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1.
Ecotoxicol Environ Saf ; 222: 112514, 2021 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-34280841

RESUMO

Pendimethalin (PND) is one of the best sellers of selective herbicide in the world and has been frequently detected in the water. However, little is known about its effects on cardiac development. In this study, we used zebrafish to investigate the developmental and cardiac toxicity of PND. We exposed the zebrafish embryos with a serial of concentrations at 3, 4, and 5 mg/L at 5.5-72 h post-fertilization (hpf). We found that PND exposure can reduce the heart rate, survival rate, and body length of zebrafish embryos. Furthermore, we identified many malformations including pericardial and yolk sac edema, spinal deformity, and cardiac looping abnormality. In addition, PND increased the expression of reactive oxygen species and malondialdehyde and reduced the activity of superoxide dismutase (Antioxidant enzymes); We examined the expression of cardiac development-related genes and the apoptosis markers, and found changes of the following marker: vmhc, nppa, tbx5a, nkx2.5, gata4, tbx2b and FoxO1, bax, bcl-2, p53, casp-9, casp-3. Our data showed that activation of Wnt pathway can rescue the cardiac abnormalities caused by PND. Our results provided new evidence for the toxicity of PND and suggested that the PND residual should be treated as a hazard in the environment.


Assuntos
Embrião não Mamífero , Peixe-Zebra , Compostos de Anilina , Animais , Apoptose , Cardiotoxicidade/metabolismo , Embrião não Mamífero/metabolismo , Estresse Oxidativo , Peixe-Zebra/metabolismo , Proteínas de Peixe-Zebra/genética , Proteínas de Peixe-Zebra/metabolismo
2.
Environ Toxicol ; 36(10): 2062-2072, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34227734

RESUMO

Quercetin is a flavonoid compound with a variety of biological properties that is widely distributed throughout the plant kingdom. Studies have found that quercetin has anti-inflammatory, antioxidant, and liver-protective effects, while thioacetamide (TAA) can cause inflammation and liver damage in zebrafish larvae. The purpose of this study was to evaluate whether quercetin can prevent TAA-induced inflammation and liver damage in zebrafish larvae and to investigate the molecular mechanisms involved. Zebrafish Tg transgenic lines were used as the experimental animals. Behavioral, oxidative stress level, proliferative antigen chromogenic antibody, and western blot analyses were carried out on zebrafish larvae in the control group and groups treated with TAA and 12 µM quercetin. The results indicated that quercetin promoted the development of zebrafish larvae damaged by TAA, exhibited antioxidant and anti-inflammatory properties, and promoted cell proliferation. Quercetin reduced the expression of p53 protein in zebrafish larvae injured by TAA, resulting in decreased levels of Bax and increased levels of Bcl-2. The findings suggested quercetin has antiapoptotic action. Quercetin reduced the expression of DKK1 and DKK2 genes related to the Wnt signaling pathway in zebrafish larvae damaged by TAA and increased the expression of Lef1 and wnt2bb. Quercetin may regulate the development of zebrafish larvae damaged by TAA through the Wnt signaling pathway. This study provides the scientific basis for the development and utilization of quercetin and the development of new related drugs.


Assuntos
Quercetina , Tioacetamida , Animais , Antioxidantes/metabolismo , Larva , Fígado/metabolismo , Estresse Oxidativo , Quercetina/farmacologia , Tioacetamida/toxicidade , Peixe-Zebra
3.
Aquat Toxicol ; 237: 105870, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34107429

RESUMO

Pyridaben is a widely used acaricide in agriculture and reaches a high concentration (97 µg/L) in paddy water for a short time when pyridaben was applied to rice. However, its toxicity to aquatic organisms is still poorly understood. Therefore, we assessed the pyridaben cardiotoxicity to aquatic organisms using the zebrafish (Danio rerio) model. We found that pyridaben is highly toxic to aquatic organisms, and LC50 of pyridaben for zebrafish at 72 hpf was 100.6 µg/L. Pyridaben caused severe cardiac malformations and functional abnormalities. Morphologic abnormity included severe pericardial edema, cardiomegaly, decreased cardiomyocytes, thinning of the myocardial layer, linear heart, and increased the distance between sinus venous and bulbus arteriosus (SV-BA). Functional failure included arrhythmia, heart failure, and reduced pumping efficiency. The genes involved in heart development, WNT signaling, BMP signaling, ATPase, and cardiac troponin C were abnormally expressed in the pyridaben treatment group. Exposure to pyridaben increased oxidative stress and induced cell apoptosis. The above causes may lead to cardiac toxicity. The results suggest that pyridaben exposure induced elevated oxidative stress through the WNT signaling pathway, which in turn led to apoptosis in the heart and cardiotoxicity. Besides, pyridaben exposure at the critical stage of cardiac looping (24-36 hpf) resulted in the greatest cardiotoxicity. The chorion reduced the entry of pyridaben and protected zebrafish embryos, resulting in cardiotoxicity second only to the stage of cardiac looping. The study should provide valuable information that pyridaben exposure causes cardiotoxicity in zebrafish embryos and have potential health risks for other aquatic organisms and humans.


Assuntos
Poluentes Químicos da Água , Peixe-Zebra , Animais , Cardiotoxicidade , Embrião não Mamífero , Humanos , Piridazinas , Poluentes Químicos da Água/toxicidade
4.
Environ Pollut ; 285: 117323, 2021 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-34091267

RESUMO

Evaluation of the toxicity of pesticide residues on non-target organisms in the ecosystem is an important part of pesticide environmental risk assessment. Flupyradifurone is a new type of butenolide insecticide produced by Bayer, who claims it to be "low toxic" to non-target organisms in the environment. However, there is little evidence in the literature to show how flupyradifurone affects aquatic organism development. In the current study, zebrafish embryos were treated with 0.1, 0.15, and 0.2 mg/mL of flupyradifurone within 6.0-72 h past fertilization (hpf). We found that the half-lethal concentration (LC50) of flupyradifurone for zebrafish embryos at 96 hpf was 0.21 mg/mL. Flupyradifurone decreases the heart rate, survival rate, and body length of zebrafish embryos. The flupyradifurone treatment also led to the failure of heart looping, and pericardial edema. Moreover, flupyradifurone increased the level of reactive oxygen species (ROS) and decreased the enzymatic catalysis of catalase (CAT) and superoxide dismutase (SOD). Alterations were induced in the transcription of apoptosis-related genes (bcl-2, bax, bax/bcl-2, p53 and caspase-9) and the heart development-related genes (gata4, myh6, nkx2.5, nppa, tbx2b, tbx5 and vmhc). In the current study, new evidences have been provided regarding the toxic effects of flupyradifurone and the risk of its residues in agricultural products and the environment.


Assuntos
Embrião não Mamífero , Peixe-Zebra , 4-Butirolactona/análogos & derivados , Animais , Apoptose , Ecossistema , Embrião não Mamífero/metabolismo , Desenvolvimento Embrionário , Estresse Oxidativo , Piridinas
5.
Environ Pollut ; 274: 116539, 2021 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-33549839

RESUMO

Bifenazate is a novel acaricide for selective foliar spraying and is widely used to control mites in agricultural production. However, its toxicity to aquatic organisms is unknown. Here, a zebrafish model was used to study bifenazate toxicity to aquatic organisms. Exposure to bifenazate was found to cause severe cardiotoxicity in zebrafish embryos, along with disorders in the gene expression related to heart development. Bifenazate also caused oxidative stress. Cardiotoxicity caused by bifenazate was partially rescued by astaxanthin (an antioxidant), accompanied by cardiac genes and oxidative stress-related indicators becoming normalized. Our results showed that exposure to bifenazate can significantly change the ATPase activity and gene expression levels of the calcium signaling pathway. These led to heart failure, in which the blood accumulated outside the heart without entering it, eventually leading to death. The results indicated that bifenazate exposure caused cardiotoxicity in zebrafish embryos through the induction of oxidative stress and inhibition of the calcium signaling pathway.


Assuntos
Cardiotoxicidade , Peixe-Zebra , Animais , Carbamatos/metabolismo , Cardiotoxicidade/metabolismo , Embrião não Mamífero/metabolismo , Hidrazinas , Estresse Oxidativo
6.
Chemosphere ; 263: 127860, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-32829219

RESUMO

Iprodione is a highly effective broad-spectrum fungicide commonly used for early disease control in fruit trees and vegetables. Pesticides often flow into watercourses due to rainfall, causing toxicity in non-target organisms, eventually entering the food chain. However, little information is available in the current literature about the toxicity of iprodione to cardiac development. The present study aimed to investigate the effect of iprodione on early embryonic development and its cardiotoxicity in aquatic animals, using zebrafish as a model. At 6-72 h post-fertilization (hpf), zebrafish were exposed to concentrations of 15 mg/L, 20 mg/L, and 25 mg/L (72 h-LC50 = 21.15 mg/L). We found that exposure to iprodione resulted in yolk edema, increased mortality, and shortened body length in zebrafish embryos. In addition, iprodione was also found to induce edema in the pericardium of zebrafish, decrease heart rate, and cause the failure of cardiac cyclization. Exposure to iprodione significantly increased the accumulation of ROS and altered the activity of antioxidant enzymes (MDA, CAT) in zebrafish embryos. Moreover, iprodione induced changes in the transcription levels of heart developmental-related genes and apoptosis-related genes. In addition, Astaxanthin (antioxidant) can partially rescue the toxic phenotype caused by iprodione. Apoptosis-related genes and heart developmental-related genes were rescued after astaxanazin treatment. The results suggest that iprodione induces developmental and cardiac toxicity in zebrafish embryos, which provides new evidence of the toxicity of iprodione to organisms in aquatic ecosystems and assessing human health risks.


Assuntos
Cardiotoxicidade , Peixe-Zebra , Aminoimidazol Carboxamida/análogos & derivados , Animais , Ecossistema , Embrião não Mamífero/metabolismo , Desenvolvimento Embrionário , Hidantoínas , Estresse Oxidativo
7.
Ecotoxicol Environ Saf ; 205: 111339, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32961491

RESUMO

Famoxadone-cymoxanil is a new protective and therapeutic fungicide, but little research has been done on it or its toxicity in aquatic organisms. In this study, we used zebrafish to investigate the cardiotoxicity of famoxadone-cymoxanil and the potential mechanisms involved. Zebrafish embryos were exposed to different concentrations of famoxadone-cymoxanil until 72 h post-fertilization (hpf), then changes of heart morphology in zebrafish embryos were observed. We also detected the levels of oxidative stress, myocardial-cell proliferation and apoptosis, ATPase activity, and the expression of genes related to the cardiac development and calcium-signaling pathway. After famoxadone-cymoxanil exposure, pericardial edema, cardiac linearization, and reductions in the heart rate and cardiac output positively correlated with concentration. Although myocardial-cell apoptosis was not detected, proliferation of the cells was severely reduced and ATPase activity significantly decreased, resulting in a severe deficiency in heart function. In addition, indicators of oxidative stress changed significantly after exposure of the embryos to the fungicide. To better understand the possible molecular mechanisms of cardiovascular toxicity in zebrafish, we studied the transcriptional levels of cardiac development, calcium-signaling pathways, and genes associated with myocardial contractility. The mRNA expression levels of key genes in heart development were significantly down-regulated, while the expression of genes related to the calcium-signaling pathway (ATPase [atp2a1], cardiac troponin C [tnnc1a], and calcium channel [cacna1a]) was significantly inhibited. Expression of klf2a, a major endocardial flow-responsive gene, was also significantly inhibited. Mechanistically, famoxadone-cymoxanil toxicity might be due to the downregulation of genes associated with the calcium-signaling pathway and cardiac muscle contraction. Our results found that famoxadone-cymoxanil exposure causes cardiac developmental toxicity and severe energy deficiency in zebrafish.


Assuntos
Acetamidas/toxicidade , Embrião não Mamífero/efeitos dos fármacos , Fungicidas Industriais/toxicidade , Coração/efeitos dos fármacos , Estrobilurinas/toxicidade , Poluentes Químicos da Água/toxicidade , Peixe-Zebra/metabolismo , Animais , Apoptose/efeitos dos fármacos , Sinalização do Cálcio/efeitos dos fármacos , Sinalização do Cálcio/genética , Cardiotoxicidade , Regulação para Baixo , Embrião não Mamífero/metabolismo , Embrião não Mamífero/patologia , Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos , Coração/embriologia , Frequência Cardíaca/efeitos dos fármacos , Fatores de Transcrição Kruppel-Like/genética , Fatores de Transcrição Kruppel-Like/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Peixe-Zebra/crescimento & desenvolvimento , Proteínas de Peixe-Zebra/genética , Proteínas de Peixe-Zebra/metabolismo
8.
Environ Pollut ; 265(Pt A): 114775, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32504889

RESUMO

Oxadiazon-Butachlor (OB) is a widely used herbicide for controlling most annual weeds in rice fields. However, its potential toxicity in aquatic organisms has not been evaluated so far. We used the zebrafish embryo model to assess the toxicity of OB, and found that it affected early cardiac development and caused extensive cardiac damage. Mechanistically, OB significantly increased oxidative stress in the embryos by inhibiting antioxidant enzymes that resulted in excessive production of reactive oxygen species (ROS), eventually leading to cardiomyocyte apoptosis. In addition, OB also inhibited the WNT signaling pathway and downregulated its target genes includinglef1, axin2 and ß-catenin. Reactivation of this pathway by the Wnt activator BML-284 and the antioxidant astaxanthin rescued the embryos form the cardiotoxic effects of OB, indicating that oxidative stress, and inhibition of WNT target genes are the mechanistic basis of OB-induced damage in zebrafish. Our study shows that OB exposure causes cardiotoxicity in zebrafish embryos and may be potentially toxic to other aquatic life and even humans.


Assuntos
Cardiotoxicidade , Peixe-Zebra , Acetanilidas , Animais , Embrião não Mamífero , Oxidiazóis , Estresse Oxidativo
9.
Chemosphere ; 256: 127038, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32470728

RESUMO

Baicalein is a flavonoid that is widely found in plants. Studies have shown that baicalein has anti-inflammatory, anti-cancer, and liver-protective effects. However, the effects of baicalein on TAA-induced toxicity and the underlying molecular mechanisms in zebrafish larvae are still unknown. Here, we investigated the effects of baicalein on liver development and its anti-inflammatory effects in zebrafish larvae. The results showed that baicalein has significant anti-embryonic developmental toxicity and significant antioxidant and anti-inflammatory capabilities in TAA-induced zebrafish larvae and promotes liver development and cell proliferation, reduces the expression of apoptotic proteins, and induces the expression of anti-apoptotic proteins. At the molecular level of TAA-treated zebrafish larvae, there was a decrease in the relative expression levels of mRNAs of three subfamilies, P38, ERK1, and ERK2, of the MAPK-signaling pathway and of the products of peroxisome proliferator-activated receptor (PPAR)α. Compared with TAA-treated zebrafish larvae, zebrafish larvae treated with baicalein showed an increase in the relative expression levels of P38, ERK1, and ERK2 mRNAs and the downstream products of PPARα. When MAPK signal inhibitor (SB203580) was added, it was found that liver development was inhibited and baicalin had no protective effect on TAA induced hepatotoxicity in zebrafish larvae. The results showed baicalein can protect the zebrafish larvae against toxicity induced by TAA through MAPK signal pathway. Several molecular mechanisms discovered in this study may help in the development of new drugs.


Assuntos
Flavanonas/toxicidade , Tioacetamida/toxicidade , Peixe-Zebra/fisiologia , Animais , Anti-Inflamatórios/metabolismo , Antioxidantes/metabolismo , Flavonoides , Larva/efeitos dos fármacos , Fígado/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , PPAR alfa , Substâncias Protetoras/metabolismo , Transdução de Sinais/efeitos dos fármacos
10.
Chemosphere ; 255: 126889, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32388256

RESUMO

Pyrimethanil is a broad-spectrum fungicide commonly used in the prevention and treatment of Botrytis cinerea. However, little information is available in the literature to show the toxicity of Pyrimethanil to cardiac development. In this study, we used an experimental animal model to explore the developmental and cardiac toxicity of Pyrimethanil in aquatic vertebrates; we exposed zebrafish embryos to Pyrimethanil at concentrations of 2, 4, and 6 mg/L from 5.5 to 72 h post fertilisation. We found that Pyrimethanil caused a decrease in the hatching rate, heart rate, and survival rate of zebrafish embryos. Pyrimethanil exposure also resulted in pericardial and yolk sac edema, spinal deformity, and heart loop failure. Moreover, Pyrimethanil increased reactive oxygen stress levels and heightened the activity of superoxide dismutase and catalase. Alterations were induced in the transcription of apoptosis-related genes (p53, Bax, Bcl2, Casp 9, and Casp6l1) and heart development-related genes (Tbx2b, Gata4, Myh6, Vmhc, Nppa, Bmp2b, Bpm 4, and Bpm 10). Our data showed that the activation of Wnt signalling by BML-284 could partially rescue the malformed phenotype caused by Pyrimethanil. Our results provide new evidence for Pyrimethanil's toxicity and the danger of its residues in the environment and agricultural products.


Assuntos
Fungicidas Industriais/toxicidade , Pirimidinas/toxicidade , Animais , Apoptose , Cardiotoxicidade , Caspase 9 , Embrião não Mamífero/metabolismo , Estresse Oxidativo , Peixe-Zebra/metabolismo , Proteínas de Peixe-Zebra/genética , Proteínas de Peixe-Zebra/metabolismo
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