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

Abstract

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<0.025); nonthyroid basal 83.0 ±21.5, ethanol maximum 137±31.1 (p<0.01) in picomoles/30 min per mg protein]. This increase was dose dependent over a range of 3–9% ethanol. There was no difference in the degree of ethanol stimulation of AC between normal (28.7±16.3) and neoplastic (21.4±7.8) thyroid or between normal (89.0±8.9) and neoplastic (75.2±23.7) nonthyroid tissues. When ethanol (5%) was given along with TSH, sodium fluoride, Gpp(NH)p, or forskolin, there was a greater increase in AC activity than when no alcohol was present. The combined effect of TSH and ethanol (140.1±49.4) at maximal concentrations was comparable or greater than the result when TSH and ethanol were added separately (121.5±41.8). Thus, ethanol stimulates TSH binding and also activates AC in nearly all normal and neoplastic human tissues. This may be important biologically as well as experimentally since some compounds used in AC assays (in particular, forskolin) are dissolved in ethanol.

Alcohol consumption is associated with reduced prevalence of goitre and solitary thyroid nodules

“…Other possibilities are that alcohol inhibits thyroid hormone metabolism in the liver or peripheral tissues and thereby decreases the need for thyroid hormone secretion. Yet another possibility is the induction by alcohol of relative resistance to TSH; experimental studies with supra-physiological doses of alcohol rather indicated increased sensitivity to TSH in the presence of alcohol (Clark & Gerend, 1986). Hegedus et al (1988) found slightly increased amount of thyroid fibrosis among alcoholics and suggested a direct detrimental effect of alcohol on the thyroid with shrinkage of the gland.…”

Thyroid function in lead smelter workers: absence of subacute or cumulative effects with moderate lead burdens

“…Least-squares regression was used to determine linear trends in each of the dependent thyroid function variables T 4 , EFT 4 , and TSH by subacute and cumulative lead exposure. Since both age (Harman et al 1984;Gustafson et al 1989) and alcohol consumption (Clark and Gerend 1986;Szilagyi 1987) are known to aect thyroid indices, analysis of covariance (ANCOVA) controlling for these potential confounders was performed to assess covariate-adjusted mean dierences in thyroid function by lead exposure category.…”