.

Feng, Huimiao / Zhou, Ping / Liu, Feixue / Zhang, Wei / Yang, Haitao / Li, Xueqing / Dong, Jingquan

Environmental science and pollution research international

2023 Volume 30, Issue 19, Page(s) 55200–55213

Abstract: Abamectin is a commonly used pesticide in agriculture and fisheries and poses a risk to aquatic species. However, the mechanism of its toxic effects on fish remains to be discovered. In this study, we explored the effects of abamectin exposure at ... ...

Abstract	Abamectin is a commonly used pesticide in agriculture and fisheries and poses a risk to aquatic species. However, the mechanism of its toxic effects on fish remains to be discovered. In this study, we explored the effects of abamectin exposure at different concentrations on the respiratory system of carp. Carp were divided into three groups, namely the control group, low-dose abamectin treatment group, and high-dose abamectin treatment group. Gill tissue was collected after abamectin exposure for histopathological, biochemical, tunnel, mRNA, and protein expression analysis. Histopathological analysis indicated that abamectin damaged the gill structure. Biochemical analysis showed that abamectin triggered oxidative stress with lowered antioxidant enzyme activities and increased MDA content. Moreover, abamectin led to enhanced INOS levels and pro-inflammatory transcription, activating inflammation. Tunnel results demonstrated that exposure to abamectin induced gill cell apoptosis through an exogenous pathway. In addition, exposure to abamectin activated the PI3K/AKT/mTOR pathway, leading to inhibition of autophagy. Overall, abamectin caused respiratory system toxicity in carp via triggering oxidative stress, inflammation, and apoptosis and inhibiting autophagy. The study suggests that abamectin has a profound toxicity mechanism in the respiratory system of carp, contributing to a better understanding of pesticide risk assessment in aquatic systems.
MeSH term(s)	Animals ; Carps/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Oxidative Stress ; Antioxidants/metabolism ; Apoptosis ; Inflammation/chemically induced ; Respiratory System/metabolism ; Pesticides/pharmacology ; Autophagy
Chemical Substances	abamectin (5U8924T11H) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Antioxidants ; Pesticides
Language	English
Publishing date	2023-03-08
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-023-26166-3
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Article ; Online: Disruption of the intestinal barrier by avermectin in carp involves oxidative stress and apoptosis and leads to intestinal inflammation

Han, Hairui / He, Nana / Pan, Enzhuang / Tan, Xuelian / Yang, Zuwang / Li, Xueqing / Shi, Dahua / Dong, Jingquan

Pesticide Biochemistry and Physiology. 2023, p.105531-

2023 , Page(s) 105531–

Abstract: Avermectin (AVM) is a widely used insecticide. Due to its sensitive toxicity to aquatic organisms, the toxicology of AVM on fish intestines remains unclear. Here, we established a 96 h AVM acute toxicity model to explore the effects of AVM on the ... ...

Abstract	Avermectin (AVM) is a widely used insecticide. Due to its sensitive toxicity to aquatic organisms, the toxicology of AVM on fish intestines remains unclear. Here, we established a 96 h AVM acute toxicity model to explore the effects of AVM on the intestinal tract of carp. The 96 h LC₅₀ of carps exposed to AVM was 24.04 μg/L, 12.02 μg/L was selected as the high-dose group and 3.005 μg/L was selected as the low-dose group. After 96 h of exposure, intestinal tissues were collected and subsequently analyzed for histopathology, the activities of antioxidant oxidases (CAT, SOD, GSH-Px), and the expression of mRNA associated with oxidative stress, inflammation, and apoptosis. Our study showed that AVM exposure caused intestinal damage in carp, decreased the expression of the tight junction protein gene, activated oxidative stress, induced apoptosis, and induced intestinal inflammation in carp. Therefore, we demonstrated that AVM exposure compromised the integrity of the intestinal barrier in carp, activated oxidative stress, induced endogenous apoptosis, and induced intestinal inflammatory responses. These results indicate that AVM, as a drug-sensitive to aquatic organisms, has a much more complex toxic effect on the fish intestinal tract, which provides a new perspective for studying the toxicology of AVM on the fish intestinal tract.
Keywords	acute toxicity ; antioxidants ; apoptosis ; avermectins ; carp ; genes ; histopathology ; inflammation ; insecticides ; intestines ; models ; oxidative stress ; oxidoreductases ; physiology ; tight junctions ; toxicology ; Avermectin ; Intestinal barrier
Language	English
Publishing place	Elsevier Inc.
Document type	Article ; Online
Note	Pre-press version
ZDB-ID	184819-7
ISSN	1095-9939 ; 0048-3583 ; 0048-3575
ISSN (online)	1095-9939
ISSN	0048-3583 ; 0048-3575
DOI	10.1016/j.pestbp.2023.105531
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Article ; Online: Protective effect of quercetin on avermectin induced splenic toxicity in carp: Resistance to inflammatory response and oxidative damage

Pan, Enzhuang / Chen, Huizhen / Wu, Xinyu / He, Nana / Gan, Jiajie / Feng, Huimiao / Sun, Yong / Dong, Jingquan

Pesticide Biochemistry and Physiology. 2023 June, v. 193 p.105445-

2023

Abstract: Avermectin pollution is an important problem that cannot be ignored in aquatic system in recent years. It has brought great trouble to freshwater aquaculture, especially fishery aquaculture. Plant-derived quercetin has anti-inflammatory and antioxidant ... ...

Abstract	Avermectin pollution is an important problem that cannot be ignored in aquatic system in recent years. It has brought great trouble to freshwater aquaculture, especially fishery aquaculture. Plant-derived quercetin has anti-inflammatory and antioxidant properties and is widely used as a dietary additive, but its protective effect on immune damage induced by avermectin in freshwater carp remains unclear. This study evaluated the role of dietary additive quercetin supplementation in chronic avermectin exposure of carp spleen. Sixty carp were divided into 4 groups (n = 15/ group), including control group, avermectin treatment group, quercetin treatment group, quercetin and avermectin co-treatment group. Carp were exposed to a 1/10 96 h LC₅₀ dose of avermectin for 30 d and fed a carp diet containing 400 mg/kg quercetin twice a day (3% body weigh/ carp). The results showed that chronic avermectin exposure caused the loose parenchymal structure of carp spleen tissue and the increase of inflammatory cells, accompanied by increased transcription levels of pro-inflammatory il-1β, il-6, tnf-α and decreased levels of anti-inflammatory factors il-10 and tgf-β1, ROS accumulation in spleen tissue. MDA content increased and T-AOC, CAT and GSH levels decreased. Quercetin down-regulates the NF-κB pathway by inhibiting the expression of iNOS and activating p38 MAPK, blocking the transcription of inflammatory factors, and alleviating the inflammation of carp spleen caused by chronic avermectin exposure. In addition, quercetin inhibits the over-activation of Nrf2/Keap-1 signaling axis, blocks ROS accumulation, and restores the spleen REDOX homeostasis. In conclusion, quercetin, as a dietary additive for carp feed, can effectively improve the immune damage caused by avermectin pollution in aquatic environment, resist spleen inflammation and oxidative stress, and provide a theoretical basis for clinical development of freshwater carp feed.
Keywords	antioxidants ; aquatic environment ; avermectins ; carp ; diet ; fisheries ; freshwater aquaculture ; homeostasis ; inflammation ; interleukin-10 ; interleukin-6 ; mitogen-activated protein kinase ; oxidative stress ; pesticides ; pollution ; protective effect ; quercetin ; spleen ; toxicity ; Avermectin ; Splenic toxicity ; Oxidative damage
Language	English
Dates of publication	2023-06
Publishing place	Elsevier Inc.
Document type	Article ; Online
ZDB-ID	184819-7
ISSN	1095-9939 ; 0048-3583 ; 0048-3575
ISSN (online)	1095-9939
ISSN	0048-3583 ; 0048-3575
DOI	10.1016/j.pestbp.2023.105445
Database	NAL-Catalogue (AGRICOLA)

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Article: Difenoconazole causes cardiotoxicity in common carp (Cyprinus carpio): Involvement of oxidative stress, inflammation, apoptosis and autophagy

Wang, Jinxin / Gao, Xuzhu / Liu, Feixue / FangWang / Dong, Jingquan / Zhao, Panpan

Chemosphere. 2022 Nov., v. 306

2022

Abstract: Difenoconazole, a commonly used broad-spectrum triazole fungicide, is widely applied to fish culture in paddy fields. Due to its high chemical stability, low biodegradability, and easy transfer, difenoconazole persists in aquatic systems, raising public ... ...

Abstract	Difenoconazole, a commonly used broad-spectrum triazole fungicide, is widely applied to fish culture in paddy fields. Due to its high chemical stability, low biodegradability, and easy transfer, difenoconazole persists in aquatic systems, raising public awareness of environmental threats. Difenoconazole causes cardiotoxicity in carp, however, the potential mechanisms of difenoconazole-induced cardiotoxicity remain unclear. Here, common carp were exposed to difenoconazole, and cardiotoxicity was evaluated by measuring the creatine kinase (CK) and the lactate dehydrogenase (LDH) in the serum. Cardiac pathological injury was determined by HE staining. The content and expression of oxidative stress indicators were detected using biochemical kits and qPCR analysis. Changes in inflammation-related cytokines were examined by qPCR. Apoptosis levels were assessed by TUNEL assay and qPCR. The occurrence of autophagy was measured by western blotting detection of autophagy flux LC3II/LC3I, and autophagy regulatory pathways were detected using qPCR. The results showed that difenoconazole exposure induced cardiotoxicity accompanied by obviously elevated LDH and CK levels and caused myocardial fibers to swell and inflammatory cells to increase. Elevated peroxide MDA and reduced transcriptional and activity levels of the antioxidant enzymes CAT, SOD and GSH-Px were dependent on the Nrf2/Keap-1 pathway. Moreover, the proinflammatory cytokines IL-1β, IL-6, and TNF-α were upregulated, iNOS activity was enhanced, whereas the anti-inflammatory cytokines TGF-β1 and IL-10 were downregulated after exposure to difenoconazole. Moreover, apoptosis was observed in the TUNEL assay and mediated through the p53/Bcl-2/Bax-Caspase-9 mitochondrial pathway. Furthermore, difenoconazole increased the autophagy markers LC3II, ATG5 and p62 and regulated them through the PI3K/AKT/mTOR pathway. Altogether, this study demonstrated that difenoconazole exposure caused common carp cardiotoxicity, which is regulated by oxidative stress, inflammation, apoptosis and autophagy, providing central data for toxicological risk assessment of difenoconazole in the ecological environment.
Keywords	Cyprinus carpio ; apoptosis ; autophagy ; biodegradability ; blood serum ; cardiotoxicity ; carp ; creatine kinase ; difenoconazole ; fish culture ; inflammation ; interleukin-10 ; interleukin-6 ; lactate dehydrogenase ; mitochondria ; oxidative stress ; paddies ; risk assessment ; toxicology ; transcription (genetics) ; triazoles
Language	English
Dates of publication	2022-11
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	120089-6
ISSN	1879-1298 ; 0045-6535 ; 0366-7111
ISSN (online)	1879-1298
ISSN	0045-6535 ; 0366-7111
DOI	10.1016/j.chemosphere.2022.135562
Database	NAL-Catalogue (AGRICOLA)

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