PUBLICATION
Sodium dehydroacetate induces cardiovascular toxicity associated with Ca2+ imbalance in zebrafish
- Authors
- Huang, X., Zhao, X., Zhu, K., Ding, S., Shao, B.
- ID
- ZDB-PUB-210106-23
- Date
- 2021
- Source
- Ecotoxicology and environmental safety 208: 111613 (Journal)
- Registered Authors
- Keywords
- Ca(2+), Cardiovascular, Metabolism, Mitochondria, Sodium dehydroacetate
- MeSH Terms
-
- Animals
- Calcium/metabolism*
- Heart/drug effects*
- Heart/embryology
- Pyrones/toxicity*
- Zebrafish*/growth & development
- Cell Line
- Dose-Response Relationship, Drug
- Cerebral Hemorrhage/chemically induced
- Apoptosis/drug effects
- Embryo, Nonmammalian/drug effects*
- Cardiotoxicity
- Embryonic Development/drug effects*
- Rats
- Pericardium/drug effects
- Pericardium/pathology
- Edema, Cardiac/chemically induced
- Myocardium/metabolism
- Myocardium/pathology
- PubMed
- 33396133 Full text @ Ecotoxicol. Environ. Saf.
Citation
Huang, X., Zhao, X., Zhu, K., Ding, S., Shao, B. (2021) Sodium dehydroacetate induces cardiovascular toxicity associated with Ca2+ imbalance in zebrafish. Ecotoxicology and environmental safety. 208:111613.
Abstract
The environmental effects of additives have attracted increasing attention. Sodium dehydroacetate (DHA-S), as an approved preservative, is widely added in processed foods, cosmetics and personal care products. However, DHA-S has been recently reported to induce hemorrhage and coagulation aberration in rats. Yet little is known about the ecotoxicological effect and underlying mechanisms of DHA-S. Here, we utilized the advantage of zebrafish model to evaluate such effects. DHA-S induced cerebral hemorrhage, mandibular dysplasia and pericardial edema in zebrafish after 24 h exposure (48-72 hpf) at 50 mg/L. We also observed the defective heart looping and apoptosis in DHA-S-treated zebrafish through o-dianisidine and acridine orange staining. Meanwhile, DHA-S induced the deficiency of Ca2+ and vitamin D3 in zebrafish. We further demonstrated that DHA-S stimulated Ca2+ influx resulting in Ca2+-dependent mitochondrial damage in cardiomyocytes. Additionally, DHA-S inhibited glucose uptake and repressed the biosynthesis of amino acids. Finally, we identified that sodium bicarbonate could rescue zebrafish from DHA-S induced cardiovascular toxicity. Altogether, our results suggest that DHA-S is a potential risk for cardiovascular system.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping