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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.

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Differential effects of propylthiouracil (PTU), methimazole (MMI) and thyroidectomy (Tx) on liver and plasma proteins have been studied in rats, some of which have been simultaneously treated with L-thyroxine (T4). Although the absolute liver weights were lower in all hypothyroid groups, the relative liver weights (g/100 g) were significantly higher in PTU and MMI groups, while in Tx group they were lower. T4 administration raised the absolute liver weights in all groups, even though there was no significant difference between relative weights in PTU and MMI groups. In Tx group, however, the relative weight was restored to control level. One of the constituents responsible for the increased relative liver weight was liver protein. The increased liver protein concentration (mg/g) was, however, not reflected in the synthesis rate which was uniformly low in all groups inspite of T4 therapy. Plasma albumin concentration was raised in hypothyroid rats which did not respond to T4 therapy. On the other hand, increased total plasma protein level was restored to normal. Relative 14C-glycine incorporation into albumin, fibrinogen, seromucoids and total proteins was reduced from 14 to 30%, 5.2 to 19% and 13 to 23% of control in PTU, MMI and Tx groups, respectively. Of these, only MMI and Tx groups appeared to be responsive to T4 therapy. Of all the protein fractions, fibrinogen synthesis was least affected by various treatments. To some extent these observations may be explained on the basis of altered general endocrine status and specific extra-thyroidal effects, rather than on the basis of thyroid status alone.

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1 Ricin is known to have diverse effects on the cells of different organs like liver, kidney, pancreas, intestines and parathyroid. 2 Acute decrease in serum thyroid hormone levels 24 h after ricin administration (1.5 μg/100 g) led us to suspect the toxic action of ricin on the thyroid. 3 We monitored the lipid peroxidation (LP) and anti oxidant status of the thyroid tissue to determine the role, if any, played by reactive oxygen species (ROS) in this pathology. 4 An increase of 39% in LP and 47% in superoxide dismutase, along with a 8.5% decrease in catalase points to the imbalance in the antioxidant defence involving hydrogen peroxide and its univalent reduc tion product, the hydroxyl radical. 5 Thyroid histopathology shows destruction of thyroid follicles and necrosis, which may be due to ROS and may partly explain the 50% reduction in circulating thyroid hormones seen after ricin administration.