Intestinal barrier dysfunction caused by chronic alcohol consumption is closely associated with disruption of the intestinal epithelial apical junction complex. The present study was undertaken to directly display by transmission electron microscopy the abnormal ultrastructure of the intestinal epithelial barrier in mice with alcoholic steatohepatitis. The results showed that chronic alcohol consumption could induce obvious liver injury, with diffuse lipid accumulation and focal inflammatory cell infiltration in the liver, assessed by hematoxylin and eosin staining. The indicators of intestinal barrier dysfunction, D-lactic acid and lipopolysaccharide, were significantly higher in alcohol-fed mice than in control mice. Alcohol exposure obviously caused high permeability in the ileum to fluorescein isothiocyanate-dextran (FD-4: molecular weight 4000). Transmission electron microscopy demonstrated that tight junctions and adherens junctions expanded noticeably in alcohol-fed mice. Although the tight junction (TJ) length of alcohol-fed mice had no significant difference compared with control mice, the adherens junction (AJ) length of alcohol-fed mice significantly decreased compared with control mice. Additionally, the ratios of both TJ(max)/TJ(min) and AJ(max)/AJ(min) were significantly larger in alcohol-fed mice than in control liquid-fed mice. In conclusion, high intestinal permeability caused by alcohol attributes to the irregular ultrastructure of the intestinal epithelial barrier. (C) 2014 Elsevier Inc. All rights reserved.