Journal
TOXICOLOGY LETTERS
Volume 324, Issue -, Pages 1-11Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2020.02.003
Keywords
Cardiotoxicity; QT duration; T-wave; Apoptosis; Zebrafish
Categories
Funding
- National Science Foundation for Young Scientists of China [81802629]
- International Science and Technology Cooperation Program of Shandong Academy of Sciences [2019GHZD10]
- Chinese Academy of Sciences (Shenyang branch) Shandong Academy of Sciences Partner Program for young scientists
- European Union's Horizon 2020 Research and innovation programme (VISGEN) [734862]
- OPEN FET RIA (NEURAM) [712821]
- Higher Education Institutional Excellence Programme of the Ministry for Innovation and Technology in Hungary
- Key Science and Technology Research Project Fund of Hebei Province of China [19227115D]
- Natural Science Foundation of Hebei Province of China [C2019209478]
- Marie Curie Actions (MSCA) [734862] Funding Source: Marie Curie Actions (MSCA)
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alpha-asarone is a natural phenylpropene found in several plants, which are widely used for flavoring foods and treating diseases. Previous studies have demonstrated that alpha-asarone has many pharmacological functions, while some reports indicated its toxicity. However, little is known about its cardiovascular effects. This study investigated developmental toxicity of alpha-asarone in zebrafish, especially the cardiotoxicity. Zebrafish embryos were exposed to different concentrations of alpha-asarone (1, 3, 5, 10, and 30 mu M). Developmental toxicity assessments revealed that alpha-asarone did not markedly affect mortality and hatching rate. In contrast, there was a concentration-dependent increase in malformation rate of zebrafish treated with alpha-asarone. The most representative cardiac defects were increased heart malformation rate, pericardial edema areas, sinus venosusbulbus arteriosus distance, and decreased heart rate. Notably, we found that alpha-asarone impaired the cardiac function of zebrafish by prolonging the mean QTc duration and causing T-wave abnormalities. The expressions of cardiac development-related key transcriptional regulators tbx5, nkx2.5, hand2, and gata5 were all changed under alpha-asarone exposure. Further investigation addressing the mechanism indicated that alpha-asarone triggered apoptosis mainly in the heart region of zebrafish. Moreover, the elevated expression of puma, cyto C, afap1, caspase 3, and caspase 9 in treated zebrafish suggested that mitochondrial apoptosis is likely to be the main reason for alpha-asarone induced cardiotoxicity. These findings revealed the cardiac developmental toxicity of aasarone, expanding our knowledge about the toxic effect of alpha-asarone on living organisms.
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