Excess iodine induced lymphocytic impairment in adult rats

Bulletin of Egyptian Society for Physiological Sciences

The aim of the current study was to investigate the effects of long term excessive iodine intake on gene expression of thyroidal sodium iodide symporter (NIS), D1 deiodinase and thyroid peroxidase (TPO), thyroid hormones, oxidative injury and anti-oxidative ability of euthyroid and hypothyroid Sprague Dawley rats. Materials and Methods: Ninety rats were divided into euthyroid and hypothyroid (thiocyanate induced) groups with or without administration of excess iodine (3000 or 6000 μg/l) for 4 weeks. Serum thyroxine (T 4 ), triiodothyronine (T 3 ), TSH, thyroid antioxidants ((glutathione S transferase, catalase, superoxide dismutase enzymes, nitric oxide and total antioxidants), lipid peroxide (malondialdehyde, MDA) were measured. RT-PCR gene expression for thyroidal NIS, D1 deiodinase and TPO were performed. Results: Thiocyanate significantly decreased thyroid hormones (T 3

Our objective was to investigate the effects of chronic excess iodine intake on thyroid functions and thyroid oxi-dative stress state in hypothyroid rats. Sixty rats were divided into euthyroid and hypothyroid (thiocyanate-induced) groups with or without administration of excess iodine (3000 or 6000 mg/L) for 8 weeks. Serum thyroxine (T 4), triiodothyronine (T 3), thyroid-stimulating hormone (TSH), thyroid antioxidants (catalase, superoxide dismutase enzymes, and total antioxi-dants), and lipid peroxide (malondialdehyde; MDA) were measured. Reverse transcription – PCR gene expression for thyroi-dal Na + /I – symporter (NIS), D1 deiodinase, and thyroid peroxidase (TPO) were performed. Thiocyanate significantly decreased thyroid hormones (T3, T4), increased lipid peroxides and antioxidants, and increased gene expression of NIS, D1 deiodinase, and TPO. Excess iodine intake in hypothyroid rats increased T3 and T4. Also, high iodine intake by hypothy-roid rats significantly decreased NIS, D1 deiodinase, and TPO genes expression. Excess iodine significantly increased MDA and antioxidants in euthyroid and hypothyroid rats. In conclusion, thiocyanate-hypothyroidism increases gene expression of NIS, TPO, and TPO and induces oxidative stress. High iodine intake decreases NIS and D1 deiodinase gene expression in hypothyroid rats. Moreover, excess iodine increase thyroid hormones, lipid peroxides, and antioxidants in hypothyroid rats. Résumé : Notre objectif était d'examiner les effets d'une prise chronique d'iode en excès sur les fonctions thyroïdiennes et sur l'état de stress oxydant de la thyroïde chez le rat hypothyroïdien. Soixante rats ont été divisés en groupes euthyroïdiens et hypothyroïdiens (induction par le thiocyanate), avec ou sans administration d'iode en excès (3000 ou 6000 mg/L) pendant 8 semaines. La thyroxine (T4), la triiodothyronine (T3) et l'hormone stimulant la thyroïde (TSH) sériques, les antioxydants de la thyroïde (catalase, superoxyde dismutase et antioxydants totaux) et le malondialdéhyde (MDA) ont été mesurés. Une analyse de l'expression génique du symporteur Na + /I – (NIS), de la déiodinase D1 et de la thyroperoxydase (TPO) a été réa-lisée par RT–PCR. Le thiocyanate a diminué significativement les niveaux d'hormones thyroïdiennes (T3, T4), augmenté les niveaux de peroxydes lipidiques et d'antioxydants, et augmenté l'expression génique du NIS, de la déiodinase D1 et de la TPO. Une prise d'iode en excès par les rats hypothyroïdiens augmentait les niveaux de T 3 et de T 4. Aussi, une forte prise d'iode diminuait significativement l'expression génique du NIS, de la déiodinase D1 et de la TPO chez les rats hypothyroï-diens. L'iode en excès augmentait de manière significative les niveaux de MDA et d'antioxydants chez les rats euthyroïdiens et hypothyroïdiens. En conclusion, l'hypothyroïdie induite par le thiocyanate augmente l'expression génique du NIS, de la diodinase D1 et de la TPO et induit un stress oxydant. Une prise d'iode à haute dose diminue l'expression génique du NIS et de la diodinase D1 chez les rats hypothyroïdiens. De plus, l'iode en excès augmente les niveaux d'hormones thyroïdien-nes, de peroxydes lipidiques et d'antioxydants chez les rats hypothyroïdiens.

Nutrition, 2009

Thyroid, 2013

Background: Seaweed is an important dietary component and a rich source of iodine in several chemical forms in Asian communities. Their high consumption of this element (25 times higher than in Western countries) has been associated with the low incidence of benign and cancerous breast and prostate disease in Japanese people. Summary: We review evidence showing that, in addition to being a component of the thyroid hormone, iodine can be an antioxidant as well as an antiproliferative and differentiation agent that helps to maintain the integrity of several organs with the ability to take up iodine. In animal and human studies, molecular iodine (I 2) supplementation exerts a suppressive effect on the development and size of both benign and cancerous neoplasias. Investigations by several groups have demonstrated that these effects can be mediated by a variety of mechanisms and pathways, including direct actions, in which the oxidized iodine dissipates the mitochondrial membrane potential, thereby triggering mitochondrion-mediated apoptosis, and indirect effects through iodolipid formation and the activation of peroxisome proliferator-activated receptors type gamma, which, in turn, trigger apoptotic or differentiation pathways. Conclusions: We propose that the International Council for the Control of Iodine Deficient Disorders recommend that iodine intake be increased to at least 3 mg/day of I 2 in specific pathologies to obtain the potential extrathyroidal benefits described in the present review.

British Journal of Nutrition, 2011

Little information is available as to whether doses of iodide similar to those recommended in clinical practice for the prevention of iodine deficiency in pregnant women affect thyroid function. The aim of the present study was to analyse whether doses of iodide can affect thyroid function in adults, and evaluate its effect on plasma markers of oxidative stress, inflammation and acute-phase proteins. A total of thirty healthy volunteers (ten men and twenty women) with normal thyroid function were randomly assigned to three groups (n 10). Each group received a daily dose of 100, 200 or 300 μg of iodide in the form of KI for 6 months. Free tetraiodothyronine (FT4) levels at day 60 of the study were higher in the groups treated with 200 and 300 μg (P = 0·01), and correlated with the increase in urinary iodine (r 0·50, P = 0·007). This correlation lost its significance after adjustment for the baseline FT4. The baseline urinary iodine and FT4 correlated positively with the baseline glut...

Interdisciplinary Toxicology, 2013

131-radioiodine has been widely used as an effective radionuclide for treatment of patients with thyroid diseases. The purpose of this study was to investigate the genotoxic effects of iodine-131 in human cultured lymphocytes. Whole blood samples from human volunteers were incubated with iodine-131 (10, 50, 100 µCi/1.5ml) for 2 h. The lymphocytes were mitogenically stimulated to allow for evaluation of the number of micronuclei in cytokinesis-blocked binucleated cells. At the dose 100 µCi, iodine-131 induced genotoxicity by an 8.5 fold increase in the frequency of micronuclei in human lymphocytes compared with the control group.

Frontiers in Veterinary Science, 2020

Background: Complexes of iodine (povidone-iodine and cadexomers) are among the most important antiseptics used in clinical and veterinary medicines. However, high local irritation activity and systemic toxicity limits their oral administration. The purpose of the study was to compare the effect of a new complex of iodine (PA, potentiator of anticancer antibiotics), in which iodine is coordinated by carbohydrates and polypeptides) on the organisms of rats and dogs treated orally with the drug for 30 days. Methods: Wistar rats and Beagle dogs served as experimental animal models. Effect of PA on the animal organism was examined through the measurements of hormones level changes, hematological and clinical chemistry parameters alterations, necropsy and histological examination. The established maximum tolerated dose (MTD) of 2,000 mg/kg PA led to a decrease in the rate of body weight gain in male and female rats. Changes in hematological and certain biochemical parameters in rats at doses of 1,000 and 2,000 mg/kg were observed. Histological study of the thyroid gland revealed changes in the shape and size of the follicles along with colloid resorption. Administration of a half of MTD (180 mg/kg) and lower doses did not result in any change in dogs (thyroid-stimulating hormone, triiodothyronine, and thyroxine). The results of our study show that the pathogenetic action of PA takes place along the path of induction of an inflammatory response with the development of thyrotoxicosis, rather than hypothyroidism. The mechanism of induction of an inflammatory response is also confirmed by histological studies of lesions of the thyroid gland and testes in rats (Figure ). The no-observed-adverse-effect level (NOAEL) of PA is estimated to be 180 mg/kg (or iodine 22.8 mg/kg) in dogs, which is equivalent to 100 mg/kg (or iodine 12.3 mg/kg) in humans.

Immunology, 1994

Evidence is accumulating that dietary iodine intake is an important modulator of autoimmune thyroid reactions. To study this role of iodine intake further, female Wistar rats were kept on an enriched iodine diet (EID, iodine intake 100 micrograms iodine/day) for a period of up to 18 weeks. Control rats were either on a normal iodine diet (NID, iodine intake 7 micrograms iodine/day) or a low iodine diet (LID, 2 days of 1% KClO4 followed by iodine-deficient drinking water/pellets). During the first 6 weeks of the EID rats developed a thyroid-associated ectopic thymic tissue (50-57% of the animals on EID versus 7-14% of NID rats and 0% of LID rats). This thyroid-associated ectopic thymic tissue showed a similar histology (cortex and medulla) and a similar marker pattern as normal rat thymus concerning TdT expression (positive cells in the cortex) and CD4/CD8 positivity (double-positive cells in the cortex, single-positive cells in the medulla). The excessive iodine diet also resulted i...

Frontiers in immunology, 2017

Iodine is an essential element required for the function of all organ systems. Although the importance of iodine in thyroid hormone synthesis and reproduction is well known, its direct effects on the immune system are elusive. Human leukocytes expressed mRNA of iodide transporters (NIS and PENDRIN) and thyroid-related proteins [thyroglobulin (TG) and thyroid peroxidase (TPO)]. The mRNA levels of PENDRIN and TPO were increased whereas TG transcripts were decreased post leukocyte activation. Flow cytometric analysis revealed that both PENDRIN and NIS were expressed on the surface of leukocyte subsets with the highest expression occurring on monocytes and granulocytes. Treatment of leukocytes with sodium iodide (NaI) resulted in significant changes in immunity-related transcriptome with an emphasis on increased chemokine expression as probed with targeted RNASeq. Similarly, treatment of leukocytes with NaI or Lugol's iodine induced increased protein production of both pro- and anti...

Acta veterinaria, 2011

Having in mind the former results which confirmed the functional relationship between the thyroid and the immune system, and the administration of potassium iodide (KI) in the therapy of auto-immune diseases, we considered it of interest to investigate the pathogenesis of KI induced experimental thyroiditis, by studying the morphology of thymus, thyroid gland and spleen, as well as the phenotype of lymphocytes in the thymus and peripheral blood in relation to the expression of CD4 and CD8 molecules. The experiments have been carried out on 30 male Wistar rats, divided in 3 groups. The first group (n=10) received KI (225 mg/g, i.p.), the second group (n=10) received KI (675 mg/g, i.p.), while the third group (n=10) received sodium chloride (0.9%, i.p.). The intensity of histological lesions in the thyroid gland, was statistically significant (p<0.01) in KI treated groups, compared to the controls. KI also significantly decreased rat body mass, and increased masses of thymus and thyroid gland (p<0.05). No statistically significant difference was found in thymocyte and peripheral blood CD4+ and CD8+ subpopulation numbers between the groups. Our experiments suggest that KI, at least in some doses could induce mild lymphocytic thyroiditis in rats, and that this simple, practical and non-expensive model of experimental thyroiditis could be of importance for further research.