Effect of chronic excess iodine intake on thyroid function and oxidative stress in hypothyroid rats

2012 ◽  
Vol 90 (5) ◽  
pp. 617-625 ◽  
Author(s):  
Abd El-Aziz M. Hussein ◽  
Amr M. Abbas ◽  
Gehan A. El Wakil ◽  
Ayman Z. Elsamanoudy ◽  
Azza Abd El Aziz

Our objective was to investigate the effects of chronic excess iodine intake on thyroid functions and thyroid oxidative 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 μg/L) for 8 weeks. Serum thyroxine (T4), triiodothyronine (T3), thyroid-stimulating hormone (TSH), thyroid antioxidants (catalase, superoxide dismutase enzymes, and total antioxidants), and lipid peroxide (malondialdehyde; MDA) were measured. Reverse transcription – PCR gene expression for thyroidal 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 hypothyroid 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.

2011 ◽  
Vol 107 (5) ◽  
pp. 674-682 ◽  
Author(s):  
Ningna Li ◽  
Yaqiu Jiang ◽  
Zhongyan Shan ◽  
Weiping Teng

Our previous epidemiological study indicated that excessive intake of iodine could potentially lead to hypothyroidism. In the present study, we aimed to investigate the time and dose effect of iodine intake on serum thyrotropin (thyroid-stimulating hormone, TSH) levels and to explore the non-autoimmune regulation of serum TSH by pituitary type 2 deiodinase (D2). A total of 360 Wistar rats were randomly divided into five groups depending on administered iodine dosages (folds of physiological dose): normal iodine (NI), 3-fold iodine (3HI), 6-fold iodine (6HI), 10-fold iodine (10HI) and 50-fold iodine (50HI). At 4, 8, 12 and 24 weeks after administration of sodium iodide, blood was collected for serum TSH measurement by chemiluminescent immunoassay. Pituitaries were also excised for measurement of TSHβ subunit expression, D2 expression and activity, monocarboxylate transporter 8 (MCT8) and thyroid hormone receptor β2 isoform (TRβ2) levels. The results showed that iodine intake of 10HI and 50HI significantly increased pituitary and serum TSH levels from 8 to 24 weeks (P < 0·05 v. NI). Excess iodine had no effect on D2 mRNA or protein expression; however, 10HI and 50HI administration significantly inhibited pituitary D2 activities from 8 to 24 weeks (P < 0·05 v. NI). Iodine had no effect on MCT8 or TRβ2 protein levels. We conclude that prolonged high iodine intake inhibits pituitary D2 activity and induces elevation of serum TSH levels. These findings may provide a potential mechanism of iodine excess-induced overt and subclinical hypothyroidism.


Author(s):  
Olha Kasiyan ◽  
Halyna Tkachenko ◽  
Natalia Kurhaluk ◽  
Svitlana Yurchenko ◽  
Alek Manenko

AbstractThe current study aimed to identify correlative and regressive dependencies between the water iodine concentration and the levels of TSH (thyroid-stimulating hormone), thyroglobulin antibodies (TgAbs), and thyroid peroxidase (TPOAb) in the serum of 168 in patients (34 men and 134 women) with a hypothyroid form of Hashimoto’s thyroiditis who use water from the supply network and individual wells. Based on the water iodine concentration, low and moderate degrees of iodine endemia in the location of the patients were determined. In the groups of men and women using water from different water supply sources, there were direct correlations between the water iodine concentrations and the TgAbs and TPOAb titers as well as an inverse dependence between iodine and TSH levels. Multivariate regressive analysis indicated that TgAb and TSH in the group of women using water from a supply network and TPOAb titers in the group of women using well water were independent factors associated with water iodine concentrations. Statistically significant correlations and regressive dependencies between the water iodine concentrations and the biomarkers of the thyroid status of the patients indicate the risk of Hashimoto’s thyroiditis progression, especially among women with additional iodine intake.


2020 ◽  
Vol 9 (6) ◽  
pp. 1679 ◽  
Author(s):  
Marco Colella ◽  
Danila Cuomo ◽  
Antonia Giacco ◽  
Massimo Mallardo ◽  
Mario De Felice ◽  
...  

Thyroid hormones (THs) exert pleiotropic effects in different mammalian organs, including gonads. Genetic and non-genetic factors, such as ageing and environmental stressors (e.g., low-iodine intake, exposure to endocrine disruptors, etc.), can alter T4/T3 synthesis by the thyroid. In any case, peripheral T3, controlled by tissue-specific enzymes (deiodinases), receptors and transporters, ensures organ homeostasis. Conflicting reports suggest that both hypothyroidism and hyperthyroidism, assessed by mean of circulating T4, T3 and Thyroid-Stimulating Hormone (TSH), could affect the functionality of the ovarian reserve determining infertility. The relationship between ovarian T3 level and functional ovarian reserve (FOR) is poorly understood despite that the modifications of local T3 metabolism and signalling have been associated with dysfunctions of several organs. Here, we will summarize the current knowledge on the role of TH signalling and its crosstalk with other pathways in controlling the physiological and premature ovarian ageing and, finally, in preserving FOR. We will consider separately the reports describing the effects of circulating and local THs on the ovarian health to elucidate their role in ovarian dysfunctions.


Author(s):  
Perin Vural ◽  
Cemil Akgül ◽  
Mukaddes Canbaz

Background: Oxidative stress has been implicated in the pathogenesis of ageing and menopause, and can arise through the increased production of lipid peroxides and/or a deficiency of antioxidant defence. Aim: To investigate the effects of the menopause and tibolone treatment (2.5 mg/day for six months) on plasma antioxidants and lipid peroxidation. Methods: Plasma concentrations of ascorbic acid, α-tocopherol, total thiol groups, caeruloplasmin, erythrocyte glutathione (GSH) and malondialdehyde (MDA) were measured in 24 postmenopausal and 24 premenopausal healthy women. Results: Data analysis indicates a significant decrease in plasma ascorbic acid, α-tocopherol, total thiol groups, caeruloplasmin, erythrocyte GSH and a significant increase in lipid peroxides (expressed as MDA concentrations) in postmenopausal women. There was no significant difference between control and study groups in the mean plasma caeruloplasmin concentrations. It was found that there is a significant increase in α-tocopherol and significant decrease in lipid peroxide concentrations in postmenopausal after tibolone treatment. Conclusions: The menopause is associated with an increase in oxidative stress and a decrease of some antioxidants, such as ascorbic acid, α-tocopherol, total thiols and erythrocyte GSH. Tibolone treatment leads to a decrease in concentrations of plasma lipid peroxide, probably by stimulating direct and indirect mechanisms of tocopherol regeneration and increasing plasma concentrations of vitamin E. However, due to the relatively small numbers involved this study can be regarded as a pilot. Further studies performed on a larger scale are necessary to establish the exact mechanisms of tibolone in inhibiting oxidative stress in postmenopausal women.


2012 ◽  
Vol 06 (02) ◽  
pp. 184-190 ◽  
Author(s):  
Mahadevi B Hosur ◽  
S R Puranik ◽  
Shrinivas Vanaki ◽  
Surekha R Puranik

ABSTRACTObjective: Apart from its well-known deleterious dental and skeletal effects, fluoride excess can have toxic effects on many other tissues. Fluoride, when in excess, is known to interfere with thyroid gland function. Fluoride-induced thyroid disturbances similar to those observed in iodine deficiency state in spite of adequate iodine intake have been documented. Similar thyroid disturbances in individuals with dental fluorosis have not been well studied in populations with endemic fluorosis. This work was undertaken to study the effects of fluoride-induced thyroid disturbances in individuals with dental fluorosis.Methods: The study group included 65 subjects with dental fluorosis from endemic fluorosis populations. An additional control group was comprised of 10 subjects without dental fluorosis. The drinking water fluoride levels of the study populations were analyzed. Serum free FT3, FT4, and TSH levels of both groups were assessed.Results: All subjects with dental fluorosis had serum levels of thyroid hormones (FT3, FT4, and TSH) within the normal range, with the exception of 1 individual, who had elevated levels of TSH. Statistical significance was found when FT3 and TSH values were compared with different Dean’s index groups by a 1-way ANOVA test: FT3 (F = 3.4572; P=.0377) and TSH (F = 3.2649 and P=.0449).Conclusions: Findings of this study did not show any significant alterations in the levels of the thyroid hormones FT3, FT4, and TSH in subjects with dental fluorosis. Our observations suggest that thyroid hormone levels were not altered in subjects with dental fluorosis. Hence, future studies of this kind, along with more detailed investigations are needed. (Eur J Dent 2012;6:184-190)


2021 ◽  
Author(s):  
Fatemeh Eftekharian ◽  
Gholamhossein Ranjbar Omrani ◽  
Mohammad Hossein Dabbaghmanesh ◽  
Reza Sahraei ◽  
Marzieh Bakhshayeshkaram ◽  
...  

Abstract Background The purpose of this study was to determine the association of sonographic parameters with the serum levels of anti-thyroid peroxidase (TPO), anti-thyroglobulin (Tg), and thyroid hormones in patients with Hashimoto's thyroiditis. Methods 149 patients (118 females, 31 males; aged 18–60 years; mean age: 38.60 ± 8.03 years) who were diagnosed with Hashimoto's thyroiditis were enrolled in the study. Blood sample was taken to measure the serum levels of free T3 and T4, thyroid stimulating hormone (TSH), anti-TPO antibody titers, and anti-Tg antibody titers. The thyroid sonography of each patient was classified into one of the five grades by real-time ultrasonography (US) based on echogenicity, thyroid size, and thyroid pattern. We evaluated whether a correlation existed between thyroid characteristics on US and serum levels of thyroid hormones, anti-TPO and anti-Tg. Results Nodular structures were detected in 54 (36.2%) patients (38 micronodular and 16 macros nodular). Echogenicity was recorded as isoechoic in 15 (10.07%) and hypoechoic in 119 (79.87%) subjects. Euthyroid ‎subjects had significantly thicker isthmus than overt and subclinical hypothyroid patients (p = 0.018). Mean serum TSH, anti-Tg and anti-TPO titers was significantly higher in patients with micronodules than those with micronodules and subjects without nodules (P < 0.05). Isthmus thickness had a significant negative correlation with FT4 and FT3 (P = 0.046; r = 0.11& P = 0.017; r = 0.15, respectively). Thyroid autoantibodies had positive significant correlations with different parameters of the thyroid volume (P < 0.05). Conclusions Thyroid’s US findings in addition to serum levels of anti-Tg and anti-TPO titers would be useful in diagnosis and evaluation of the severity and extent of Hashimoto's thyroiditis, but further evaluations are needed. Trial registration: Trial registry identifier IR.SUMS.REC.1395.S161 (2015/11/30).


2011 ◽  
Vol 165 (5) ◽  
pp. 745-752 ◽  
Author(s):  
Christine D Thomson ◽  
Jennifer M Campbell ◽  
Jody Miller ◽  
Sheila A Skeaff

ObjectiveIodine deficiency has re-emerged in New Zealand, while selenium status has improved. The aim of this study was to investigate the effects of excess iodine intake as iodate on thyroid and selenium status.MethodsIn a randomized controlled trial on older people (mean±s.d. 73±4.8 years;n=143), two groups received >50 mg iodine as iodate/day for 8 weeks because of supplement formulation error, either with 100 μg selenium (Se+highI) or without selenium (highI). Four other groups received 80 μg iodine as iodate/day with selenium (Se+lowI) or without selenium (lowI), selenium alone (Se+), or placebo. Thyroid hormones, selenium status, and median urinary iodine concentration (MUIC) were compared at weeks 0, 8, and 4 weeks post-supplementation.ResultsMUIC increased nine- and six-fold in Se+highI and highI groups, decreasing to baseline by week 12. Plasma selenium increased in selenium-supplemented groups (P<0.001). The level of increase in whole blood glutathione peroxidase (WBGPx) in the Se+highI group was smaller than Se+ (P=0.020) and Se+lowI (P=0.007) groups. The decrease in WBGPX in the highI group was greater than other non-selenium-supplemented groups, but differences were not significant. Ten of 43 participants exposed to excess iodate showed elevated TSH (hypothyroidism) at week 8. In all but two, TSH had returned to normal by week 12. In three participants, TSH decreased to <0.10 mIU/l (hyperthyroidism) at week 8, remaining low at week 12.ConclusionsExcess iodate induced hypothyroidism in some participants and hyperthyroidism in others. Most abnormalities disappeared after 4 weeks. Excess iodate reduced WBGPx activity and resulted in smaller increases in WBGPx after selenium supplementation.


2015 ◽  
Vol 34 (3) ◽  
pp. 323-331 ◽  
Author(s):  
Maureen Jepkorir Cheserek ◽  
Gui-Rong Wu ◽  
Arsene Ntazinda ◽  
Yong-Hui Shi ◽  
Li-Ye Shen ◽  
...  

SummaryOxidative stress plays a role in the pathogenesis of many chronic diseases. It is recognized in overt hypothyroidism while its existence in subclinical hypothyroidism (SCH) is not well established. The aim of this study was to determine whether there was increased oxidation of lipids and proteins in SCH, and examine their association with lipids and thyroid hormones.Methods: Male adults (35-59 years) with SCH (n=467) and euthyroid controls (n=190) were studied. Anthropometric measurements, plasma lipids, thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), total antioxidant capacity (T-AOC), lipid peroxidation products, malondialdehyde (MDA), advanced oxidation protein products (AOPP) and dityrosine concentrations were measured.Results: Plasma concentrations of MDA were significantly higher (p<0.05) in SCH (8.11±1.39 nmol/mL) compared with euthyroid controls (7.34±1.31 nmol/mL) while AOPP, dityrosine and T-AOC levels were not different. MDA was not associated with TSH (β=-0.019, P=0.759), FT4 (β=-0.062, P=0.323) and FT3 (β=-0.018, P=0.780) in SCH while levels increased with elevated total cholesterol (β=0.229, P=0.001), LDL (β=0.203, P=0.009) and triglycerides (β=0.159, P=0.036) after adjustment for ageand body mass index. T-AOC reduced (β=-0.327, P=0.030) with increased MDA in euthyroid controls and not in SCH (β=-0.068, P=0.349), while levels increased with elevated triglycerides in both groups.Conclusion: Oxidative stress was increased in subclinical hypothyroidism as evidenced by the elevated lipid peroxidation product, malondialdehyde, while protein oxidation was absent. Thus, reduction of oxidative stress may be beneficial in patients with subclinical hypothyroidism


2013 ◽  
Vol 91 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Bharathinagar S. Suresha ◽  
Kuntavalli Y. Vasantha ◽  
Avinash P. Sattur ◽  
Krishnapura Srinivasan

Oxidative stress plays a key role in the progression of diabetes and its complications. In this study, the beneficial influence of the fungal metabolite nigerloxin, a new aldose reductase inhibitor and a free-radical scavenger, was investigated on oxidative stress in streptozotocin-induced diabetic rats. Groups of diabetic rats were orally administered nigerloxin for 30 days at a dose of 25 and 100 mg·(kg body mass)−1·day−1. Diabetic rats showed significantly increased lipid peroxide levels in blood and liver, which was accompanied by lowered concentrations of antioxidant molecules and activities of antioxidant enzymes in blood and liver. Administration of nigerloxin for 30 days at a daily dose of 100 mg∙(kg body mass)–1 to diabetic rats significantly decreased plasma and liver lipid peroxides, elevated the nonenzymatic antioxidants ascorbic acid, reduced glutathione, and total thiols, and elevated the activities of antioxidant enzymes in blood and liver. Nigerloxin showed a tendency to counter lipid abnormalities in diabetic animals, while fasting glucose and body mass were unaffected by nigerloxin treatment. Thus, this animal study has indicated the beneficial influence of nigerloxin on oxidative stress associated with diabetes that may have an implication in delaying or ameliorating the secondary complications.


2020 ◽  
pp. 206-212
Author(s):  
A. F. Verbovoy ◽  
Yu. A. Dolgikh

Hypothyroidism is the most common endocrine disease after diabetes mellitus. Its frequency depends on age, sex and iodine intake. The highest prevalence of hypothyroidism is observed in older women. Chronic autoimmune thyroiditis is the most common cause of this condition. The peculiarity of hypothyroidism is an erased clinical picture, diversity and nonspecific symptoms. This makes it difficult to diagnose the disease, leads to an erroneous diagnosis and later detection of thyroid insufficiency. This article discusses the various «masks» of hypothyroidism and peculiarities of clinical manifestations. The main «masks» are: cardiological, dermatological, urological, gastroenterological, endocrine and reproductive system disorders, neurological, psychiatric, hematological, rheumatological. Free thyroxine and thyroid-stimulating hormone are used to diagnose hypothyroidism, as well as antibody titer to thyroid peroxidase and thyroglobulin to detect chronic autoimmune thyroiditis. Levothyroxine preparations are used as a substitution therapy. The dose of the drug depends on the age of the patient and the presence of cardiovascular disease. Patients under 50 years of age without a severe concomitant cardiovascular disease are given 1.6 µg of levothyroxine per kg of body weight. In persons over 50 years of age with cardiovascular diseases, the drug dose is prescribed at the rate of 0.9 µg per kg of body weight. The therapy starts with small doses, slowly increasing it under the control of electrocardiography. At occurrence or strengthening of symptoms of angina a dose of levothyroxine is reduced to the previous one and the cardiovascular therapy is corrected. Evaluation of the effectiveness of the treatment is carried out on the level of thyroid hormone.


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