Effect of Thyroid Status on Ouabain Binding to the Human Lymphocyte

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Abstract
Lymphocyte Na-K ATPase was evaluated as an index of thyroid status in man. Lymphocytes from 24 untreated hypothyroid patients and 11 hyperthyroid subjects were sampled n i parallel with normal lymphocytes, and Na-K ATPase activity was assessed by measurements of ouabain binding to a plasma membrane fraction or to whole cells. In both systems, ouabain bound saturably and specifically, resulting in linear Scatchard plots. Normal lymphocyte plasma membranes bound 2.30 ± 0.16 pmol ouabain⁄mg protein (mean ± SEM; n = 11), with a Kd of 68 ± 12 nM. Intact normal lymphocytes bound 3.24 ± 0.30 pmol ouabain⁄10(7) cells (n = 14), representing 189,000 sites⁄cell. In hypothyroidism, ouabain binding, when compared with normal cells sampled on the same day, was reduced by 22.0 ± 5.3% (n = 11; P < 0.001) in plasma membranes and by 29.1 ± 3.5% (n = 14) in whole lymphocytes (P < 0.001), but there was no signif(icant change in the K)d in the membrane fraction. In 6 subjects, the decrease in ouabain binding to lymphocytes was reversed by thyroid hormone replacement. Red cells from hypothyroid subjects showed normal ouabain binding. Ouabain binding to hy-perthyroid plasma membranes (2.42 ± 0.18 pmol⁄mg protein) was not significantly different from normal. The results in hypothyroid subjects are consistent with the hypothesis that lymphocyte Na-K ATPase is regulated by thyroid hormones. However, lymphocyte Na-K ATPase does not increase in parallel with elevated thyroid hormone levels in hyperthyroidism. The mechanisms underlying these observations remain to be clarified. (J Clin Endocrinol Metab54: 1150, 1982)