PUBLICATION
Chronic exposure to ethanol causes steatosis and inflammation in zebrafish liver
- Authors
- Schneider, A.C., Gregório, C., Uribe-Cruz, C., Guizzo, R., Malysz, T., Faccioni-Heuser, M.C., Longo, L., da Silveira, T.R.
- ID
- ZDB-PUB-170331-4
- Date
- 2017
- Source
- World journal of hepatology 9: 418-426 (Journal)
- Registered Authors
- Keywords
- Alcoholic fatty liver, Ethanol, Hepatic steatosis, Inflammation, Zebrafish
- MeSH Terms
- none
- PubMed
- 28357029 Full text @ World J Hepatol
Citation
Schneider, A.C., Gregório, C., Uribe-Cruz, C., Guizzo, R., Malysz, T., Faccioni-Heuser, M.C., Longo, L., da Silveira, T.R. (2017) Chronic exposure to ethanol causes steatosis and inflammation in zebrafish liver. World journal of hepatology. 9:418-426.
Abstract
Aim To evaluate the effects of chronic exposure to ethanol in the liver and the expression of inflammatory genes in zebrafish.
Methods Zebrafish (n = 104), wild type, adult, male and female, were divided into two groups: Control and ethanol (0.05 v/v). The ethanol was directly added into water; tanks water were changed every two days and the ethanol replaced. The animals were fed twice a day with fish food until satiety. After two and four weeks of trial, livers were dissected, histological analysis (hematoxilin-eosin and Oil Red staining) and gene expression assessment of adiponectin, adiponectin receptor 2 (adipor2), sirtuin-1 (sirt-1), tumor necrosis factor-alpha (tnf-a), interleukin-1b (il-1b) and interleukin-10 (il-10) were performed. Ultrastructural evaluations were conducted at fourth week.
Results Exposing zebrafish to 0.5% ethanol developed intense liver steatosis after four weeks, as demonstrated by oil red staining. In ethanol-treated animals, the main ultrastructural changes were related to cytoplasmic lipid particles and droplets, increased number of rough endoplasmic reticulum cisterns and glycogen particles. Between two and four weeks, hepatic mRNA expression of il-1b, sirt-1 and adipor2 were upregulated, indicating that ethanol triggered signaling molecules which are key elements in both hepatic inflammatory and protective responses. Adiponectin was not detected in the liver of animals exposed and not exposed to ethanol, and il-10 did not show significant difference.
Conclusion Data suggest that inflammatory signaling and ultrastructural alterations play a significant role during hepatic steatosis in zebrafish chronically exposed to ethanol.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping