期刊
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
卷 216, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2021.112227
关键词
Difenoconazole; Cardiovascular toxicity; Oxidative stress; Apoptosis; Antioxidant; Zebrafish
资金
- National Natural Science Foundation of China [81671359, 81903353]
- Subproject of National Key Research and Development Program of China [2016YFC1000204-6]
- Technology Development Fund of Nanjing Medical University [NMUB2018001, NMUB2020117]
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- Collegiate Natural Science Foundation of Jiangsu Province [19KJB330003]
The study found that DIF induced cardiovascular toxicity in zebrafish embryos, resulting in decreased hatching rate, survival rate, heart rate, and increased malformation rate. DIF exacerbated oxidative stress, triggering cardiovascular apoptosis and inhibiting cardiac muscle contraction, which could be restored by the antioxidant N-acetyl-L-cysteine (NAC).
Difenoconazole (DIF), a common broad-spectrum triazole fungicide, is associated with an increased risk of cardiovascular diseases. Unfortunately, little attention has been paid to the mechanisms underlying this association. In this study, zebrafish embryos were exposed to DIF (0, 0.3, 0.6 and 1.2 mg/L) from 4 to 96 h post fertilization (hpf) and cardiovascular toxicity was evaluated. Our results showed that DIF decreased hatching rate, survival rate and heart rate, with increased malformation rate. Cardiovascular deformities are the most prominent, including pericardial edema, abnormal cardiac structure and disrupted vascular pattern in two transgenic zebrafish models (myl7:egfp and fli1:egfp). DIF exacerbated oxidative stress by via accumulation of reactive oxygen species (ROS) and inhibition of antioxidant enzyme. Cardiovascular apoptosis was triggered through increased expression of p53, bcl-2, bax and caspase 9, while DIF suppressed the transcription of key genes involved in calcium signaling and cardiac muscle contraction. These adverse outcomes were restored by the antioxidant N-acetyl-L-cysteine (NAC), indicating that oxidative stress played a crucial role in DIF-induced cardiovascular toxicity caused by apoptosis and inhibition of cardiac muscle contraction. Taken together, this study revealed the key role of oxidative stress in DIF-induced cardiovascular toxicity and provided novel insights into strategies to mitigate its toxicity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据