Iodide supplementation: 200 micrograms daily or 1,500 micrograms weekly?

25 euthyroid volunteers were divided into two groups. Each participant of group A received 200 micrograms iodine in the form of diiodotyrosine per day for a period of eight weeks, i.e. 7 x 200 micrograms iodine/week. Each participant of group B received 1,500 micrograms iodide once a week for a period of eight weeks. In addition to the basal excretion of iodine with the collected urine, the excretion values in group A amounted to 67% of the applied dose in the eighth week. In group B, the excretion values amounted to 65% of the applied dose in the eighth week. Hence, no significant difference between both groups was found.

Pharmacokinetics and urinary excretion of orally administered diiodotyrosine.

Serum levels of diiodotyrosine (DIT) and urinary excretion rates of DIT and iodine were measured in 10 normal subjects after oral administration of 1.57 mumol of DIT corresponding to 400 micrograms of iodine. Serum DIT concentrations rose promptly from a mean endogenous basal level of 0.23 nmol/l to maximum values between 6.0 and 20 nmol/l within 30 min to 1 h after DIT ingestion. Decreasing DIT levels were found in all subjects 2 h after DIT intake. Urinary excretion of intact DIT was low, being less than 1% of the administered dose of exogenous DIT within 2 days. In contrast, 52% of the iodine administered in the form of DIT was excreted in the urine in the same time interval. The rapid absorption of DIT from the gastrointestinal tract combined with rapid and almost complete metabolic degradation by deiodination make orally applied DIT seem a suitable iodine carrier compound for therapeutic purposes.

[Use of levamisole in the complex treatment of patients with thyrotoxicosis]. / Primenenie levamizola v kompleksnom lechenii bol'nykh tireotoksikozom.

The immune status was studied in patients with a familial nature of thyrotoxicosis and without complicated heredity. Disorders in the immune homeostasis, mostly expressed in thyrotoxicosis of familial nature, were revealed. Proceeding from the above the authors proposed a method of multimodality therapy of thyrotoxicosis with antithyroid drugs and immunomodulator levamisole causing a fast disappearance of the clinical signs of thyrotoxicosis, a decrease in thyroid activity and density and the reduction of the number of surgical interventions. The effect may be probably due to the normalization of the immune status.

Experimental observations on the mechanism of hormonal imprinting: influence of actinomycin D, methylamine and colchicine on receptor memory in a unicellular model system.

The first interaction between target cell and hormone gives rise to hormonal imprinting, which accounts for greater responsiveness of the cell at later interactions. The mechanism of hormonal imprinting is obscure; we based experimental approach to its closer study on combined treatment of Tetrahymena, as model cells, with diiodotyrosine (T2), which stimulates the division, and cell growth inhibitors, which interfere with different stages of cell reproduction, and methylamine, which inhibits cluster formation in the membrane. Of these, actinomycin D and methylamine inhibited the growth of the Tetrahymena, while colchicine did not, and all three suppressed the division stimulating action of T2, but could not prevent hormonal imprinting, as demonstrated on later re-exposure to T2 of cells preexposed and not preexposed to T2 in combination with the inhibitors. It appears that the underlying mechanism of hormonal imprinting is highly complex, and involves many subcellular mechanisms and structures, but suppression of, or gross interference with, one or another of these cannot delete, only quantitatively reduce, the consequence of the first interaction with the hormone, i.e. hormonal imprinting.

Involvement of selection and amplification mechanisms in hormone receptor development in a unicellular model system.

It was demonstrated earlier, that long lasting exposure of Tetrahymena to a hormone (histamine) resulted in an increased responsiveness to a later re-exposure. However, it was difficult to establish whether selection or amplification plays a role in receptor differentiation. As diiodotyrosine (T2) enhances the growth of Tetrahymena, in the present experiment the effect of T2-treatment on a long-term culture of Tetrahymena pyriformis was analysed by mathematical-statistical methods to differentiate the effects of selection and amplification mechanisms on hormone receptor development. Although continuous and periodic treatment with T2 enhanced cell division equally, the resulting populations differed in structure. On continuous treatment the population tended to become inhomogenous. The variance tended to increase for 9 days and decreased afterwards without, however, returning to the control level. On periodic treatment the variance was the same as in the control group, but the second and third exposure were significantly more effective than the first treatment, suggesting that the primary encounter with the hormone had given rise to lasting alterations (hormonal imprinting). It follows that continuous exposure involves a selection process which does not, however, account for a steady increase of the growth rate; for initial amplification, taking place also in this condition, and selection which takes effect later, compensate one another's effects. Regarding the unicellular experimental system as a phylo- and ontogenetic model, the conclusion lies close at hand that the selection and amplication mechanisms promote hormone receptor development by joint rather than alternate action.

Enhancement of the sensitivity of Tetrahymena to a second hormonal influence by hormone pretreatment.

Diiodotyrosine and serotonin enhance the growth of Tetrahymena. A second exposure of the unicellular to these hormones accounts for a still greater increase of its growth rate, probably due to the amplification of the receptor induced by the first exposure.