Bifenazate exposure induces cardiotoxicity in zebrafish embryos

Ma, Jinze; Huang, Yong; Peng, Yuyang; Xu, Zhaopeng; Wang, Ziqin; Chen, Xiaobei; Xie, Shuling; Ping, Jiang; Zhong, Keyuan; Lu, Huiqiang

doi:10.1016/j.envpol.2021.116539

Cited by 23 publications

(7 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The antioxidant mechanisms of astaxanthin include the direct scavenging of cellular ROS retained within and on the surface of phospholipid membranes, the protection of mitochondrial redox status and functional integrity, the enhancement of antioxidant enzyme activities such as GSH-Px and SOD [ 68 ], and the activation of antioxidant-related signaling pathways such as the Nrf-2/ARE pathway [ 69 ]. In previous studies, 30 nM astaxanthin demonstrated no cardiotoxicity in zebrafish and was able to inhibit cardiotoxicity induced by pesticides such as 1.0 mg/L benoxacor and 10 mg/L bifenadril [ 31 , 70 ]. In our study, astaxanthin reduced MP-induced ROS levels and alleviated pericardial edema and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Methyl Parathion Exposure Induces Development Toxicity and Cardiotoxicity in Zebrafish Embryos

Chen

Wang

et al. 2023

Toxics

View full text Add to dashboard Cite

Methyl parathion (MP) has been widely used as an organophosphorus pesticide for food preservation and pest management, resulting in its accumulation in the aquatic environment. However, the early developmental toxicity of MP to non-target species, especially aquatic vertebrates, has not been thoroughly investigated. In this study, zebrafish embryos were treated with 2.5, 5, or 10 mg/L of MP solution until 72 h post-fertilization (hpf). The results showed that MP exposure reduced spontaneous movement, hatching, and survival rates of zebrafish embryos and induced developmental abnormalities such as shortened body length, yolk edema, and spinal curvature. Notably, MP was found to induce cardiac abnormalities, including pericardial edema and decreased heart rate. Exposure to MP resulted in the accumulation of reactive oxygen species (ROS), decreased superoxide dismutase (SOD) activity, increased catalase (CAT) activity, elevated malondialdehyde (MDA) levels, and caused cardiac apoptosis in zebrafish embryos. Moreover, MP affected the transcription of cardiac development-related genes (vmhc, sox9b, nppa, tnnt2, bmp2b, bmp4) and apoptosis-related genes (p53, bax, bcl2). Astaxanthin could rescue MP-induced heart development defects by down-regulating oxidative stress. These findings suggest that MP induces cardiac developmental toxicity and provides additional evidence of MP toxicity to aquatic organisms.

show abstract

Section: Discussionmentioning

confidence: 99%

Methyl Parathion Exposure Induces Development Toxicity and Cardiotoxicity in Zebrafish Embryos

Chen

Wang

et al. 2023

Toxics

View full text Add to dashboard Cite

show abstract

“…Therefore, the lethal concentration 50 (LC 50 ) of diflubenzuron for zebrafish at 96 hpf was analyzed (3.5 mg/L), which is lower than those of other insecticides. For example, LC 50 of bifenazate and thiophanate-methyl for zebrafish at 72 hpf was 14.5 mg/L [ 20 ] and 50.45 mg/L [ 21 ], respectively. Flupyradifurone is a new butenolide insecticide, and it was found that the LC 50 of flupyradifurone to zebrafish embryos at 96 hpf is 210 mg/L [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Diflubenzuron Induces Cardiotoxicity in Zebrafish Embryos

Han

et al. 2022

IJMS

View full text Add to dashboard Cite

Diflubenzuron is an insecticide that serves as a chitin inhibitor to restrict the growth of many harmful larvae, including mosquito larvae, cotton bollworm and flies. The residue of diflubenzuron is often detected in aquaculture, but its potential toxicity to aquatic organisms is still obscure. In this study, zebrafish embryos (from 6 h to 96 h post-fertilization, hpf) were exposed to different concentrations of diflubenzuron (0, 0.5, 1.5, 2.5, 3.5 and 4.5 mg/L), and the morphologic changes, mortality rate, hatchability rate and average heart rate were calculated. Diflubenzuron exposure increased the distance between the venous sinus and bulbar artery (SV-BA), inhibited proliferation of myocardial cells and damaged vascular development. In addition, diflubenzuron exposure also induced contents of reactive oxygen species (ROS) and malondialdehyde (MDA) and inhibited the activity of antioxidants, including SOD (superoxide dismutase) and CAT (catalase). Moreover, acridine orange (AO) staining showed that diflubenzuron exposure increased the apoptotic cells in the heart. Q-PCR also indicated that diflubenzuron exposure promoted the expression of apoptosis-related genes (bax, bcl2, p53, caspase3 and caspase9). However, the expression of some heart-related genes were inhibited. The oxidative stress-induced apoptosis damaged the cardiac development of zebrafish embryos. Therefore, diflubenzuron exposure induced severe cardiotoxicity in zebrafish embryos. The results contribute to a more comprehensive understanding of the safety use of diflubenzuron.

show abstract

“…After the removal of flumioxazin residues with egg water, acridine orange was used to stain live zebrafish at 72 hpf according to Ma, Huang, Jiang, et al (2021). Apoptotic cells appeared as yellow–green spots in microfluorescence images, which were captured under a fluorescence stereomicroscope after elution with egg water (Ma, Huang, Peng, et al, 2021).…”

Section: Methodsmentioning

confidence: 99%

“…A 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) probe is a cell-permeable probe for the detection of intracellular ROS. At 72 hpf, live zebrafish with typical phenotypes that had been exposed to flumioxazin or rescued with 20 nM astaxanthin were stained with a DCFH-DA probe for 30 min in a dark environment at 37 °C after flumioxazin and astaxanthin residues had been removed with egg water (Ma, Huang, Peng, et al, 2021). Fluorescence microscopy images were taken under a fluorescence stereomicroscope after elution with egg water.…”

Section: Oxidative Stress Analysismentioning

confidence: 99%

“…Therefore cardiotoxicity induced by environmental pollutants may disrupt blood circulation and threaten the development of other organs or even life (Ma, Huang, Jiang, et al, 2021). Zebrafish is an ideal vertebrate model widely used to assess the cardiotoxicity of environmental pollutants (Ma, Huang, Peng, et al, 2021). Cardiac morphology (degree of cardiac looping, distance between sinus venous and bulbus arteriosus), area, function (heart rate, number of red blood cells), and expression levels of related genes ( nkx2.5 , nppa , gata4 , myh6 , tbx2b , tbx5 , and vmhc , etc.)…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oxidative stress contributes to flumioxazin‐induced cardiotoxicity in zebrafish embryos

Ma,

Jiang,

Huang

et al. 2023

Enviro Toxic and Chemistry

Self Cite

View full text Add to dashboard Cite

Flumioxazin is a widely applicated herbicide in the control of aquatic plants. Current evidence suggested that flumioxazin could induce cardiac defects (ventricular septal defects) in vertebrates, but the underlining mechanisms remain unclear. Because of the inhibitory effect of flumioxazin on polyphenol oxidase (PPO), the assumption is made that flumioxazin‐induced cardiotoxicity is caused by oxidative stress. The results show that flumioxazin induced cardiac malformations and abnormal gene expression associated with cardiac development. Cardiac malformations include pericardium edema, cardiac linearization, elongated heart, cardiomegaly, cardiac wall hypocellularity, myocardial cell atrophy into granular, and a significant gap between the myocardial intima and the adventitia. An increase in oxidative stress and apoptosis was observed in the cardiac region of zebrafish after exposure to flumioxazin. Antioxidant astaxanthin reversed the cardiac malformations, excessive ROS production and expression of genes for cardiac developmental and apoptosis regulation induced by flumioxazin. In addition, flumioxazin also activated AHR signaling pathway genes (ahr2, cyp1a1, and cyp1b1) and increased porphyrins concentration. In conclusion, the results suggest that excessive ROS production, which could be mediated through AHR, led to apoptosis, contributing to the cardiotoxicity of flumioxazin in zebrafish embryos.

show abstract

Bifenazate exposure induces cardiotoxicity in zebrafish embryos

Cited by 23 publications

References 37 publications

Methyl Parathion Exposure Induces Development Toxicity and Cardiotoxicity in Zebrafish Embryos

Methyl Parathion Exposure Induces Development Toxicity and Cardiotoxicity in Zebrafish Embryos

Diflubenzuron Induces Cardiotoxicity in Zebrafish Embryos

Oxidative stress contributes to flumioxazin‐induced cardiotoxicity in zebrafish embryos

Contact Info

Product

Resources

About