Abstract

Thifluzamide is a new amide fungicide, and its extensive application may have toxic effects on zebrafish. To better understand the underlying mechanism, we investigated in detail the potential toxic effects of thifluzamide on zebrafish embryos. In the present study, embryos were exposed to 0, 0.19, 1.90, and 2.85 mg/L thifluzamide for 4 days. Obvious pathological changes were found upon a histological exam, and negative changes in mitochondrial structure were observed under Transmission Electron Microscopy (TEM), which qualitatively noted the toxic effects of thifluzamide on embryos. Moreover, we quantitatively evaluated the enzyme activities [succinate dehydrogenase (SDH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), caspases], the contents of malonaldehyde (MDA) and interleukin-8 (IL-8) and the expression levels of the related genes. This study suggests that the negative changes in mitochondrial structure and SDH activity might be responsible for oxidative damage, cell apoptosis and inflammation, which would facilitate the action of these factors in cell death and might play a crucial role during toxic events. In addition to providing the first description of the mechanism of the toxic effects of thifluzamide on embryos, this study also represents a step towards using embryos to assess mitochondrial metabolism and disease.

Highlights

  • Thifluzamide is a new amide fungicide, and its extensive application may have toxic effects on zebrafish

  • The methods used by experts in conducting toxic evaluations and exploring the toxicity mechanism are many and varied and reflect the particular question or hypothesis being examined

  • The lethality result indicated that embryos were more sensitive to thifluzamide than adult zebrafish[4]

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Summary

Introduction

Thifluzamide is a new amide fungicide, and its extensive application may have toxic effects on zebrafish. To better understand the underlying mechanism, we investigated in detail the potential toxic effects of thifluzamide on zebrafish embryos. In addition to providing the first description of the mechanism of the toxic effects of thifluzamide on embryos, this study represents a step towards using embryos to assess mitochondrial metabolism and disease. Embryos undergo anatomical and physical changes, and their detoxification mechanisms are not completely developed yet[13,14]; toxic effect might be rapid Embryos complete their development into juveniles in approximately 26 days[15]. Measurements of the enzyme activities [SDH, superoxide dismutase (SOD), catalase (CAT), peroxidase (GPx), caspases], the malonaldehyde (MDA) and interleukin-8 (IL-8) contents, and the related gene expression levels were used to quantitatively assess mitochondrial damage, oxidative stress, cellular apoptosis and immune response to comprehensively explore the toxicity mechanism. The present study aimed to provide new insight into the application of embryos to assess mitochondrial diseases

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