Toxicity induced by emodin on zebrafish embryos
- Authors
- He, Q., Liu, K., Wang, S., Hou, H., Yuan, Y., and Wang, X.
- ID
- ZDB-PUB-110816-13
- Date
- 2012
- Source
- Drug and chemical toxicology 35(2): 149-154 (Journal)
- Registered Authors
- Keywords
- zebrafish, emodin, developmental toxicity, CYP3A
- MeSH Terms
-
- ATP Binding Cassette Transporter, Subfamily B, Member 1/genetics
- ATP Binding Cassette Transporter, Subfamily B, Member 1/metabolism
- Animals
- Cytochrome P-450 CYP3A/genetics
- Cytochrome P-450 CYP3A/metabolism
- Embryo, Nonmammalian
- Embryonic Development/drug effects*
- Emodin/toxicity*
- Female
- RNA/chemistry
- RNA/genetics
- Reverse Transcriptase Polymerase Chain Reaction
- Survival Analysis
- Zebrafish
- PubMed
- 21834668 Full text @ Drug Chem. Toxicol.
Emodin, a widely available herbal remedy, has a variety of pharmacological actions and valuable clinical applications. The potential effect of emodin on zebrafish (Danio rerio) embryos was evaluated. Zebrafish embryos were incubated with 0.1–2 μg/mL of emodin from 7 hours to 6 days postfertilization (dpf). Emodin, at concentrations of 0.25 μg/mL and above, negatively affected embryo survival and hatching success. Emodin induced a large suite of abnormalities on zebrafish embryos, such as edema, crooked trunk, and abnormal morphogenesis. To elucidate the mechanism of action, the transcript levels of drug-metabolism genes (CYP3A) and a multiple drug-resistance gene (MDR1) were detected by reverse-transcript polymerase chain reaction. Embryos showed increases in mRNA accumulation of CYP3A and MDR1. The above-described results indicated that emodin impaired zebrafish embryo development and some organ morphogenesis, and CYP3A and MDR1 were involved in the process. These findings suggest that emodin was toxic to zebrafish lavae at relatively low concentrations.