Effect of ethyl alcohol on the TSH‐receptor‐cyclase system in thyroid and nonthyroid tissues

Alcohol has been documented to be an excellent stimulator of calcitonin secretion in patients with C‐cell hyperplasia and medullary thyroid carcinoma (MTC). We, therefore, investigated the effects of 3–9% ethyl alcohol (ethanol) on the binding of tracer quantities of125I‐labeled bovine thyroid‐stimulating hormone (125I‐bTSH) to its receptor in normal and neoplastic thyroid tissue as well as its effects on adenylate cyclase (AC) stimulation in an 8,000 × g particulate fraction from normal and neoplastic nonmedullary thyroid tissue from 10 patients (20 specimens). We also studied the effect of ethanol on AC activity in 16 other nonthyroidal tissues (5 parathyroid adenoma, 1 pheochromocytoma, 1 sarcoma, and normal and neoplastic breast, kidney, parotid, and colon). These studies demonstrated that ethanol increased the binding of125I‐bTSH to normal and neoplastic thyroid tissue. It also increased AC activity in all but 3 of the 20 thyroid tissues and in all but 3 of the 16 nonthyroid tissues [thyroid basal 20.9±7.1, ethanol maximum 45.9±12.3 (p