PUBLICATION
Copper impair autophagy on zebrafish (Danio rerio) gill epithelium
- Authors
- Luzio, A., Parra, S., Costa, B., Santos, D., Álvaro, A.R., Monteiro, S.M.
- ID
- ZDB-PUB-210525-16
- Date
- 2021
- Source
- Environmental Toxicology and Pharmacology 86: 103674 (Journal)
- Registered Authors
- Keywords
- Apoptosis, Autophagosome, Cell death, LC3, Ultrastructure
- MeSH Terms
-
- Autophagy/drug effects*
- Copper/toxicity*
- Water Pollutants, Chemical/toxicity*
- Zebrafish Proteins/genetics
- Animals
- Epithelium/anatomy & histology
- Epithelium/drug effects*
- Epithelium/metabolism
- Epithelium/ultrastructure
- Zebrafish
- Gills/anatomy & histology
- Gills/drug effects*
- Gills/metabolism
- Gills/ultrastructure
- Microtubule-Associated Proteins/genetics
- PubMed
- 34029728 Full text @ Environ. Toxicol. Pharmacol.
Citation
Luzio, A., Parra, S., Costa, B., Santos, D., Álvaro, A.R., Monteiro, S.M. (2021) Copper impair autophagy on zebrafish (Danio rerio) gill epithelium. Environmental Toxicology and Pharmacology. 86:103674.
Abstract
Copper (Cu) is an essential element for organism's metabolism, being controversially listed as a priority pollutant. Importantly, the toxicity of Cu has been linked to several cell death pathways. Thus, this study aimed to assess if macroautophagic pathways are triggered by Cu in zebrafish gill, the main target of waterborne pollutants. The electron microscopy findings indicated that Cu induced profound impacts on zebrafish gill structure and functions, being this tissue a biomarker sensitive enough to indicate early toxic effects. The findings also support a clear impairment of autophagy, througth the absence of phagossomes and the significant down-regulation mRNA transcript levels of microtubule-associated protein light chain 3 (LC3). The reduction of LC3 levels was often associated to an increase of apoptotic activation, indicating that the inhibition of macroautophagy triggers apoptosis in zebrafish gills. This study highlighted that the autophagic down-regulation might be affected through the activation of other cell death signaling pathway.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping