Cholestasis occurs in a wide variety of liver diseases and causes hepatic damage by an accumulation of toxic hydrophobic bile salts in the liver. Our aim was to investigate the effect of several bile acids: chenodeoxycholic (QCA), taurochenodeoxycholic (TQA), deoxycholic (DCA), taurodeoxycholic (TDA), ursodeoxycholic (UDA), lithocholic (LCA) and taurolithocholic (TLC) in inducing lipid and protein oxidative damage in hepatic cell membranes both in the presence and absence of iron. Hepatic membranes were isolated from male Sprague-Dawley rats (225–250g) by differential centrifugation and incubated at 37ordm;C for 2h with or without 1mM of each bile acid, in the presence and absence of 0.1 mM FeCl3 and 0.1 mM ascorbic acid. Malondialdehyde (MDA) + 4-hydroxyalkenals (4-HDA) concentrations and carbonyl content of the cell membranes were used as indices of lipid and protein oxidation, respectively. In the absence of FeCl3 and ascorbic acid several bile acids increased (p<0.05) MDA+4-HDA concentrations (LCA, 68%; TDA, 69%; UDA, 72%; DCA, 73%; and TLC, 350%) and carbonyl content in the membrane proteins (LCA, 133%; TQA, 147%; DCA, 150%; UDA, 175%; TDA, 201%; and TLC, 311%). In addition, some bile acids enhanced (p<0.05) lipid (UDA, 10%; TQA, 21%; TDA, 24% and TLC, 29%) and protein (DCA, 30%; TDA, 33%; TQA, 41% and TLC, 74%) oxidations due to iron and ascorbic acid. The ability of the bile acids to increase iron-induced lipid peroxidation may be related to their hydrophobicity. These results suggest that oxidative stress due to bile acids may be involved in the physiopathology of the cholestasis.