The Inhibitory Effect of Acute Administration of Excess Iodide on the Formation of Adenosine 3′,5′-Monophosphate Induced by Thyrotropin in Mouse Thyroid Lobes

Abstract

In a previous paper, we demonstrated that an inhibitory action of excess iodide on thyrotropin-induced thyroid hormone secretion occurs at a site subsequent to the generation of cyclic AMP. In the present study, however, we have found that thyroidal cyclic AMP formation induced by thyrotropin in vitro was markedly inhibited by the acute administration of excess iodide to mice fed a low iodine diet. In contrast, excess iodide failed to produce inhibition in animals fed a regular diet. In vitro stimulation by long-acting thyroid stimulator (LATS), prostaglandin E2, and 4-methylhistamine of cyclic AMP formation in mouse thyroid lobes was also significantly inhibited by the acute in vivo administration of excess iodide. The inhibition was completely relieved by the administration of methimazole prior to excess iodide. Furthermore, it has been shown that thyroid adenylate cyclase activity induced by thyrotropin was markedly depressed by excess iodide under similar experimental conditions. Therefore, it is suggested that one of the inhibitory actions of excess iodide is on the adenylate cyclase-cyclic AMP system and further, that iodide can elicit its inhibitory action after its conversion to some form of organic iodine.

Thyroid function and polyamines. III. Changes in ornithine decarboxylase activity and polyamine contents in the rat thyroid during hyperplasia and involuton.

“…If thyroid ODC activation is mediated via cyclic AMP, the inhibitory effect of excess iodide on the thyroid ODC would be exerted through the inhibition of the adenylate cyclase-cyclic AMP system. It has repeatedly been shown that iodide dramatically reduces TSH stimulation of adenylate cyclase activity both in vivo and in vitro (Van Sande et al, 1975;Sherwin and Tong, 1975;Hashizume et al, 1976).…”

“…Since the inhibitory action of iodide on the adenylate cyclase responsiveness to TSH is abolished by propylthiouracil, methimazole or perchlorate, it has been postulated that the prior organification of iodide is required in its inhibition (Burke, 1970;Ingbar, 1972;Van Sande et al, 1975;Sherwin and Tong, 1975;Hashizume et al, 1976). In the present experiment, however, it is unlikely that other iodinated products such as iodotyrosines and iodohistidines within thyroglobulin act as the inhibitor of thyroid ODC activation, for "organic iodine" has remained decreased all through the KI treatment.…”

An Analysis for Aggravation of Thyroid Function After Discontinuing Potassium Iodine in Graves’ Patients Treated With Methimazole and Potassium Iodine

“…Therefore, KI has been generally prescribed in limited situations such as preparation for thyroidectomy, treatment after radioactive iodine therapy for GD and correction of thyroid function of patients suffering from adverse effects of ATDs [6,7,13,14]. In addition, iodine administration in combination with ATDs has been reported to reduce the efficacy of ATDs in vitro [15][16][17]. There are also some reports that the combination of ATDs with iodine was not effective and KI monotherapy of GD impaired the efficacy of subsequent ATDs therapy [18,19].…”

Characterization of regulation of thyrotropin (TSH) receptor function in thyroid plasma membrane: Interaction between TSH receptor function and activation of adenosine 3',5'-monophosphate-dependent protein kinase.

“…LATS activity was measured as previously described (Hashizume et al, 1976 However, a decrease was also observed in the membranes incubated with buffer alone. In addition to the finding that the decrease was stimulated by adding cyclic AMP to the incubation medium, we observed that cyclic AMP production in the membrane occurred spontaneously even in the absence of TSH in vitro, and we also observed that the decrease was temperature dependent, suggesting that the decrease in the number may be due to a physiological process which requires cyclic AMP.…”

“…Agents which stimulate adenylate cyclase activity, such as prostaglandins (Hashizume et al, 1975(Hashizume et al, , 1976, biogenic amines (Hashizume et al, 1976, Onaya et al, 1977 and immunoglobulin G from patients with Graves' disease (Hashizume et al, 1976) also could release TSH binding activities from thyroid plasma membranes (Hashizume and DeGroot, 1985). In these conditions, one might predict that the TSH binding activity in the thyroid plasma membrane may also be modified by preceding activation of adenylate cyclase or by activation of cyclic AMP-dependent protein kinase.…”