Exposure to ionizing radiation causes radiolysis of water in tissues leading to generation of reactive oxygen species (ROS), which are known to affect the antioxidant defense systems and induce lipid peroxidation (LP). Use of radioactive iodine (131I) for diagnosis and therapy of thyroid disorders may also generate ROS in the thyroid. Early (24 and 48 hours) and late (18 days) effects of subablation doses of 131I (370/555/1110 kBq) on the antioxidant defense and LP in the thyroid tissues have been studied. LP was elevated in all 131I treated groups by 10% to 41%. Although there was no change in catalase (CAT), the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities showed evidence of change from 48 hours onwards--SOD decreased by 32% to 56% and GPx increased by 15% to 43%. Nonprotein thiols (reduced glutathione, GSH) showed an elevation of 16% at 24 hours, but later declined by 15% by day 18 after 370 KBq of 131I. Thus, the increase in LP observed may be due to beta irradiation induced ROS by 131I. The parallel decrease in SOD could be due to inactivation by ROS. The increase in GPx may be a consequence of induction due to elevated LP and/or ROS, which may be inadequate to lower the LP. In spite of elevated LP, the thyroid function appears to be normal.