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L. Kayser, P. E. Høyer, H. Perrild, A. M. Wood, and W. R. Robertson


The present study was undertaken to investigate the regulation of intracellular pH in human thyroid epithelial cells and to characterize the kinetics of the acid-extruding processes operating in the absence and presence of HCO 3, Na+ and Cl. A dynamic technique of dual excitation microfluorimetry and the pH-sensitive fluorescent probe 2′,7′-bis-(2-carboxyethyl)-5(and-6)-carboxyfluorescein was employed.

The intracellular pH was 7·01 ± 0·27 (n = 29) and 6·94 ± 0·25 (n = 54) in the absence and presence of HCO 3 respectively. Both in the absence and presence of HCO 3, the recovery from intracellular acid loads was not only due to an Na+/H+ exchange, but also to an Na+-dependent HCO 3/Cl exchange. In alkaline conditions caused by NH4Cl pulsing, an HCO 3/Cl exchange was also found. The cells in HCO 3 responded with a wide range of maximal hydrogen efflux rates in experiments where cells were either pretreated with 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid or incubated with amiloride. The heterogeneity might be due to subpopulations of thyrocytes in different metabolic states or at different points in the cell cycle.

It is concluded that recovery from intracellular acidification in human thyroid cells is due to both Na+/H+ exchange and Na+-dependent Cl/HCO 3 exchange even in nominally HCO 3-free conditions, and that recovery from intracellular alkalinization is due to a Cl/HCO 3 exchange which needs to be characterized further.

Journal of Endocrinology (1992) 135, 391–401

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N Knudsen, I Bulow, P Laurberg, H Perrild, L Ovesen, and T Jorgensen

Tobacco smoking increases the risk of goitre and Graves' disease, but the association with thyroid nodularity and hypothyroidism has not been settled. We investigated 4649 subjects from the general population with questionnaires, thyroid ultrasonography and blood tests. The results were analysed in multivariate regression models. Tobacco smoking was associated with an increased prevalence of thyroid multinodularity (odds ratio (OR) 1.9; 95% confidence interval (CI) 1.4-2.5), but not with increased prevalence of solitary thyroid nodules. The tendency was for a stronger association in the area with the most pronounced iodine deficiency (P for interaction=0.08). Lower levels of serum TSH were found among tobacco smokers (P<0.001), but this association disappeared when adjustment was made for thyroid nodularity and thyroid Volume. The prevalence of elevated TSH levels was markedly reduced among smokers (OR 0.47; 95% CI 0.33-0.67). No association was found between smoking and hyperthyroidism. The observed associations seem to be explainable by the blocking of iodine uptake and organification in the thyroid by thiocyanate, a degradation product of cyanide in tobacco smoke.