PUBLICATION
Exposure to diclofenac alters thyroid hormone levels and transcription of genes involved in the hypothalamic-pituitary-thyroid axis in zebrafish embryos/larvae
- Authors
- Wang, H., Dong, F., Zhao, Y., Fu, S., Zhao, H., Liu, S., Zhang, W., Hu, F.
- ID
- ZDB-PUB-220331-8
- Date
- 2022
- Source
- Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 257: 109335 (Journal)
- Registered Authors
- Keywords
- Diclofenac, Embryonic development, Heartbeat, Thyroid disruption, Zebrafish
- MeSH Terms
-
- Animals
- Thyroid Gland
- Diclofenac/toxicity
- Larva/genetics
- Thyroid Hormones
- PubMed
- 35351617 Full text @ Comp. Biochem. Physiol. C Toxicol. Pharmacol.
Abstract
Diclofenac (DCF), one of typical non-steroidal anti-inflammatory drugs (NSAIDs), has been frequently detected in various environmental media. Nevertheless，the potential endocrine disrupting effects of DCF on fish were poorly understood. In the present study, zebrafish embryos/larvae were used as a model to evaluate the adverse effects of DCF on development and thyroid system. The results demonstrated that DCF only significantly decreased the heart rate at 72 h post-fertilization (hpf), exhibiting limited influence on the embryonic development of zebrafish. Treatment with DCF significantly reduced whole-body thyroxine (T4) levels, and changed transcriptional levels of several genes related to the hypothalamic-pituitary-thyroid (HPT) axis. These findings provide important information regarding to the mechanisms of DCF-induced developmental toxicity and thyroid disruption in fish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping