Chronic exposure to ethanol causes steatosis and inflammation in zebrafish liver.

AIM

To evaluate the effects of chronic exposure to ethanol in the liver and the expression of inflammatory genes in zebrafish.

METHODS

Zebrafish ( = 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 (), sirtuin-1 (), tumor necrosis factor-alpha (), interleukin-1b () and interleukin-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 , and were upregulated, indicating that ethanol triggered signaling molecules which are key elements in both hepatic inflammatory and protective responses. was not detected in the liver of animals exposed and not exposed to ethanol, and 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.