The acute and subacute oral toxicity of selenocystine was assessed in ICR male mice. In the acute study, the estimated LD50 value for a single oral dose was 76.0 mg/kg (confidence limit : 64.4-89.7 mg/kg) and the minimal lethal dose was 43.2 mg/kg. In the mice administered 50 mg/kg, the liver and kidney injuries were assumed by increase in aspartate aminotransferase, alanine aminotransferase, urea nitrogen and phosphorus, and a decrease of calcium in plasma. In the subacute study, the body weight gain of animals orally administered 10, 20, 30 and 40 mg/kg/d for 30 d significantly decreased with the dosage, and all mice given 30 or 40 mg/kg/d died within the exposure period. Although renal damage was not recognized by biochemical measurements and histopathological examinations, liver damage was apparent by increase in aspartate aminotransferase and alanine aminotransferase in plasma and histopathological findings, vacuolation of centrilobular and/or peripheral hepatocytes. Gel chromatography was carried out on the cytosol from kidney and liver of mice following a single and consecutive administrations of selenocystine. In the kidney, selenium following a single dosage of 50 mg/kg was eluted around the void volume and another fraction in Sephadex G-25 gel chromatography ; most of the selenium following consecutive dosages of 20 mg/kg/d for 30 d, however, was eluted only in the void volume. In Sephadex G-150 gel chromatography of the liver, most of the selenium following a single administration was eluted in the low-molecular fraction, whereas a major peak of selenium following consecutive administrations was eluted in the high-molecular fraction. The findings thus indicate that in the acute toxicity study selenocystine caused hepatic damage and renal damage and in the subacute toxicity liver damage, depending on selenium behavior in these organs.