PUBLICATION
Oxidative stress in bisphenol AF-induced cardiotoxicity in zebrafish and the protective role of N-acetyl N-cysteine
- Authors
- Gu, J., Wang, H., Zhou, L., Fan, D., Shi, L., Ji, G., Gu, A.
- ID
- ZDB-PUB-200515-11
- Date
- 2020
- Source
- The Science of the total environment 731: 139190 (Journal)
- Registered Authors
- Keywords
- Bisphenol AF (BPAF), Cardiotoxicity, Human cardiac myocytes (HCM), Oxidative stress, Zebrafish
- MeSH Terms
-
- Acetylcysteine*
- Animals
- Benzhydryl Compounds
- Cardiotoxicity
- Humans
- Oxidative Stress
- Phenols
- Zebrafish*
- PubMed
- 32408210 Full text @ Sci. Total Environ.
Citation
Gu, J., Wang, H., Zhou, L., Fan, D., Shi, L., Ji, G., Gu, A. (2020) Oxidative stress in bisphenol AF-induced cardiotoxicity in zebrafish and the protective role of N-acetyl N-cysteine. The Science of the total environment. 731:139190.
Abstract
Research has shown that there is a relationship between bisphenol A (BPA) exposure and the incidence of cardiovascular diseases. However, the effect of bisphenol AF (BPAF), a main substitute for BPA, on heart development remains unclear. In this study, the cardiotoxicity of BPAF was evaluated in zebrafish in vivo and in human cardiac myocytes (HCMs) in vitro. Our results showed that BPAF at a concentration of 200 μg/L results in cardiotoxicity, including a reduced number of cardiomyocytes and endocardial cells in the heart, and reduced heart size in two transgenic zebrafish models (myl7:: dsred2-nuc and fli1a::nGFP). An increase in apoptosis was observed along with antioxidant enzyme inhibition and lipid peroxidation. In addition, the mRNA expression levels of several key genes involved in cardiac development were suppressed by BPAF treatment. In the HCM cell model, BPAF at 2 mg/L induced reactive oxygen species generation, antioxidant enzyme inhibition, mitochondrial dysfunction and oxidative DNA damage. These adverse outcomes can be attenuated by the antioxidant N-acetyl-L-cysteine (NAC), suggesting that oxidative stress is involved in BPAF-induced cardiotoxicity. These data indicated that BPAF exposure increased oxidative stress and apoptosis and that it suppressed the expression of genes involved in cardiac development, which may play crucial roles in the mechanisms of BPAF-induced cardiotoxicity.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping