The structural and functional changes of mitochondrial monoamine oxidase (MAO) in livers of rats fed a selenium (Se)-deficient diet from an endemic area of Keshan disease were investigated. The results indicate that after intake of the Se-deficient diet for 12-14 weeks, MAO activity and lipid fluidity in the mitochondrial membranes were significantly lower than those of the control rats; on the contrary, MAO degradation and lipid peroxides were significantly higher. Concomitantly, Se content and glutathione peroxidase (GPX) activity in hepatic homogenates of Se-deficient rats markedly decreased. These changes could be prevented or returned to the control levels when the rats were fed the same diet but one supplemented with 0.5 mg/kg N a2 SeO3. In vitro, we also showed that adding 0.5 ppm Na2SeO3 in hepatic submitochondria could significantly decrease MAO degradation induced by the intermediates of lipid peroxidation generated through radiolysis of submitochondria with a 6°Co source. Our results suggest that Se may be important for preventing lipid peroxidation in hepatic mitochondrial membranes, thus maintaining structural and functional integrity of MAO.