Showing papers on "Iodine published in 1975"

Iodine-induced thyrotoxicosis in apparently normal thyroid glands.

Abstract: Although iodine-induced thyrotoxicosis was reported to occur in patients with obvious underlying thyroid disorders, it is not known to occur in patients with apparently normal thyroid glands. From ten such cases evidence is presented that thyrotoxicosis: a) appeared during treatments by iodide or organic-iodine-containing drugs, in the absence of any past history of thyroid disorder; b) was accompanied by almost undetectable radioiodine uptake which nevertheless could be activated by TSH; c) subsided spontaneously within a few weeks or months after stopping the high intake of iodine; d) and left, after a period of hypothyroidism, an apparently normal thyroid gland which had resumed normal size, function, uptake, and suppressibility.

Iodine absorption in burn patients treated topically with povidone-iodine

Abstract: Providone-iodine is used as a topical antimicrobial in burn patients. Although absorption of iodine has been thought to be negligible, several patients have recently been noted with substantial elevations of serum free iodide. Unexplained abnormalities occurred in several of these patients, renal failure, metabolic acidosis, and elevation of serum glutamic oxaloacetic transaminase. It is conceivable that the large iodide loads noted were at least in part responsible for these abnormalities.

Lithium iodine battery

Abstract: A lithium-iodine cell including a lithium anode, a lithium iodine electrolyte and a cathode comprising a source of iodine in the form of a substantially solid block or pellet of iodine and iodine-containing depolarizer material applied in the form of a relatively thin layer or coating to a lithium surface of the anode and to a surface of the iodine block. The depolarizer material serves to transport iodine ions from the source to the electrolyte, and the material is a charge transfer complex of an organic donor component and iodine such as 2-vinyl pyridine iodide.

Iodine and goiter in children.

Abstract: Goiter examination was performed on 7,785 children aged 9 to 16 years in four areas of the United States--Michigan, Kentucky, Texas, and Georgia. Urinary iodine and creatinine, thyroxine, protein-bound iodine, and plasma inorganic iodide determinations were made on 377 matched pairs of goitrous and nongoitrous control children. The overall prevalence of goiter was 6.8%. Most children with goiter had palpably but not visibly enlarged thyroids and showed no evidence of clinical or biochemical thyroid abnormalitymmean urinary iodine excretion was 452 mug/gm of creatinine, many times the 50 mug/gm of creatinine level used to define deficiency. Children with goiter and areas with high goiter prevalence tended to have higher rather than lower iodine excretion. These findings are consistent with other data indicating high iodine intakes in the United States and suggest that goiter in American children cannot be assumed to be related to iodine deficiencymthe possible role of high iodine intake in the causation of goiter is discussed.

Thyroidal triiodothyronine and thyroxine in Graves' disease: correlation with presurgical treatment, thyroid status, and iodine content.

Abstract: To evaluate the potential contribution of thyroidal secretion to the relative excess of triiodothyronine (T3) production in hyperthyroidism and to investigate the effects of treatment, iodine (127I), T3 and thyroxine (T4) were measured in digests of thyroid tissue obtained at surgery from 13 patients with Graves' disease. In 11 normal human thyroid glands, 127I content was 630 +/- 60 (all values mean +/- SE in mug/ wet weight) T4, 254 +/- 39 and T3 21 +/-3. The T4I was 26 +/- 3% of the total iodine and the molar ratio T4/T3 was 11 +/- 1. The 13 patients with Graves' disease were divided into three groups. Eleven were clinically euthyroid (Groups I and II) and had received either iodide or iodide plus a thiourea derivative before surgery. Two subjects (Group III) received only propranolol. In Group I (n = 8), mean thyroidal 127I content was 320 +/- 50, T4 was 115 +/- 9 and T3 22 +/- 4. The molar ratio T4/T3 was 5.9 +/- 1 and T4I was 26 +/- 2% of the total. Group II patients (3) had the lowest preoperative serum T4 (less than 2.5 mug/dl) and T3 (less than ng/dl) concentrations with TSH elevated in only one (7 muU/ml). Thyroidal 127I was 100 +/- 26, T49 +/- and T3 1.3 +/- 0.3. The % T4I was 5 +/-2. The two chemically hyperthyroid subjects had a mean tissue 127I of 450; T4, 295 and T3, 56, the T4/T3 ratio was 4.5 and % T4I was 42. There was no correlation between tissue 127I and T4/T3 within either the normal or Graves' disease group. Since adequate clinical and chemical control of hyperthyroidism with antithyroid drugs and iodine was attained in the 8 Group I subjects without a decrease in the % T4I or T3I below that of normal thyroids, it suggests that inhibition of iodotyrosine coupling is not required for this effect. The % T4I was below normal only in patients with marked suppression of serum T4 and T3 concentraions. The lack of correlation between tissue 127I and T4/T3 ratio in the treated patients suggests that the lower T4/T3 ratio in Graves' thyroids is independent of intrathyroidal iodine concentrations. This hypothesis is strengthened by the similarly low T4/T3 ratio in untreated subjects with near normal tissue 127I content. Assuming that the thyroid hormones are secreted in the ratios present in these digests, one can estimate that direct secretion by the thyroid could contribute most, of not all, of the excess T3 production in Graves' disease.

The automatic determination of iodide or iodate in solution by catalytic spectrophotometry, with particular reference to river water

Abstract: A catalytic procedure, in which a Technicon AutoAnalyzer(I) is used, for determining iodide or iodate (50 µg l–1) added to river water (during river-flow gauging operations by the dilution method) is described. The maximum error of the analytical procedure, as determined by replicate analysis of six sets of eleven samples, is ± 0·36 per cent. in the range 20–100 µg l–1. The setting up of the procedure is described in detail, according to Mark's (1973) recommendations. The shape of the most appropriate calibration graph is considered. Also, the effects of changes in temperature, reaction period and spectrophotometric variables are discussed. This information could be used directly in the development of methods for determining iodine in other types of sample, e.g., protein-bound iodine in blood or urine and iodate or iodide in sea water, etc. Further, it could also be used in developing other automatic procedures that rely upon catalytic reactions that follow a pseudo-first-order behaviour.

Free diiodotyrosine effects on protein iodination and thyroid hormone synthesis catalyzed by thyroid peroxidase.

Abstract: Free diiosotyrosine exerts two opposite effects on the reactions catalyzed by thyroid peroxidase, thyroglobulin iodination and thyroid hormone formation. 1 Inhibition of thyroglobulin iodination catalyzed by thyroid peroxidase was observed when free diiodotyrosine concentration was higher than 5 μM. This inhibition was competitive, suggesting that free diiodotyrosine interacts with the substrate site(s) of thyroid peroxidase. Free diiodotyrosine also competitively inhibited iodide peroxidation to I2. 2 Free diiodotyrosine, when incubated with thyroid peroxidase in the absence of iodide was recovered unmodified; in the presence of iodide an exchange reaction was observed between the iodine atoms present in the diiodotyrosine molecule and iodide present in the medium. Using 14C-labelled diiodotyrosine, 14C-labelled non-iodinated products were also observed, showing that deiodination occurred as a minor degradation pathway. However, no monoiodo[14C]tyrosine or [14C]tyrosine were observed. Exchange reaction between free diiototyrosine and iodide is therefore direct and does not imply deiodination-iodination intermediary steps. Thyroglobulin inhibits diiodotyrosine-iodide exchange and vice versa, again suggesting competition for both reactions. These results support, by a different experimental approach, the two-site model for peroxidase previously described by us in this journal. 3 Free diiodotyrosine when present at a very low concentration, 0.05 μM, exerts a stimulatory effect on thyroid hormones synthesis. The relationship between diiodotyrosine concentration and thyroid hormone synthesis give an S-shaped curve, suggesting that free diiodotyrosine acts as a regulatory ligand for thyroid peroxidase. Evidence is also presented that free diiodotyrosine is not incorporated into thyroid hormones. Therefore, thyroid peroxidase catalyzes only intra-molecular coupling between iodotyrosine hormonogenic residues. 4 Finally, although no direct proof exists that these free diiodotyrosine effects upon thyroglobulin iodination and thyroid hormone synthesis are physiologically significant, such a possibility deserves further investigation.

Alimentärer Jodmangel in der Bundesrepublik Deutschland

Abstract: Urinary iodine excretion of 1945 schoolchildren aged 13 to 15-years from 24 cities throughout the Federal Republic of Germany (FRG) was measured. For comparison, urinary excretion of 5678 adults from 20 cities was calculated from the 24-hour radio-iodine uptake (RIU) by the method of Oddie. On the average the schoolchildren excreted 25.1 mug iodine per g creatinine: by WHO criteria this can be classified as a grade II iodine deficiency. There was a significant decline of urinary iodine excretion from North to South of the FRG. Urinary iodine excretion of children with thyroid enlargement (21.9 mug/g) was significantly less than that of normal children (26.1 mug/g creatinine; P less th that 0.0005). Urinary iodine excretion of adults averaged 25 to 35 mug/g creatinine, values calculated from RIU agreeing well with those determined chemically. Alimentary iodine intake was found to vary between 30 and 70 mug/d throughout the FRG, which is less than 30% of WHO recommended figures for optimal goitre prevention (150-200 mug iodine per day). Alimentary iodine deficiency has been demonstrated throughout the FRG, increasing from North to South in parallel with an increase in goitre rate. Goitre prevention through compulsory iodinization of salt is recommended.

Iodoglucagon. Preparation and characterization.

Abstract: Iodinated derivatives of glucagon containing an average of 1 to 5 g-atoms of 127I per mol have been prepared by reacting the hormone with increasing amounts of iodine monochloride. Their iodoamino acid composition has been determined by ion-exchange chromatography and electrophoresis, following hydrolysis by pronase. Iodination of the two tyrosyl residues occurs first and is nearly complete after addition of a 4-fold molar excess of ICl. Iodination of the single histidyl residue is a later event and does not exceed an average of one atom per residue. Hydrolysis of iodoglucagon by trypsin and subsequent separation of the iodotyrosyl peptides shows that iodine is equally distributed between tyrosyl residues 10 and 13. Crude iodoglucagon containing an average of 1 g-atom of iodine per mol has been resolved into several components of differing iodine content and iodoamino acid composition by chromatography on DEAE-cellulose. Monoiodoglucagon isolated by this procedure shows a single band when analyzed by polyacrylamide gel electrophoresis. Iodoglucagons containing an average of 1 to 4 g-atoms of iodine per mol are more potent than native glucagon in their ability to stimulate adenylate cyclase activity and to bind to glucagon receptors of liver cell membranes of the rat. The maximal increase in biological potency occurring upon iodination is about 5-fold with respect to adenylate cyclase activity, and 2-fold with respect to binding to receptors; tetra and triiodinated derivatives show, respectively, the highest potency. Similar effects occur whether inactivation by liver membranes is inhibited or not, indicating an enhancement in the intrinsic affinity of iodoglucagon for the receptors. Iodination beyong 4 g-atoms per mol slightly decreases the affinity of the hormone for adenylate cyclase and for the receptors. Iodination causes a 2-20 fold decrease in the ability of liver plasma membranes and of blood plasma to inactivate glucagon in vitro; these effects correlate with the degree of iodination. With liver microsomal membranes, a decrease in glucagon inactivation occurs only at iodine contents exceeding 4 g-atoms per mol, and lower degrees of iodination result in opposite effects. Monoiodination causes a 4-6-fold increase in the plasma concentration of glucagon within the first 18 min following a single intrvenous injection of the hormone to rats. More extensive iodination results, in addition, in a marked decrease in the rate of dissappearance of glucagon from the blood. The immunological reactivity of glucagon is little affected by monoidination, but strongly depressed by higher degrees of iodination...

35-S-antithyroid drug concentration and organic binding of iodine in the human thyroid.

Abstract: 35S-methimazole (MMI), 35S-carbimazole or 35S-propylthiouracil (PTU) were given orally to fifty-five patients at various times up to 12 h before surgical thyroidectomy. The amount of 35S radioactivity and labelled drug in thyroid and plasma samples was measured. Intrathyroidal inhibition or organic binding of iodine by MMI, carbimazole and PTU was measured after intravenous administration of 131I, 132I or 125I-iodide. After administration of 35S-carbimazole or 35S-MMI the thyroid to serum (T/S) ratio of 35S radioactivity was greater in thyrotoxic glands than in non-toxic adenoma tissue. 35S-MMI was found in thyroid and plasma samples after administration of 35S-carbimazole. The T/S 35S-MMI was greater than 1 in most but not all patients. 35S radioactivity was also concentrated in the thyroid after administration of 35S-PTU. In thyrotoxic glands there was an 80% inhibition of iodine organification in patients receiving MMI and 60% for those receiving PTU. It is suggested that carbimazole and MMI can be given once or twice daily in some patients but PTU would be less suitable for this dose schedule.

Uptake by perennial ryegrass of iodide, elemental iodine and iodate added to soil as influenced by various amendments.

Abstract: Perennial ryegrass was grown in pots in a sandy loam soil, into which iodide, elemental iodine or iodate had been incorporated at a rate of 20 mg I/kg. The uptake of iodine into the herbage was much greater from iodate than from the other two forms. Replacement of 5 % of the soil by well-decomposed farmyard manure reduced uptake from all three forms of iodine more than ten-fold. Similar replacement by chalk reduced uptake from iodide but increased uptake from iodate. The recovery of added iodine in three successive harvests of ryegrass ranged from 0.03% for elemental iodine in combination with soil + FYM to 2.16% for iodate in combination with soil + chalk.

Acute effects of thyroxine, triiodothyronine, and iodide on thyrotropin secretion.

Abstract: Rats fed a Purina or low-iodine diet (LID) for varying periods were serially sampled before and after a single iv injection of T4, T3, iodide or saline. Suboptimal replacement doses of T4 and T3 were given to rats fed LID for 2 months or 1 year (basal TSH, approximately 1000 and 2000 muU/ml, respectively). Both 1 mug T4 and 0.25 mug T3/100 g BW dropped plasma TSH to 70% of the initial level at 15 min and to 10--20% at 4 h. By 12 h TSH had begun to rise in 2-month LID rats, followed by a secondary decline 3--5 days after injection. Statistical comparison of the slopes of the initial TSH decline indicated there was no significant difference between the effect of T4 and T3. There effect of graded doses of T3 (0.01--0.3 mug/100 g) was also examined. There was a highly significant correlation of the magnitude of TSH suppression with the dose of T3 administered. Saline had no effect but 0.65 mug iodide/100 g BW (equal to that in 1 mug T4) had a delayed effect, depressing TSH to a minimum of 25% of the initial value at 48 h in 2-month LID rats. There was no difference in the effect of these doses of T4, T3, or saline in purina-fed rats (basal TSH, 170 muU/ml). T4 or T3 in physiologically equivalent doses thus produces an identical prompt rate of decrease in plasma TSH, indicating that both hormones possess intrinsic hormonal activity. The delayed effect of iodide is presumably because it must first be incorporated into T4 and T3 and secreted by the thyroid gland. The similarity of depression of plasma TSH by thyroid hormones or saline injection in Purina-fed rats is believed due to a nonspecific stress effect in these animals with a low basal rate of TSH secretion. The non-specific inhibition of TSH secretion is minimal in the iodine-deficient rats with a much higher basal rate of TSH secretion, presumably because of relative vectorial influences.

Purification of acetic acid

Abstract: A process is provided for purification and drying of acetic acid containing water and methyl iodide and hydrogen iodide as contaminants. The process comprises distillation in a two-zone system wherein the major part of the methyl iodide and hydrogen iodide and some water are removed as overhead and bottoms, respectively, from the first zone; a stream from the middle section of the first zone is introduced into a second zone into which there is also introduced a stream of methanol; and a stream of dry purified acid is recovered from the bottom of said second zone. The process provides both for the recovery of the iodine components and the methanol added for re-use in production of additional acetic acid by the reaction of methanol and/or methyl acetate with carbon monoxide in contact with a catalyst system formed on mixing of a rhodium or iridium component and an iodine component in the presence of carbon monoxide.

Deficient cytochrome b5 reductase activity in nontoxic goiter with iodide organification defect.

Abstract: A 37-yr-old woman with nontoxic goiter is presented. The thyroid 131 I uptakes at 3 and 24 hr were, respectively, 77.1% and 81.4% dose. Thiocyanate discharged 65.5% of the accumulated 131 I in 30 min. In vitro organification of iodine in the thyroid homogenate from the patient was impaired and it was restored to normal by the addition of H 2 O 2 , glucose, and glucose oxidase system, FAD, or reduced cytochrome b 5 . Riboflavin, FMN, oxidized cytochrome b 5 , oxidized or reduced cytochrome c, NAD(H), and NADP(H) were ineffective in the reaction. The microsomal NADH-cytochrome b 5 reductase activity was definitely low in the patient's thyroid. It was augmented to a normal level by incubation of the microsomes with FAD for 30 min or more. The activities of thyroid peroxidase, G6-PD, 6-PGD, catalase, protease, and NADPH-cytochrome c reductase were within normal limits. The major thyroid protein was normal thyroglobulin which could be readily iodinated in the presence of H 2 O 2 and horse radish peroxidase. These findings suggest the correlation of an iodide organification defect with a cytochrome b 5 reductase deficiency. Administration of high doses of FAD led to the restoration of thyroidal iodide organification mechanism associated with an increased thyroid hormone production and to a marked decrease of the goiter. Riboflavin was given without effect even at a high dosage level. Consequently, it seems likely that the deficient cytochrome b 5 reductase activity in this patient is due to a defect in the biosynthesis of FAD, the coenzyme of the reductase, from riboflavin.

The effect of excess dietary iodine on pregnant mares and foals.

Abstract: On a thoroughbred stud four foals were born with greatly enlarged thyroids and leg weakness. Two foals died within 18 hours of birth, the others subsequently recovered. An enlarged thyroid was also evident in one of the resident mares. The thyroids from the dead foals were hyperplastic. Feed analyses showed that the mares had an iodine intake of about 83 mg daily, 8-8 ppm of the dietary dry matter, due almost entirely to the high iodine content of a proprietary compound horse nut which had been fed at the daily rate of 12 lb per head. It was concluded from the histology of the thyroids, the high intake of iodine, the lack of response to treatment with potassium iodide and the elevated levels of serum protein bound iodine that the condition of the foals on the stud was caused by an excess of iodine fed to the mares during pregnancy.

Rat Mammary Gland Atypia Produced by Iodine Blockade with Perchlorate

Abstract: Summary Prior published work from our laboratory concluded that there was a need for appropriate metabolic activity of iodine in breast tissue for normal growth and development. Results from studies in rats that were made iodine deficient showed histological changes in the breasts that were atypical and dysplastic. These tissue findings were further affected by the presence of estrogen and thyroxine. These changes parallel the iodine uptake of the tissues, thus representing a difference in the utilization of iodine by the mammary glands. Using an ion blockade agent, sodium perchlorate, breast tissues lacking iodine were evaluated by both endocrine and histological techniques. A dose-response series was completed that showed that perchlorate therapy for 8 weeks at 400 mg/100 ml produced breast blockade by a reduction in iodine uptake of greater than 52% of the control. At these levels, the histological experimentation showed atypia and some pleomorphism of the cells, particularly in the glands of the lobules. Blockade was less effective in estrogentreated groups. It is especially notable that both histological changes and uptake reduction were greatest in those breasts that had been rendered euthyroid by thyroxine replacement, thus clearly indicating the necessity of iodine itself for maintenance of normal breast development. By this blockade the responses of iodine inadequacy in the breast were shown to cause abnormal tissue changes relative to the percentage of the block obtained.

Electrochemical chlorine flux monitor

Abstract: This apparatus for monitoring the chlorine concentration of water has a uue internal calibration capability and a high sensitivity. A water sample is mixed with a solution of potassium iodide and the reaction produces a mole of iodine for every mole of chlorine present in the water. The mixture is passed through a detection and calibration assembly wherein the iodine is detected amperometrically by a detection cell. Calibrant (known) iodine fluxes, equivalent in effect to the unknown chlorine-produced iodine fluxes, are supplied to the detection cell during calibration runs by means of an upstream calibration cell which electrolyzes the iodide (preferably added to distilled water) to iodine at flux rates given simply by the electrolyzing currents divided by Faraday's constant. An electronics package having gain and offset controls and a concentration display is provided.

The iodine requirement and influence of iodine intake on iodine metabolism and thyroid function in the adult beagle.

Abstract: Various aspects of iodine metabolism were studied in adult beagles maintained at iodine intake levels ranging from 480 to 20 mug/day. On the basis of changes in radioiodine metabolism, the minimum daily iodine requirement of the adult beagle was found to be 140 mug. Although striking changes were observed in radioiodine metabolism when iodine intake was reduced to 90mug/day, serum T4 and T3 levels were unaffected. Marked reductions in serum T4 occurred in dogs restricted to an iodine intake of 50 or 20 mug/day, but even at these low levels of iodine intake there were only slight reductions in serum T3 concentration and a eumetabolic state was maintained. Prolonged iodine deficiency (8-12 months) resulted in variable patterns of thyroid histology, which were related to differences in thyroidal 127I content and in the rate of release of radioiodine from the thyroid. The heterogeneity in thyroid morphology and iodine kinetics did not, however, have a significant effect on serum T4 and T3 levels.

Effects of TSH on Iodide Transport by MouseThyroid Lobes in Vitro

Abstract: Thyroidal iodide concentration by in vitro mouse thyroid lobes was studied by determining the equilibrium tissue/medium iodide concentration ratio (T/M[I-]), thyroidal I- influx, and thyroidal I- efflux in the presence and absence of CIO4-. Chronic thyroid stimulation by low dietary iodine increased the T/M[I-], and the increase was linearly related to I- influx. There was no difference in efflux rate when animals fed low and high iodine diets were compared, although the efflux with C1O4- added to block influx was increased by low iodine diet. Addition of TSH in vitro caused a delayed fall in T/M[I-] with a similar TSH concentrationdependence as colloid droplet formation. The TSH effect was mimicked by exogenous cyclic AMP but could be dissociated from stimulation of hormone release by colchicine. Thyroidal I- efflux was increased up to 20-fold by C104-. In the presence of C104- short-term and equilibrium-labeled I- exited at the same rate, but in the absence of C1O4- short-term-labeled I- efflux was cons...

Methods for preparing solid iodine carrier mixtures and solid formulations of iodine with iodine carriers

Abstract: The improved approach to the direct formulation of solid iodine carriers containing poly (N-vinyl-2-pyrrolidone) and an iodide, as disclosed in copending application Ser. No. 360,338, has been extended to the direct formulation of solid products containing, in addition to the PVP and iodide, compatible additives such as nonionic detergent, anionic detergent, elemental iodine and mixtures thereof, as well as to the direct formulation of other solid iodine carriers.