Superoxide dismutase (SOD) activity and its concentration were measured in thyroid tissues obtained from patients with
Graves' disease, Hashimoto's
thyroiditis, 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/micrograms
DNA; P less than 0.02] and concentration (mean, 0.2 +/- 0.1 vs. 0.8 +/- 0.5 ng SOD/microgram
DNA; P less than 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.