Effects of bromoethylamine on antioxidant capacity,lipid peroxidation,and morphological characteristics of rat liver

Administration of bromoethylamine (BEA, 1.2 mmol/kg) to fed rats induced a significant diminution in the activity of hepatic superoxide dismutase (at 1 h after treatment), catalase, and glutathione peroxidase and in the content of nonprotein sulfhydryls (at 15 h after treatment). The content of thiobarbituric acid reactants by the liver was enhanced by 1.9 times over control values (at 3 h). Light microscopy studies revealed that BEA (72 h after treatment) induced periportal fatty accumulation, focal liver cell necrosis, and diffuse inflammatory infiltrates, in addition to hypertrophic Kupffer cells and mitotic hepatocytes. Also, hypertrophic middle tunic or hypertrophic smooth muscle layers of arterioles was observed in the periportal space, with dilated sinusoidal capillaries and free macrophage infiltration. It is concluded that BEA induces a derangement in the antioxidant status of the liver with the consequent lipid peroxidation response, which may constitute a significant hepatotoxic mechanism of the haloaklylamine. © 1998 John Wiley & Sons, Inc. J Biochem Mol Toxicol 13: 47–52, 1999