Showing papers on "Iodine published in 1992"
TL;DR: The data of iodide transport kinetics suggest that thiocyanate can be an antithyroid agent particularly in iodine deficiency.
Abstract: We studied the antithyroid action of cigarette smoking products (nicotine, cotinine, and thiocyanate) in the physiological culture system of porcine thyroid follicles. Iodide uptake, iodine organification, de novo thyroid hormone formation, and iodide efflux were measured in the presence of 0-200 mumol/l nicotine, cotinine, or potassium thiocyanate. Nicotine and cotinine did not inhibit iodide transport or thyroid hormone formation. Thiocyanate concentrations equivalent to serum levels of smokers showed three independent antithyroid actions: (i) inhibition of iodide transport, (ii) inhibition of iodine organification, and (iii) increased iodide efflux. Inhibition of iodide transport by thiocyanate was competitive with iodide and independent of TSH concentration. Thiocyanate did not inhibit TSH mediated cAMP production or Na+K+ ATPase activity, a sodium pump for iodide transport. When 50 mumol/l thiocyanate was added 2 h after incubation with iodide or when 1 mumol/l thiocyanate was added from the beginning of incubation, iodine organification was inhibited without changing iodide transport. De novo thyroid hormone formation was clearly inhibited by 50 mumol/l thiocyanate. Thiocyanate increased iodide efflux although the degrees of iodide efflux by 10 mumol/l and 100 mumol/l thiocyanate did not differ significantly. In summary, thiocyanate, a product of smoking, has three independent antithyroid activities. The data of iodide transport kinetics suggest that thiocyanate can be an antithyroid agent particularly in iodine deficiency.
102 citations
TL;DR: In this paper, the mean air concentration of methyl iodide was 2.4 pptv with a corresponding seawater concentration of 2.6 ng l −1, and chloroiodomethane (CH 2 ClI) was detected in some of the seawater samples as a second volatile organoiodine species.
98 citations
TL;DR: Evidence has been presented to support the idea that iodine plays an important role in autoimmune thyroiditis, and several hypotheses have been proposed.
Abstract: Evidence has been presented to support the idea that iodine plays an important role in autoimmune thyroiditis. Excessive amounts induce thyroiditis in genetically susceptible animal strains, while intrathyroidal depletion of iodine prevents disease in strains susceptible to severe thyroiditis. While the mechanisms by which iodine promotes thyroiditis is unknown, several hypotheses have been proposed. (1) T and/or B cells may react specifically to iodinated portions of thyroglobulin (Tg) so that severe iodine depletion renders Tg non-immunogenic. (2) A defect in the iodine processing machinery in thyroid epithelial cells of a susceptible person or animal may, in the presence of iodine, result in elevated levels of oxygen or iodine radicals, which could damage membrane lipids or proteins. (3) Defective iodine processing may result in the iodination of lipid or proteins (other than Tg) which could act either as immunogens or polyclonal activators.
95 citations
Journal Article•
TL;DR: Results indicate that with increased ingestion of supplemented (I- and F-) NaCl, almost the totality of I- is excreted in the urine while fluoride is either incompletely absorbed or retained by the body to a higher extent.
Abstract: Iodide and fluoride supplemented food grade salt (NaCl) is a common source of these two micronutrients. In a pilot study, we investigated whether increased intake of NaCl supplemented with iodide (I-) and fluoride (F-) results in their higher bioavailability. Twelve healthy adult human volunteers ingested increasing quantities (1, 3, 6 and 9 g) of NaCl with usual diet over 8 days. Sodium (Na+), I- and F- were measured in 24 hour urine specimen. During the 4 day basal period when no additional NaCl was ingested, ingestion of NaCl calculated from urinary Na+ concentration and diuresis was 8.25 +/- 0.67 g/24 h. During the same period 0.11 +/- 0.01 and 0.61 +/- 0.04 mg of I- and F- respectively were excreted in the urine per 24 h. Increased ingestion of supplemented NaCl resulted in higher urinary excretion of sodium while urinary creatinine remained stable. 92% of I- and 40% of F- contained in the additional amount of NaCl ingested were excreted in the urine. These results indicate that with increased ingestion of supplemented (I- and F-) NaCl, almost the totality of I- is excreted in the urine while fluoride is either incompletely absorbed or retained by the body to a higher extent. I- and F- supplemented NaCl is, therefore, an effective vehicle to provide these micronutrients when ingested with diet.
92 citations
TL;DR: The oral administration of a single small dose of iodized oil is capable of correcting iodine deficiency for about a year, and is likely to be more effective, efficient, and acceptable than the administration of either intramuscular or large oral doses of iodization oil.
Abstract: Background. About one billion people world-wide are at risk for iodine deficiency. Despite existing programs of prophylaxis, the prevention of iodine deficiency is still a challenge throughout the developing world. We studied the efficacy of low doses of iodized oil in an area of severe iodine deficiency in Zaire. Methods. Seventy-five subjects with visible goiter were randomly assigned to receive a single oral dose of placebo or either 0.1 or 0.25 ml of iodized oil, corresponding to 0, 47, and 118 mg of iodine, respectively. The mean ages of the subjects in the three groups were 23, 22, and 22 years, respectively, and the ratios of males to females were 0.25, 0.32, and 0.19. Efficacy was assessed by evaluating goiter size and measuring urinary iodine and serum thyroid hormone concentrations for 12 months. Results. Goiter size decreased in most of the subjects who received either dose of iodized oil. Their urinary iodine concentrations were normal for six to nine months and their serum thyroxine ...
83 citations
TL;DR: These effects were directly proportional to the severity of iodine deficiency or extent of iodine excess and suggest that each condition has a different thyroid tumor promotion mechanism.
Abstract: Thyroid tumor-promoting effects of iodine deficiency and iodine excess were investigated in a rodent 2-stage model to estimate an optimal iodine intake range that would not effectively promote development of thyroid neoplasia. Six-week-old male F344 rats were given a single subcutaneous injection of 2,800 mg/kg body weight N-bis(2-hydroxypropyl)-nitrosamine (DHPN) or saline vehicle, maintained on Remington's iodine-deficient diet (21 +/- 2 ng/g iodide), and supplemented with various amounts of potassium iodide up to 260 mg/liter in drinking water to generate conditions ranging from severe iodine deficiency to severe iodine excess. In DHPN-treated rats, both conditions significantly increased thyroid follicular tumorigenesis. In DHPN-untreated rats, iodine deficiency produced diffuse thyroid hyperplasia, characterized by small follicles with tall epithelium and reduced colloid, together with a decrease in thyroxine (T4) and an increase in thyroid-stimulating hormone (TSH). On the other hand, iodine excess produced colloid goiter, characterized by large follicles with flat epithelium and abundant colloid admixed with normal or small-sized follicles lined by epithelium of normal height, together with normal serum T4 and slightly decreased TSH. These effects were directly proportional to the severity of iodine deficiency or extent of iodine excess and suggest that each condition has a different thyroid tumor promotion mechanism. Iodine intakes that showed the least tumor promotion were 2.6 and 9.7 micrograms/rat/day in this study. Promoting mechanisms and the problem of statistically estimating recommended daily iodine intake range are briefly discussed.
80 citations
TL;DR: Five healthy male volunteers were studied both after 4 weeks of treatment with 200 micrograms iodine/d orally (PO) and following experimental iodine depletion by treatment with 3 x 300 mg perchlorate/d PO over a 4-week period, in an attempt to better define the early adaptive responses to an alteration in iodine supply in thyroid function.
Abstract: Five healthy male volunteers (aged 25 to 28 years) were studied both after 4 weeks of treatment with 200 μg iodine/d orally (PO) and following experimental iodine depletion by treatment with 3 × 300 mg perchlorate/d PO over a 4-week period, in an attempt to better define the early adaptive responses to an alteration in iodine supply in thyroid function. Intrathyroidal iodine, serum triiodothyronine (T3), free T3 (FT3), thyroxine (T4), free T4 (FT4), reverse T3 (rT3), thyroxine-binding globulin (TBG), thyroglobulin (Tg), and thyrotropin (TSH) levels (10-minute sampling over 24 hours) were measured at the end of iodine administration and at the end of perchlorate treatment. Thyroid volume was determined by sonography, and iodine content was determined by fluorescence scintigraphy. TSH pulses were analyzed by computer-assisted programs. Comparing both experimental situations, perchlorate treatment significantly reduced intrathyroidal iodine concentration (4.0 ± 1.3 to 3.0 ± 1.2 nmol/mL, P < .05), but thyroid volume and total serum T4, T3, FT3, and TBG levels were not altered. Mean 24-hour serum TSH levels (1.8 ± 0.3 to 1.0 ± 0.3 mU/L, P < .001), amount of TSH secreted/pulse (0.5 ± 0.1 to 0.3 ± 0.1 mU/L, P < .001), and FT4 levels (15.7 ± 1.7 to 14.3 ± 1.4 pmol/L, P < .005) were significantly diminished, whereas Tg levels (18.6 ± 10.0 to 35.1 ± 14.0 ng/mL, P < .01) were significantly increased. Thyroid-specific antibodies were normal and were not altered by treatment. These data suggest a higher sensitivity of the thyroid to TSH in the early adaptation to iodine depletion; thus, less TSH is sufficient to maintain normal thyroid function.
74 citations
TL;DR: In this article, chemical forms of iodine in soil solutions under non-flooded oxidizing and flooded reducing soil conditions were quantitatively analyzed, and the results showed that I¯ (oxidation number −1) was the dominant chemical form (86.8% of water soluble iodine), followed by IO3¯ (11.9%).
Abstract: Chemical forms of iodine in soil solutions under non-flooded oxidizing and flooded reducing soil conditions were quantitatively analyzed. The results showed that IO3¯ (oxidation number +5) was the dominant chemical form under non-flooded soil condition (85.8% of water soluble iodine), although most of the iodine was combined with the soil in an insoluble form. In contrast, under the flooded soil condition, a considerable portion of the insoluble iodine combined with the soils was transformed to water soluble iodine, where the concentration of soluble iodine became much higher than that under non-flooded soil condition, and I¯ (oxidation number −1) was the dominant chemical form (86.8% of water soluble iodine), followed by IO3¯ (11.9%). It was assumed that the redox potential was an important factor affecting the concentration of soluble iodine or the ratio of I¯ to IO3¯ in the soil solution.
72 citations
TL;DR: The uptake of radioactive iodide or chloride by plasma membrane vesicles of bovine thyroid was studied by a rapid filtration technique and the data support the existence of two anionic channels.
Abstract: The uptake of radioactive iodide or chloride by plasma membrane vesicles of bovine thyroid was studied by a rapid filtration technique. A Na(+)-I- cotransport was demonstrated. When this Na(+)-I- cotransport is inactive (i.e., at 4 degrees C and in the absence of Na+), an uptake of iodide above chemical equilibrium could be induced, driven by the membrane potential. The latter was set up by allowing potassium to diffuse into the membrane vesicles in the presence of valinomycin and of an inward K+ gradient. This potential difference (positive inside) induced the uptake of iodide (or other anion present). The data support the existence of two anionic channels. The first one, observed at low near-physiological iodide concentration (micromolar range), which exhibits a high permeability and specificity for iodide (hence called the iodide channel), has a Km of 70 microM. The other one appears similar to the epithelial anion channel as described by Landry et al. (J. Gen. Physiol. 90: 779-798, 1987); it is still about fourfold more permeable to iodide than to chloride and presents a Km of 33 mM. Under physiological conditions the latter channel would mediate chloride transport, and the iodide channel, which is proposed to be restricted to the apical plasma membrane domain of the thyrocyte, transports iodide from the cytosol to the colloid space.
64 citations
TL;DR: The present results suggest that some patients with a previous history of AIT may be at risk to develop hypothyroidism when given excess iodine, and excess iodine may not be the cause of the hyperthyroidism associated with amiodarone therapy.
Abstract: Amiodarone-induced thyrotoxicosis (AIT) occurs most frequently in patients with underlying thyroid disease and is generally believed to be due to the iodine contamination of amiodarone and iodine released by the metabolism of the drug. We and others have suggested that the thyrotoxicosis may also be secondary to amiodarone-induced thyroiditis. To further determine the etiology of AIT, we administered large doses of iodides [10 drops saturated solution of potassium iodide (SSKI) daily] to 10 euthyroid patients long after an episode of AIT believed to be due at least in part to amiodarone-induced thyroiditis. Six of these 10 patients had an abnormal iodide-perchlorate discharge test before SSKI administration, indicating a subtle defect in the thyroidal organification of iodide. During SSKI administration, 6 patients developed marked iodine-induced basal and/or TRH-stimulated serum TSH elevations, 2 had suppressed basal and TRH-stimulated TSH values, and 2 had normal TSH responses compared to SSKI-treated e...
52 citations
TL;DR: In this paper, the authors studied the recovery of thyroid function in patients with both thyroid and renal dysfunction, and found that impaired renal handling of iodine rather than autoimmune mechanism may have a significant role in the pathogenesis of reversible hypothyroidism.
Abstract: Recovery of thyroid function in patients with both thyroid and renal dysfunction was studied. Among 245 patients with primary hypothyroidism (serum TSH greater than 10 mU/l), 36 had mild to severe renal dysfunction (serum urea nitrogen greater than 7.1 mmol/l and creatinine greater than 106 mumol/l). Of these 36 patients, recovery of the thyroid function after iodine restriction was observed in 30 (83%), in whom an elevated serum non-hormonal iodine level (median 236, range 67-15,591 micrograms/l, N = 19) and a high thyroidal radioactive iodine uptake (51.5 +/- 29.3% at 24 h, N = 26) were observed. The perchlorate discharge test was positive in 7 of 13 patients examined, suggesting an iodide organification defect rather than an atrophic or destructive change in the thyroid. Antithyroid antibodies were negative in 22 patients (73%) and an almost normal thyroid gland or colloid goitre was confirmed histologically in 8 of them. After a 13.2 mg potassium iodide loading test, 24 h urinary excretion of iodine was about 60% in normal controls, but only 10% in a different group of six euthyroid patients with renal dysfunction. These findings suggest that impaired renal handling of iodine rather than autoimmune mechanism may have a significant role in the pathogenesis of reversible hypothyroidism found in patients with renal dysfunction, probably through a prolonged Wolff-Chaikoff effect.
TL;DR: Excessive or insufficient iodine intake or wide swings in iodine intake over prolonged periods may contribute to thyroid disorders in cats.
Abstract: Twenty-eight varieties of commercially-available cat food (23 canned, 5 dried) were analysed for iodine. The iodine concentration varied from less than 0.37 micromol/kg to 41.8 pmol/kg, wet weight (less than 1.48 micromol/kg to 167 micromol/kg, dry weight). Excessive or insufficient iodine intake or wide swings in iodine intake over prolonged periods may contribute to thyroid disorders in cats.
TL;DR: In this paper, the chemistry of methyl iodide on Ni(100) surfaces has been studied by using x-ray photoelectron spectroscopy (XPS) and the activation energy for the C-I bond scission was estimated to be about 3.5 kcal/mol based on results from isothermal XPS experiments.
Abstract: The chemistry of methyl iodide on Ni(100) surfaces has been studied by using x‐ray photoelectron spectroscopy (XPS). Methyl iodide adsorption is molecular below 100 K, but the C–I bond begins to cleave around 120 K and is completely broken by 160 K. The activation energy for the C–I bond scission was estimated to be about 3.5 kcal/mol based on results from isothermal XPS experiments.
TL;DR: The duration and the extent of the antithyroid effect of lodides in hyperthyroldlsm is clarified and whether Iodides have an additional perlpheral effect on the metabollsm of thyrold hormones is investigated.
Abstract: OBJECTIVE To clarify the duration and the extent of the antithyroid effect of lodides In hyperthyroldlsm, and to Investigate whether Iodides have an additional perlpheral effect on the metabollsm of thyrold hormones, as has been reported for some organic IodIne compounds.
DESIGN The effect on the perIpheral thyroId hormone levels of 150 mg of potassIum Iodide dally (equIvalent to 114 mg of IodIde) foro 3–7 weeks was compared In 21 hyperthyroId patients and 12 healthy controls. A possible effect of IodIde on the perIpheral metabollsm of thyroId hormones was Investigated by assessing the serum levels of thyroid hormone In 12 hypothyroid patients on thyroxine replacement for 2 weeks.
PATIENTS There were 21 thyrotoxic patients, 12 healthy hospital controls, and 12 patients with complete or near-complete hypothyroldlsm, on thyroxine replacement.
MEASUREMENTS The following were measured before and at weekly intervals after Iodide administration: (1) pulse rate, (2) serum T4, (3) serum T3, (4) serum TSH, (5) serum thyroxlne-binding capacity (TBC), (6) serum rT3, (7) serum thyroxine-binding globulln (TBG), (8) the free-T4 Index, calculated as T4/TBC.
RESULTS In the hyperthyroid patients serum T4, T3 and rT3 decreased, whereas serum thyroxlne-binding globulin and thyroxine binding capacity Increased. Serum T3, however, did not become completely normal In all cases. After 21 days, serum T4 and T3 started Increasing again in some cases, but other patients remained outhyrold even after 6 weeks. In the normal controls there was a small but significant and consistent decrease In serum T4, T3 and rT3 and an Increase In serum TSH. Finally, In the T4-treated hypothyroid patients there was no consistent change, except for an Increase of serum T4 at 1 and 14 days and a decrease of serum TSH the first day.
CONCLUSION Iodides in hyperthyroldlsm have a variable and unpredictable Intensity and duration of antlthyrold effect. Their antithyroid effect Is smaller In normal controls. They have no Important effect on the peripheral metabolism of thyroid hormones.
01 May 1992
TL;DR: In this paper, the authors found that the concentration of iodide was inversely related to that of iodate with a ratio of about −1 suggesting that the in situ reduction of iodates to iodide may play an important role in determining the distribution and speciation of iodine in these waters.
Abstract: The hydrographic front that separates the turbid inner shelf water from the “clearer” midshelf water on the southeastern U.S. continental shelf is accompanied by dramatic changes in the speciation of iodine. The total iodine to salinity ratio, or specific iodine, in the inner shelf was slightly lower, usually about 10% lower, than that in the midshelf, which was in turn slightly lower than those observed in the open oceans. This suggests that the efficiency for the removal of dissolved iodine to the particulate phase may increase progressively from the open ocean to the midshelf water to the inner shelf water. On the other hand, the average concentration of iodate increased by a factor of about three from the inner shelf to the midshelf water while the concentration of iodide decreased by about 30%. Above a concentration of iodate of about 0.05 μM, the concentration of iodide was inversely related to that of iodate with a ratio of about −1 suggesting that the in situ reduction of iodate to iodide may play an important role in determining the distribution and speciation of iodine in these waters. The relationship between the concentration ratio of iodate to iodide and the concentration of nitrate plus nitrite also falls into a definable pattern. Waters with high concentration ratios of iodate to iodide (>0.5) were found mostly when the concentration of nitrate plus nitrite fell below 0.5 μM. Above this concentration of nitrate plus nitrite, the iodate to iodide ratio was almost invariably below 0.5.
Journal Article•
TL;DR: The levels of contaminant, free inorganic iodide and iodine were determined in several commonly used ionic and nonionic intravenous contrast media to gain a better understanding of the roles of these compounds in radioactive iodine uptake inhibition.
Abstract: The levels of contaminant, free inorganic iodide and iodine were determined in several commonly used ionic and nonionic intravenous contrast media to gain a better understanding of the roles of these compounds in radioactive iodine uptake inhibition. The method, which involved a reduction-oxidation reaction using sodium nitrite, yielded accurate and precise data for the iothalomate based ionic contrast media as well as the nonionic contrast media. There was no free iodine in any of the contrast media tested. There was considerable variation in free iodide levels, ranging from 1.38 microgram/ml to 20.84 microgram/ml among the different contrast media, although significant differences between the ionic and nonionic media were not found. These levels of contaminant iodide are thought to play a role in the short-term inhibition of radioactive iodine uptake.
TL;DR: An introductory description of the main phenomena connected with ultrasonic induced cavitation is given in this article, which mainly describes the motion of microbubbles present in a cavitating liquid, and the sonolysis of carbon tetrachloride is described in aqueous solutions of potassium iodide.
TL;DR: Enhanced iodine uptake by the mammary gland of the lactating mothers from endemic goiter area in the presence of low iodine supply can account for the above findings.
Abstract: Iodine balance during pregnancy and lactation was investigated by measuring iodine con-centration in the urine of 11 pregnant women, born and living in a moderately iodine deficient endemic goiter area in Northeastern Sicily, collected during the last week of pregnancy, and between the 5th and 7th day after delivery, and in their milk sampled simultaneously with the urine of their newborns. The results were compared with those obtained on similar samples from 16 euthyroid age-matched nongoitrous women and their offspring from an iodine sufficient area. Urinary iodine concentration in pregnant women from the endemic area (1.28 ± 0.13 gMg/dl, mean ± SE) was significantly lower than that of pregnant women from the iodine sufficient area (3.77 ± 0.57 gMg/dl) (t = 3.56, p < 0.005). The longitudinal measurement of iodine concentration in each nursing woman showed a marked increase (≈90%) when compared with the values obtained during pregnancy in both endemic and control groups (2.32 ± 0.36 and 7.76 ± 2.08 gMg/dl; t = 2.13 p < 0.05, respectively). The slight difference in milk iodine concentration between the endemic (3.25 ± 0.77 gMg/dl) and the control (4.33 ± 0.57 gMg/dl) group was not statistically significant (t = 1.14; p < 0.5, NS). Similarly no difference was found in urinary iodine excretion between the endemic and the control newborn groups (3.41 ± 0.76 and 4.30 ± 0.65 gMg/dl, respectively, t = 0.88 p < 0.1, NS). The similarity between milk and urinary iodine content of newborns in the two areas was in contrast with the greatly different daily iodine intake of the mothers (endemic area 45 ± 6 gMgl/24h vs control area 106 ± 23 gMgl/24h, t = 2.14 p < 0.05 estimated in general population). An explanation for this was given by the calculation of milk iodine uptake (% intake) by the mammary gland, which was higher in endemic as compared with the control group (45 ± 6% vs 34 ± 4%). Enhanced iodine uptake by the mammary gland of the lactating mothers from endemic goiter area in the presence of low iodine supply can account for the above findings. This enhanced concentrating capacity, being inversely related to daily iodine intake (r = -0.41 p < 0.05), appears to be a further effort to effectively compensate for iodine deficiency, in order to prevent congenital hypothyroidism and to correct transient hypothyroidism of the infant.
TL;DR: The method provides a detection limit of 0·4 ng and a sensitivity of 40 pg and is also applicable for the determination of iodine in serum, urine and other biological materials.
TL;DR: It is concluded that the serum free thyroxine level in cats, as measured by a kit designed for human serum, is acutely responsive to changes in iodine intake.
Abstract: Because of a perceived increase in the incidence of toxic multinodular goitres in cats in recent years, we investigated the iodine content of three varieties of commercial canned cat foods and studied the acute effects of 'ingestion of these preparations on urinary iodine excretion and serum free thyroxine levels in young, healthy cats. Ten castrated male cats were fed from a common source. The type of food was changed every 2 weeks. Urine and blood specimens were obtained weekly. Serum free thyroxine levels were determined and iodine concentrations in urine were assayed. The iodine content of the cats' food was also assayed. Food varieties of high, intermediate and low iodine content were fed for 2-week periods. There was a consistent, reciprocal relationship between the mean urinary iodine concentration and the mean serum free thyroxine level for each 2-week period. The difference in the mean serum free thyroxine concentrations for the high and low iodine intake periods was highly significant (p<0.01). When the serum free thyroxine level and the urinary iodine level for each cat at each collection throughout the 12-week study were analysed (66 paired results), a strong inverse correlation (r=0.59, p<0.01) was found. We concluded that the serum free thyroxine level in cats, as measured by a kit designed for human serum, is acutely responsive to changes in iodine intake.
TL;DR: A method has been designed for the reduction of iodate to iodide in seawater and subsequent determination of total dissolved iodine as iodide by cathodic stripping square wave voltammetry.
TL;DR: The data indicate that the effects of iodide on thyroid growth and function may be mediated by a process that involves organification of iodides and increases in TGF-β1 mRNA levels.
Abstract: We examined TGF-beta mRNA levels in primary sheep thyroid cell cultures to determine whether the inhibitory effects of iodide on thyroid cells could be explained by an induction of TGF-beta mRNA and if this induction was mediated by iodine organification. Thyroid cells were incubated with TSH and five additives (insulin, somatostatin, growth hormone, transferrin, and glycyl-L-histidyl-L-lysin) for 2-3 weeks and then were exposed to sodium iodide (NaI) or 1-methylimidazole-2-thiol (methimazole, MMI), or both for 72 h. Iodide at 10(-6) M and 10(-4) M significantly increased the amount of TGF-beta mRNA as determined by Northern blot analysis with a rat TGF-beta 1 cDNA probe. This increase in TGF-beta 1 mRNA was abolished by the addition of methimazole, an inhibitor of organification. These data indicate that the effects of iodide on thyroid growth and function may be mediated by a process that involves organification of iodide and increases in TGF-beta 1 mRNA levels.
TL;DR: TFCs produce TGF-beta 1 mRNA and TGF -beta 1 peptide, which are both increased by iodide treatment in vitro, and the inhibitory activity of TFC-CM was increased when the TFCs were preincubated with 10 mumol NaI/1, and lost when T FCs were exposed to MMI.
Abstract: The present studies have demonstrated the production of transforming growth factor-beta 1 (TGF-beta 1) by porcine thyroid follicular cells (TFCs) maintained in vitro as subconfluent monolayers, and have confirmed a stimulatory effect of iodide on thyroidal TGF-beta 1 mRNA and peptide release. RNA extracted from TFCs maintained in the absence of iodide contained a 2.5 kb transcript which hybridized specifically with a cDNA probe for human TGF-beta 1, and which showed an approximate doubling in intensity in cells exposed to 10 mumol NaI/1. In the presence of the anti-thyroid thionamide drug methimazole (MMI; 1 mmol/l), the action of iodide on TGF-beta 1 mRNA was attenuated, although MMI alone had no effect on the control level of TGF-beta 1 mRNA. The TGF-beta 1 peptide content of TFC-conditioned media (TFC-CM) was assessed using the fetal mink lung cell line Mv1Lu, in which activated TGF-beta 1 specifically suppresses trichloroacetic acid-precipitable [methyl-3H]thymidine incorporation. Newly conditioned TFC-CM stimulated [methyl-3H]thymidine incorporation into Mv1Lu cells, but after heat treatment to inactivate growth stimulators and activate the latent TGF-beta 1 component this medium inhibited [methyl-3H]thymidine incorporation. This inhibitory effect was prevented by immunoadsorption of TFC-CM with a TGF-beta 1-neutralizing antiserum, confirming the specificity of the inhibitory response. The inhibitory activity of TFC-CM was increased when the TFCs were preincubated with 10 mumol NaI/1, and lost when TFCs were exposed to MMI. In conclusion, TFCs produce TGF-beta 1 mRNA and TGF-beta 1 peptide, which are both increased by iodide treatment in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: It is suggested that shock wave-gas bubble interaction is an important mediator of iodine release and cell killing by shock waves.
Abstract: Exposure of a potassium iodide solution to lithotripter shock waves resulted in formation of iodine with the amount of iodine depending on the gas dissolved in the solution. Iodine yield was higher with O 2 and Ar, as compared to CO 2 and N 2 O; degassed solution revealed the lowest iodine yield. Exposure of L1210 mouse leukemia cells to shock waves reduced the number of viable cells with no difference between O 2 -, Ar-, or N 2 O-equilibrated and degassed conditions. CO 2 equilibration resulted in a more pronounced reduction. The difference between chemical and biological effects argues against the involvement of free radicals in cell killing by shock waves. In additional experiments, gas bubbles of various sizes were introduced into the test vials. Addition of a 10 μL gas bubble revealed an over 10-fold increase in iodine yield from degassed potassium iodide solution with all gases. Addition of a gas bubble also reduced the number of viable cells again with no difference between the gases. It is suggested that shock wave-gas bubble interaction is an important mediator of iodine release and cell killing by shock waves.
Patent•
26 May 1992
TL;DR: In this paper, a solid, storage-stable, germicidal, pre-iodine composition comprises in dry admixture with each other, a solid oxy-compound of iodine, a solvating agent for the oxycompound, and a solid desiccant used in amount sufficient to combine during the storage cycle of the composition with ambient and/or endogenous water.
Abstract: A solid, storage-stable, germicidal, pre-iodine composition comprises in dry admixture with each other, a solid oxy-compound of iodine, a solid reducing agent for the oxy-compound of iodine, and a solid desiccant used in amount sufficient to combine during the storage cycle of the composition with ambient and/or endogenous water. The oxy-compounds of iodine are iodic acid, iodine pentoxide, potassium iodate and sodium iodate. Preferred reducing agents are ascorbic acid, dihydroxy fumaric acid, the thiol sugars and cysteine. A preferred combination desiccant and iodine solvating agent is polyvinyl pyrrolidone having a molecular weight of from 10,000 to 1,000,000. The composition is storage-stable for an indefinite period. Upon the addition of water, the oxy-compound of iodine is reduced to nascent iodine, which, in application, serves its well-known germicidal function.
TL;DR: Aqueous iodine and triiodide ion react rapidly with thiosulfate ion in a multistep mechanism: rate constants (25.0±0.2 o C, μ=010 M) are measured by pulsed-accelerated-flow and stopped-flow methods.
Abstract: Aqueous iodine and triiodide ion react rapidly with thiosulfate ion in a multistep mechanism:... Rate constants (25.0±0.2 o C, μ=010 M) are measured by pulsed-accelerated-flow and stopped-flow methods.
TL;DR: CF3l was synthesized in high yields by treatment of XCF2CO2Me(X = Cl or Br) with iodine in the presence of potassium fluoride and copper iodide under similar conditions to CF2l2.
Abstract: CF3l was synthesized in high yields by treatment of XCF2CO2Me(X = Cl or Br) with iodine in the presence of potassium fluoride and copper iodide; if Kl was used instead of KF under similar conditions, CF2l2 was obtained in moderate yields.
TL;DR: In this paper, the authors used polytetrafluoroethylene membrane tubing to assemble a newly designed gas diffusion unit and was applied to the permeation of halogens.
TL;DR: Grey-scale values after nine months were interpreted as reflecting a decrease in follicle size and colloid content of the thyroid which takes place after iodide supplementation, which is observed after combined treatment with levothyroxine and iodide.
Abstract: The effects of oral iodide, levothyroxine and of iodide and levothyroxine in combination were studied in three groups of 30 children, age 13-15 years, with euthyroid goitre. As endpoints of this study, we used thyroid volume reduction, thyroid hormones, thyrotropin and thyroid grey-scale histograms by computerized analysis. The three groups were well matched with respect to mean age, body weight and pretreatment thyroid volumes and thyroid hormones. Mean urinary iodide excretion before treatment was in the range of 30 micrograms/g creatinine, since the study was conducted in an iodine-deficient area. All three treatment regimens led to significant reductions in thyroid volume within one month. After six months on 100 micrograms of levothyroxine, thyroid volume had decreased from 14.1 +/- 4.2 ml to 8.3 +/- 2.6 ml (mean +/- SD); on 150 micrograms of iodide, from 18.5 +/- 6.2 ml to 8.8 +/- 2.7 ml; and on 100 micrograms of iodide plus 50 micrograms of levothyroxine, from 17.2 +/- 3.1 ml to 8.3 +/- 2.0 ml. When treatment was discontinued for three months, or the dosage reduced, thyroid volume increased again in the levothyroxine (to 11.3 +/- 2.5 ml) but not in the iodide group. Grey-scale values (by ultrasound, computer-aided estimation) after nine months were significantly different between the three treatment groups; no change was observed with levothyroxine, but after 150 micrograms of iodide as well as after combined treatment with levothyroxine and iodide there were marked decreases of grey-scale values; this is interpreted as reflecting a decrease in follicle size and colloid content of the thyroid which takes place after iodide supplementation.(ABSTRACT TRUNCATED AT 250 WORDS)