Intermittent alcohol consumption changes the hepatocyte ploidy

Abstract

Introduction: Alcohol is mainly metabolized by hepatocytes in the liver. These cells should be the direct targets of stress, which can culminate in cellular adaptations earlier than alcoholic liver disease progression. Polyploidization has been suggested as a genetic adaptation to hepatotoxic stress. This study aimed to investigate how intermittent alcohol administration could affect hepatocyte nuclear phenotypes. Methods: Rats were treated with 5% (v/v) and 20% (v/v) ethanol in drinking water overnight for 80 days. Thereafter, their liver was dissected and histologically processed. Histopathological analysis was performed using hematoxylin and eosin (H&E)-stained sections. Histomorphometric analysis of hepatocyte nuclei were performed in Feulgen stained sections using ImageJ. Results: Severe congestion was observed in the group treated with 20% ethanol. No difference in fat accumulation in hepatocytes or infiltration of inflammatory cells was observed between the control and ethanol-treated groups. After hepatocytes had different ploidies, the DNA content of nuclei was determined based on the integrated optical density values obtained from digital image analysis of liver sections stained with Feulgen stain. More nuclei with high DNA content (8C) were found in the ethanol-treated animals. Conclusion: It is concluded that alcohol induces hepatocyte polyploidization, even at doses when typical signs of alcohol-induced liver disease, such as steatosis and hepatitis, are not significant.