PUBLICATION
Bifenazate induces developmental and immunotoxicity in zebrafish
- Authors
- Peng, Y., Li, M., Huang, Y., Cheng, B., Cao, Z., Liao, X., Xiong, G., Liu, F., Hu, C., Lu, H.
- ID
- ZDB-PUB-210115-8
- Date
- 2021
- Source
- Chemosphere 271: 129457 (Journal)
- Registered Authors
- Lu, Huiqiang
- Keywords
- Astaxanthin, Bifenazate, Immunotoxicity, Oxidative stress, Zebrafish
- MeSH Terms
-
- Animals
- Hydrazines
- Oxidative Stress
- Zebrafish*
- Carbamates
- Embryo, Nonmammalian*/metabolism
- PubMed
- 33445023 Full text @ Chemosphere
Citation
Peng, Y., Li, M., Huang, Y., Cheng, B., Cao, Z., Liao, X., Xiong, G., Liu, F., Hu, C., Lu, H. (2021) Bifenazate induces developmental and immunotoxicity in zebrafish. Chemosphere. 271:129457.
Abstract
Bifenazate is a widely used acaricide, but its biological safety remains unknown. In the present study, the immunotoxic effects of exposure to bifenazate on zebrafish larvae were evaluated for the first time. Firstly, after exposure to bifenazate, the body length of the zebrafish larvae became shorter and the yolk sac swelled. Secondly, the number of innate immune cells and adaptive immune cells was greatly reduced. Following exposure to bifenazate, oxidative stress levels in the zebrafish increased significantly, antioxidant activity was inhibited, and the expression of genes related to antioxidants, such as those of the glutathione metabolism pathway, changed, including gclm, prdx1, serpine1, and gss. In addition, inflammatory factors such as CXCL-c1c, IFN-γ, iL-8, iL-6, and MYD88 were abnormally expressed. The use of astaxanthin was effective in rescuing the developmental toxicity caused by bifenazate exposure. In summary, bifenazate exposure is immunotoxic and can cause oxidative stress in zebrafish larvae.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping