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1.
John R. Arthur Fergus Nicol Geoffrey J. Beckett 《Biological trace element research》1992,33(1-3):37-42
Selenium deficiency impairs thyroid hormone metabolism by inhibiting the synthesis and activity of the iodothyronine deiodinases,
which convert thyroxine (T4) to the more metabolically active 3,3′-5 triiodothyronine (T3). Hepatic type I iodothyronine deiodinase, identified in partially purified cell fractions using affinity labeling with [125I]N-bromoacetyl reverse triiodothyronine, is also labeled with75Se by in vivo treatment of rats with75Se-Na2SeO3. Thus, the type I iodothyronine 5′-deiodinase is a selenoenzyme. In rats, concurrent selenium and iodine deficiency produces
greater increases in thyroid weight and plasma thyrotrophin than iodine deficiency alone. These results indicate that a concurrent
selenium deficiency could be a major determinant of the severity of iodine deficiency. 相似文献
2.
The effects of supplementing selenium on thyroid hormone metabolism were studied on mice with excessive iodine exposure. The
serum concentrations of thyroxine (T4) and triiodothyronine (T3) and the activities of iodothyronine 5′ and 5-deiodinase (D2, D3) were measured in the brain of filial mice to study the
influence of selenium on thyroid hormone metabolism. Measurements were carried out on postnatal day 0, 14, and 28. It was
found that selenium supplementation alleviated the adverse effects of excessive iodine on progeny. The serum TT4 level as well as TT4 and TT3 concentrations and D3 activity in cerebrum of progeny decreased, whereas D2 activity increased in the cerebrum of progeny
on postnatal day 0 and 14. Selenium supplementation exerted some favorable effects on thyroid hormone metabolism in cerebrum
of progeny of dam with excessive iodine intake. 相似文献
3.
J R Arthur 《Canadian journal of physiology and pharmacology》1991,69(11):1648-1652
In animals, decreases in selenium-containing glutathione peroxidase activity and the resultant impairment of peroxide metabolism can account for many, but not all of the biochemical and clinical changes caused by selenium deficiency. Recently, however, type I iodothyronine 5'-deiodinase has also been shown to be a selenium-containing enzyme. This explains the impairment of thyroid hormone metabolism caused by selenium deficiency in animals with a normal vitamin E status. Since iodothyronine 5'-deiodinases are essential for the production of the active thyroid hormone 3,5,3'-triiodothyronine, some of the consequences of selenium deficiency may result from thyroid changes rather than inability to metabolise peroxides. In particular, the impaired thyroid hormone metabolism may be responsible for decreased growth and resistance to cold stress in selenium-deficient animals. A further consequence of the role of selenium in thyroid hormone metabolism is the exacerbation of some of the thyroid changes in iodine deficiency by a concurrent selenium deficiency. Selenium status may therefore have a major influence on the outcome of iodine deficiency in both human and animal populations. 相似文献
4.
Mario Calomme Jean Vanderpas Baudouin François Micheline Van Caillie-Bertrand Nicole Vanovervelt Christian Van Hoorebeke Dirk Vanden Berghe 《Biological trace element research》1995,47(1-3):349-353
Type I 5′-deiodinase was recently characterized as a selenocysteine-containing enzyme in humans and other mammals. Up to now,
the effect of selenium (Se) supplementation on thyroid hormone metabolism in humans has only been reported in the very peculiar
nutritional environment of Central Africa, where combined severe iodine and Se deficiency occurs. In this study, a group of
phenylketonuria subjects with a low selenium status, but a normal iodine intake were supplemented with selenium to investigate
changes in their thyroid hormone metabolism. After 3 wk of selenium supplementation (1 μg/kg/d), both the concentrations of
the prohormone thyroxine (T4) and the metabolic inactive reverse triiodothyronine (rT3) decreased significantly. Clinically,
the phenylketonuria subjects remained euthyroid before and after selenium supplementation. The individual changes of plasma
Se and glutathione peroxidase activity were closely associated with individual changes of plasma T4 and rT3. 相似文献
5.
Karin P. L. T. M. K. Janssen Daan van der Heide Theo J. Visser Ellen Kaptein Anton C. Beynen 《Biological trace element research》1994,40(3):237-246
The hypothesis tested was whether marginal iodine deficiency for a period of 6 wk affects iodothyronine deiodinase activities
in liver and brain of rats. Male rats were fed purified diets either deficient or sufficient in iodine; the diets were fed
on a restricted basis (60% ofad libitum intake). Body weight gain of the two groups was comparable. Iodine deficiency was evidenced by increased thyroid weight (26%),
reduced urinary iodine excretion (80%), and reduced plasma T4 concentrations (22%). Activities of liver type I and brain type III deiodinase were unchanged, but the activity of type II
deiodinase in brain was increased (28%) in the iodine-deficient rats. Food restrictionper se significantly lowered T3 (30%) and T4 (22%) concentrations in plasma and decreased type III deiodinase activity in brain (30%). These results indicate that in
marginal iodine deficiency the activities of hepatic type I deiodinase and brain type III deiodinase are unchanged, whereas
that of brain type II deiodinase is increased. 相似文献
6.
Iodine deficiency (ID) and related disorders are still major, yet unresolved health concerns. Recently, in a systematic survey
of schoolage children (SAC), we reported severe to moderate ID, in Ankara and three cities from Black Sea region of Turkey.
The current study attempted to evaluate selenium (Se) status, thiocyanate (SCN−) overload, and their possible contribution to the goiter endemics and thyroid hormone profile observed in these cities. Thyroid
ultrasonography was performed and serum Se, SCN−, thyroid hormones, sensitive TSH (sTSH) levels, and urinary iodine concentrations (UICs) were determined from 251 SAC (9–11
yr old).
Thyroid volumes (TVs) exceeding recommended upper normal limits and median UIC indicated goitre endemics and moderate to severe
ID in the areas studied. Mean serum SCN− concentrations were found to be greater than the controls from the literature. The UIC/SCN− ratio was found to be lowest in Bayburt and Trabzon denoting that SCN− overload may contribute to the goiter endemics. Serum Se concentrations represent a marginal deficiency in the four areas
studied. No significant correlations between serum Se concentrations and the other parameters studied (i.e., TV, SCN−, thyroid hormones, sTSH, UIC) was detected.
In conclusion, this study showed that selenium is also marginally deficient in the iodine-deficient endemic areas studied,
but this has little or no impact on the thyroid hormone profile and the goiter endemics. SCN− overload may contribute to the endemics, especially for the areas where iodine is severely deficient. An effective iodine
supplementation program will not only resolve the goiter endemics but also the consequence of SCN− overload as well in the endemic goiter areas studied. 相似文献
7.
Effect of selenium supplementation on thyroid hormone levels and selenoenzyme activities in growing lambs 总被引:1,自引:1,他引:0
Chadio SE Kotsampasi BM Menegatos JG Zervas GP Kalogiannis DG 《Biological trace element research》2006,109(2):145-154
The aim of the present study was to evaluate the effects of selenium supplementation on thyroid hormone metabolism and selenoenzyme
activities in lambs. Twelve 20-d-old male lambs were assigned to one of two diets: A (0.11 ppm Se) and B (supplemented with
0.2 ppm selenium as sodium selenite). Blood samples were collected weekly for the determination of T3, T4, and selenium levels. The response to thyrotropin-releasing hormone (TRH) challenge was estimated at the 11th and 20th wk.
Animals were slaughtered at wk 20 and tissues were collected for enzyme determination. Plasma selenium concentration was significantly
higher in supplemented lambs (p<0.001). Plasma T3 and T4 levels remained similar in both groups. Type I deiodinase activity (ID-I) was decreased in the liver (p<0.05) and increased in the pituitary (p<0.01) of supplemented animals. No ID-I activity was detected in the thyroid. Pituitary type II deiodinase activity (ID-II)
remained unchanged. The response to TRH challenge did not differ between the two groups for both challenges, but in group
B, the second TRH challenge (20th wk) resulted in a significantly higher T3 response compared to the first one (11th wk) (p<0.05). In conclusion, the lack of effects of Se supplementation on thyroid hormone metabolism demonstrates that enzyme activity
is homeostatically controlled and selenium is incorporated in that order to ensure the maintenance of thyroid hormone homeostasis. 相似文献
8.
Male New Zealand White rabbits were divided into three groups: (I) control, (II) high-fat-diet (HFD) fed, and (III) HFD fed+selenium
supplemented. After 3 mo of treatment, there was a significant increase in serum cholesterol and triglycerides in the HFD-fed
group as compared to the control. However in the selenium (Se)-supplemented group, the levels of serum cholesterol and triglycerides
were significantly less as compared to group II. HFD feeding resulted in decreased serum Se levels, but supplementation of
dietary Se along with HFD, as in group III, showed an apparent increase in its levels. The Se-dependent glutathione peroxidase
(GSH-Px) activity in the liver and the aorta increased significantly in HFD-fed animals and also showed an additional significant
increase on Se supplementation. Both serum T3 and T4 levels showed a significant decrease on HFD feeding. However, supplementation of Se led to a significant increase in the
levels of these parameters viz-à-viz HFD-fed animals. HFD feeding significantly decreased the activity of type I iodothyronine
5′-deiodinase (5′-DI) in the liver from group II rats. On supplementation of Se along with HFD, the activity increased in
the liver. However, there was no significant change in its activity in the aorta. The 5′-DI activity in the thyroid showed
an opposite trend in comparison with peripheral tissues (i.e., liver). The important finding of this study is that in the
hyperlipidemic state, deiodinase in the thyroid behaves in a different manner as compared to its activity in extrathyroidal
tissues. 相似文献
9.
A. de Luze J. Leloup M. Olivereau 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1984,154(2):199-205
Summary In the eel, ovine prolactin (oPrl) treatment (0.018 IU/day·g body weight), for 8 to 13 days modifies neither iodide absorption from the water nor excretion, extrathyroidal metabolism and plasma level of iodide.Thyroid activity, evaluated by epithelial cell height, radioiodine uptake and absolute iodide uptake is approximately twice that of controls. However, the amounts of total iodine, thyroxine (T4) and triiodothyronine (T3) in thyroid are unaltered by oPrl. Therefore, the decrease of plasma T4 and the increase of plasma T3, previously observed in oPrl-treated eels, do not result from a preferential thyroidal secretion of T3, but only from a stimulation of peripheral conversion of T4 to T3. Furthermore, the increased thyroid activity probably originates from a decreased feedback inhibition following the fall of circulating T4 induced by oPrl.Abbreviations
oPrl
ovine prolactin
-
T
4
Thyroxine
-
T
3
3.5.3 triiodothyronine
-
TRH
thyrotropin releasing hormone
-
TSH
thyroid stimulating hormone
-
PBI
protein bound iodine 相似文献
10.
Presently, the effect of selenium (Se) deficiency and excess of Se (1 ppm) on the activity of selenoenzymes type 1 5′-iodothyronine
deiodinase (5′-DI), glutathione peroxidase (GSH-Px), and level of thyroid hormones (T3 and T4) was studied in rats. Se levels in the serum and liver, T3 and T4 in the serum, GSH-Px levels in the liver, and 5′-DI activity in the liver/aorta/thyroid were estimated after 1, 2, and 3
mo of Se-deficient (0.02 ppm), Se-adequate (0.2 ppm), and Se-excess (1 ppm) diet feeding. All of these parameters decreased
significantly in the Se-deficient group as compared to the adequate group. Within the deficient group, as the Se deficiency
progressed, all of the parameters except 5′-DI decreased after 2 and 3 mo in comparison to 1-mo data. Thyroidal 5′-DI activity
in Se deficiency showed the maximum increase. A significant increase was observed in all of the above parameters in the 1
ppm Se-supplemented diet group when compared with the adequate Se group; also, as the Se deposition increased within the Se-excess
diet group, a significant increase was observed in all of the above parameters. However, as observed by others, the intake
of excess of Se (i.e., 2 ppm in the diet) did not elevate the activities of selenoenzymes and thyroid hormones; rather, it
had adverse effects. The present study concludes that Se supplementation at least up to 1 ppm enhances the selenoenzyme activities,
and above this level, it may not be considered as an indicator of selenoenzyme activities. 相似文献
11.
Selenoenzyme activities in selenium- and iodine-deficient sheep 总被引:3,自引:0,他引:3
Voudouri AE Chadio SE Menegatos JG Zervas GP Nicol F Arthur JR 《Biological trace element research》2003,94(3):213-224
This study was conducted to evaluate the effects of single and combined deficiencies of selenium and iodine on selenoenzyme
activities in sheep. Twenty-four male lambs were assigned to one of four semisynthetic diets: combined deficient A (Se−I), Se-deficient B (Se−I+), I-deficient C (Se+I−), and basal diet D (Se+I+). Thyroid hormones (T3, T4), thyroid stimulating hormone (TSH), and inorganic iodine (PII) were determined in plasma. Selenium and glutathione peroxidase
activity (GSH-Px) were determined in erythrocytes, and tissue samples, including the thyroid, liver, kidney, and brain, were
taken for selenoenzyme analysis. Plasma T3, T4, and TSH concentrations were similar in all groups. Type I deiodinase (ID-I) activity in liver and kidney remained unchanged
in Se or I deficiency. In contrast, hepatic ID-I activity was increased by 70% in combined Se-I deficiency. Thyroidal cystolic
GSH-Px (c-GSH-Px) and phospholipid GSH-Px (ph-GSH-Px) activities remained constant in both Se-deficient groups, whereas thyroidal
c-GSH-Px activity increased (57%) in I deficiency. Type II deiodinase (ID-II) activity was not detectable in the cerebrum
and cerebellum, whereas cerebellum Type III deiodinase (ID-III) activity was decreased in I deficiency and combined Se-I deficiencies.
The results of the present study support a sensitive interaction between Se and I deficiencies in sheep thyroid and brain.
Furthermore, the lack of thyroidal ID-I activity, the presservation of the thyroidal antioxidant enzymes, and the increases
in hepatic ID-I indicate that a compensatory mechanism(s) works toward retaining plasma T3 levels, mostly by de novo synthesis of T3 and peripheral deiodination of T4 in Se- and I-deficient sheep. 相似文献
12.
Responses of mycelia ofGanoderma lucidum to vanadium, selenium and germanium were examined over a wide range of concentrations (10–1, 120 μg/ml) in pure culture.
Se and V were found to be highly toxic, but Ge was not toxic at the levels tested.Ganododerma lucidum cultivated on substrates of sawdust with V (30–80 μg/g) developed mature fruitbodies, but the bioaccumulation of V was quite
low (2.5–7 μg/g in pileus, 12.5–21.5 μg/g in stipe and <1 μg/g in basidiospores). Se as Na2SeO4 labeled with75Se was effectively taken up from substrates and accumulated in fruitbodies (mainly in pileus), then depleted by discharge
of basidiospores. Ge as GeCl4 labeled with77Ge was easily uptaken and translocated into fruitbodies. 相似文献
13.
The effect of manganese supply on thyroid hormone metabolism in the offspring of manganese-depleted dams 总被引:1,自引:0,他引:1
Klaus Eder Angelika Kralik Manfred Kirchgessner 《Biological trace element research》1996,55(1-2):137-145
The present study was performed to investigate the effect of manganese (Mn) supply on metabolism of thyroid hormones in the
rat. A study with rats was carried out over two generations. Female rats were raised with a Mn-deficient diet (0.1 mg Mn/kg),
and mated to produce a second generation. The male rats of the second generation were used as subjects for the investigation.
They were divided into five groups and fed diets with Mn concentrations of 0.1, 0.5, 2.2, 10, and 46 mg/kg for 40 d. For assessment
of thyroid hormone metabolism, concentrations of thyroid hormones in serum and activity of hepatic type I 5′ deiodinase (5′
D-I) were measured. Feeding diets with 0.1 mg Mn/kg impaired growth and food conversion, influenced parameters of thyroid
hormone metabolism, and changed some clinical-chemical parameters, such as concentrations of total protein, albumin, calcium
(Ca) and magnesium (Mg) as well as activity of alkaline phosphatase in serum. Regarding the thyroid hormone metabolism, rats
fed the diet with a Mn level of 0.1 mg/kg had a higher 5′D-I activity in liver, and consequently a higher concentration of
triiodothyronine in serum than the rats fed the other diets. In contrast, the concentrations of total and free thyroxine were
not influenced by the Mn intake. Growth, clinical-chemical parameters, concentrations of thyroid hormones in serum, and activity
of hepatic 5′ D-I were similar in the rats fed diets with Mn concentrations between 0.5 and 46 mg/kg. The present study shows
that feeding a diet with a very low Mn concentration affects growth and thyroid hormone metabolism and that a dietary level
of 0.5 mg Mn/kg is adequate for growth and thyroid hormone metabolism in the off-spring of Mn-depleted dams. 相似文献
14.
Bernard A. Eskin Carolyn E. Grotkowski Christopher P. Connolly William R. Ghent 《Biological trace element research》1995,49(1):9-19
This research describes the effects of short-term elemental iodine (I2) and iodide (I−) replacement on thyroid glands and mammary glands of iodine-deficient (ID) Sprague-Dawley female rats. Iodine deficiency
causes atypical tissue and physiologic changes in both glands. Tissue histopathology and the endocrine metabolic parameters,
such as serum TT4, tissue and body weights, and vaginal smears, are compared. A moderate reduction in thyroid size from the ID control (IDC)
was noted with both I− and I2, whereas serum total thyroxine approached the normal control with both I− and I2, but was lower in IDC. Thyroid gland IDC hyperplasia was reduced modestly with I2, but eliminated with I−. Lobular hyperplasia of the mammary glands decreased with I2 and increased with I− when compared with the IDC; extraductal secretions remained the same as IDC with I2, but increased with I−; and periductal fibrosis was markedly reduced with I2, but remained severe with I−. Thus, orally administered I2 or I− in trace doses with similar iodine availability caused different histopathological and endocrine patterns in thyroid and
mammary glands of ID rats. The significance of this is that replacement therapy with various forms of iodine are tissue-specific. 相似文献
15.
L. S. Jensen G. L. Colnago K. Takahashi Y. Akiba 《Biological trace element research》1986,10(1):11-18
Experiments were conducted to study the effect of marginal levels of selenium and vitamin E on plasma thyroid hormones of
meattype chicks. Plasma thyroxine (T4) was significantly increased when a semipurified diet was supplemented with either selenium or vitamin E. Triiodothyronine
(T3) was also significantly increased by vitamin E and in one experiment with selenium supplementation. No significant increase
in these hormones was observed in birds fed a corn-soybean-meal diet supplemented with these nutrients. Plasma corticosterone
level was reduced and weight of the bursa of Fabricius increased by selenium or vitamin E supplementation. These nutrients
may be necessary for providing the optimum thyroid conditions for activity of thyroid peroxidase. 相似文献
16.
Julius Brtko Peter Filipčík Soňa Hudecová Anastázia Brtková Janette Bransová 《Biological trace element research》1998,62(1-2):43-50
The present study was undertaken to investigate the effects of selenite (SeIV) and selenate (SeVI) on the all-trans retinoic acid (RA)-nuclear retinoic acid receptor (RAR) complex formation in rat liver. We also present
the data on the in vitro effects of SeIV on the RARα and the type I iodothyronine 5′-deiodinase gene expression in the GH4C1 rat pituitary tumor cells. SeIV at 1.0 μmol/L was found to reduce (p<0.05) the RA specific binding to RAR in rat liver. Dithiothreitol (DTT), a protective agent for sulfhydryl groups, was found
to be slightly effective in protecting the RAR binding properties when affected by SeIV. SeVI at 0.1 μmol/L reduced (p<0.05) the RA specific binding to RAR in liver, as well. Seleno-l-methionine (Se-II) when compared tol-methionine did not exert any inhibitory effect on the formation of the RA-RAR complex. SeIV (up to 2.5 μmol/L) has no inhibitory effect on GH4C1 cell proliferation as well as the prolactin secretion. SeIV at 1.0 μmol/L significantly decreases the rate of mRNA synthesis and/or degradation of the α form of the RAR and causes the
enhancement of the type I iodothyronine 5′-deiodinase gene expression in GH4C1 cells.
The results based on in vitro experiments suggest that inorganic selenium may affect the RA specific binding to their cognate
receptor molecules, and it may reduce expression of the gene encoding the RARα, with the cell vitality and the cell growth
remaining unchanged. 相似文献
17.
Chanoine JP 《BioFactors (Oxford, England)》2003,19(3-4):137-143
Selenium is an integral component of the enzymes glutathione peroxidase (GPx) and iodothyronine deiodinases. Although selenium nutrition could conceivably affect thyroid function in infants, children and adolescents, available data suggest that the effect of selenium deficiency on thyroid function is relatively modest. In patients with isolated selenium deficiency (such as patients with phenylketonuria receiving a low-protein diet), peripheral thyroid hormone metabolism is impaired but there are no changes in thyrotropin (TSH) or clinical signs of hypothyroidism, suggesting that these patients are euthyroid. Selenium supplementation may be advisable to optimize tissue GPx activity and prevent potential oxidative stress damage. In areas where combined selenium and iodine deficiencies are present (such as endemic goiter areas in Central Africa), selenium deficiency may be responsible for the destruction of the thyroid gland in myxoedematous cretins but may also play a protective role by mitigating fetal hypothyroidism. In these areas, selenium supplementation should only be advocated at the same time or after iodine supplementation. In patients with absent or decreased production of thyroid hormones and who rely solely on deiodination of exogenous L-thyroxine for generation of the active triiodothyronine (such as patients with congenital hypothyroidism), selenium supplementation may optimize thyroid hormone feedback at the pituitary level and decrease stimulation of the residual thyroid tissue. 相似文献
18.
Giovanna Bermano Fergus Nicol John A. Dyer Roger A. Sunde Geoffrey J. Beckett John R. Arthur John E. Hesketh 《Biological trace element research》1996,51(3):211-223
Selenium repletion of selenium-deficient rats with 20 μg selenium/kg body weight as Na2SeO3 was used as a model to investigate the mechanisms that control the distribution of the trace element to specific selenoproteins
in liver and thyroid. Cytosolic glutathione peroxidase (cGSHPx), phospholipid hydroperoxide glutathione peroxidase (PHGSHPx),
and iodothyronine 5′-deiodinase (IDI) activities were all transiently increased in liver 16 to 32 h after ip injection with
selenium. However, only cGSHPx and PHGSHPx activities increased in the thyroid where IDI activity was already increased by
selenium deficiency. These responses were owing to synthesis of the seleoproteins on newly synthesised and/or existing mRNAs.
The selenoprotein mRNAs in the thyroid gland were increased two- and threefold after the transitory increases in selenoprotein
activity. In contrast, there were parallel changes in selenoprotein mRNAs and enzyme activities in the liver, with no prolonged
rises in mRNA levels. The organ differences suggest that increased thryotrophin (TSH) concentrations, which are known to induce
thyrodial IDI and mRNA, may control the mRNAs for all the thyroidal selenoproteins investigated and be a major mechanism for
the preservation of thyroidal selenoproteins when selenium supplies are limited. 相似文献
19.
Eduard Kühn Rudi Van Cauwenbergh Leo Huybrechts Hendrik Deelstra 《Biological trace element research》1992,32(1-3):289-292
Plasma concentrations of cGH, T3, and T4 were not different between dwarf and normal broiler breeders. Normal hens had a liver selenium content of 710±35 ng/g, and
dwarf hens 656 ±nine ng/g (n=8). Following injections into a wing vein of different doses (1.5, 3, 6, 12, and 24 μg/kg) of the hypothalamic hormone TRH,
GH was increased after 15 min. This effect seemed to last longer in dwarf chickens. Plasma concentrations of T3 increased significantly 1 h after TRH in normal hens, but TRH was ineffective in raising T3 levels in dwarf animals. The selenium content of livers obtained following decapitation after 2 h was also increased in normal
hens up to 902±42 ng/g using the highest dose of TRH (24 μg/kg). This seemed not to be the case for dwarf animals. A much
smaller. number of hepatic cGH receptors was also found in dwarf hens, whereas the affinity of the hepatic GH receptor was
not influenced by the genotype. It is concluded that the sex-linked dwarf hens are unable to increase their hepatic T4 into T3 conversion following a TRH challenge probably because of a deficiency in hepatic GH receptors. The lower content of selenium
in dwarfs and their inability to increase its uptake after TRH seem therefore to support the hypothesis that selenium has
a direct role in the activity of the 5′-deiodinase complex. 相似文献
20.
The weanling Wistar rats of iodine deficiency were divided into three groups for supplementation of different levels of iodine
(iodine-excessive [IE], iodine-adequate [IA], and iodine-deficient [ID]), with a control group (C). The iodine content in
the thyroid was determined by epithermal neutron activation analysis. The activities of 5′-deiodinase and 5-deiodinase in
the brains were assayed by determining the conversion ratios of T4 to T3 and rT3, respectively. The thyroid hormones levels
in serum were also tested. The results indicated that the ID group had a goiter containing a small amount of iodine, but the
IE group had a slightly swollen thyroid with rich iodine; the concentration of iodine per unit mass of thyroid was lower in
group IE than in groups IA and C. The highest 5′-deiodinase and lowest 5-deiodinase activities in group ID and the lowest
5′-deiodinase activity in group IE were found. The iodine deficiency or excess resulted in a compensated hypothyroid state.
The results suggest that the iodine status and the deiodinases activities would become normal for the rats of iodine deficiency
if adequate iodine is supplemented soon after birth. Meanwhile, it is also critical to avoid excessive intake of iodine to
reduce the risk for overcorrecting. 相似文献