The mercurial forms [inorganic divalent mercury, Hg(II) and methylmercury, CH3Hg] produce neurological and immune effects as well as hematological and renal alterations. The main route of exposure is through the diet. Consequently, the gastrointestinal mucosa is exposed to these mercurial forms, though the potential toxic effects upon the mucosa are not clear. The present study evaluates the toxicity of Hg(II) and CH3Hg (0.1-2 mg/L) in an intestinal epithelium model using the differentiated and undifferentiated human Caco-2 cell line.The experiments made show the mercurial forms generate reactive oxygen and/or nitrogen species and a significant decrease in glutathione contents. This redox imbalance could be the cause of the lipid peroxidation observed after short exposure times. Such conditions of stress lead to a modulation of stress proteins, intercellular junction proteins and tumor necrosis factor-alpha expression and to a redistribution of F-actin and ZO1 protein in the intestinal monolayer. The abovementioned effects may be the cause of the increase in permeability in the differentiated cells observed at concentrations similar to those found in food products (0.5-1 mg/L). The increase in permeability could produce an impairment of the barrier function of the intestinal epithelium.