Deficiency of Superoxide Dismutase in Endemic Goiter Tissue*

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Abstract
Superoxide dismutase (SOD) activity and its concentration were measued in thyroid tissues obtained from patients with Graves'' disease, Hashimoto''s thyroidits, differentiated thyroid cancer, and endemic goiter (before and after iodine supplementation) as well as in normal thyroid tissue (paranodular tissue) from patients with follicular adenomas. SOD activity was measured by pyrogallol assay in ethanol-chloroform extracts of the thyroid homogenates. The SOD concentration in the thyroid extract was measured as immunoreactive SOD by electroimmunoassay. Endemic goiter tissues (n = 10) contained significantly lower SOD activity [mean, 1.9 .+-. 1.9 ( .+-. SD) vs. 7.5 .+-. 3.9 ng purified SOD/.mu.g DNA: P < 0.02] and concentration (mean, 0.2 .+-. 0.1 vs. 0.8 .+-. 0.5 ng SOD/.mu.g DNA: P < 0.01) compared with those of normal tissues. No other pathological thyroid tissues had such consistently low SOD levels. Lactate dehydrogenase activity, a marker of cytosolic enzyme, was not lower in endemic goiter tissues than in normal tissues, suggesting that both tissues possessed functioning cells capable of producing cytosolic enzyme. Thyroid tissue from endemic goiter patients previously treated with iodized oil injection also had low SOD activity and concentration. Western blot analysis indicated that SOD protein in the endemic goiter tissue did not differ from that in normal thyroid tissue. We conclude that there is deficiency of cytosolic SOD in endemic goiter tissue. Since the deficiency of cytosolic SOD causes more prolonged exposure to oxygen free radicals, the decrease in SOD might contribute to the degenerative changes frequently found in these tissues.