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Carboxin is a heterocyclic systemic fungicide, mainly used to prevent and control grain smut and wheat rust. Although its mammalian toxicity has been reported, its toxicity to acute exposure to aquatic animals is unknown. In our study, we used zebrafish as aquatic organisms to study Carboxin toxicity. Carboxin can cause developmental toxicity and cardiotoxicity in zebrafish embryos. Histopathological staining of cardiac sections reveals structural changes in zebrafish hearts, and fluorescence quantitative PCR results shows the heart developmental genes mRNA expression levels were disrupted significantly. Besides, carboxin can also cause oxidative stress and reactive oxygen species (ROS) accumulation in zebrafish embryos. The accumulation of ROS causes mitochondrial damage, which is where ATP energy is produced. So ATPase activities and gene expression level were measured and significantly decreased after exposure to carboxin. From the confocal images, the number of blood cells in the heart were decreased significantly after carboxin exposure. Besides, Carboxin exposure can inhibit myocardial cell proliferation. These are all causes to the heart failure, eventually leading to embryos death., (Copyright © 2022. Published by Elsevier Inc.)

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

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 β-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., Competing Interests: Declaration of competing interest The author reports no conflicts of interest in this work., (Copyright © 2020. Published by Elsevier Ltd.)

Benoxacor (BN) is a highly effective antidote of dichloroacetamide herbicides generally used to protect crops from herbicidal damage. As a commonly used agrochemical, this herbicide antidote is continuously discharged in watercourses thus causing toxicity to aquatic organisms, and ultimately leading to contamination of the food chain. To date, its potential toxicity to the cardiac development of aquatic organisms has not been evaluated. In the present study, we have selected the zebrafish as a model to study the impact of BN on embryonic developmental and cardiac toxicity. The zebrafish embryos were exposed in 0.5, 1.0 and 2.0 mg/L BN from 5.5 to 72 h post-fertilization (hpf). The results indicated that the exposure to BN led to increased mortality and diminished heart and hatching rates in the embryos. BN exposure also brought pericardial edema (PE) and linear stretching of heart. Besides, exposure to BN induced an excessive accumulation of reactive oxygen species (ROS) in the zebrafish embryos and abnormal activities of the antioxidant enzymes, including catalase (CAT) and malondialdehyde (MDA). Moreover, exposure to BN caused serious cardiac toxicity of the embryos, accompanied by abnormality of heart development- and apoptosis-related genes. Surprisingly, astaxanthin (ASTA), as a common antioxidant, was found to be able to partially rescue the cardiac toxicity caused by BN, which indicated that ROS are probably the major reason for the resulting cardiotoxicity in zebrafish embryos. Our results suggest the need for a comprehensive safety evaluation of the regular consumption of benoxacor, which provides scientific basis for the development of health standards and assessment of potential risk in aquatic organisms or even human. • Benoxacor increased mortality, decreased heart and hatching rates in the embryos. • Benoxacor induced pericardial edema, led to linear stretching of heart. • Exposure to benoxacor induced oxidative stress in zebrafish embryos. • Benoxacor caused changes in the transcription levels of heart development genes. • Astaxanthin was able to partially rescue cardiac toxicity caused by benoxacor. [ABSTRACT FROM AUTHOR]