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Sulfation is an important pathway of triiodothyronine (T3) metabolism. Increased serum T3 sulfate (T3S) values have been observed during fetal life and in pathological conditions such as hyperthyroidism and selenium deficiency. Similar variations have also been reported in a small number of patients with systemic non-thyroidal illness, but the underlying mechanisms have not been elucidated. In this study, serum T3S concentrations have been measured by a specific radioimmunoassay in 28 patients with end-stage neoplastic disease (ESND) and in 44 patients with chronic renal failure (CRF); 41 normal subjects served as controls. Both ESND and CRF patients had lower serum total T4 (TT4) and total T3 (TT3) than normal controls, while serum reverse T3 (rT3) was increased significantly in ESND (0.7 +/- 0.5 nmol/l; p < 0.001 vs. controls) but not in CRF (0.3 +/- 0.1 nmol/l). The TT3/rT3 ratio, an index of type I iodothyronine monodeiodinase (type I MD) activity, was reduced significantly in both groups of patients. Serum T4-binding globulin (TBG) was decreased in CRF but not in ESND patients. Serum T3S was significantly higher both in ESND (71 +/- 32 pmol/l) and CRF (100 +/- 24 pmol/l) than in controls (50 +/- 16 pmol/l, p < 0.001). Serum T3S values showed a positive correlation with rT3 values and a negative correlation with both TT3 and FT3 values in ESND, but not in CRF. In the latter group a positive correlation was observed between T3S and TBG values. The T3S/FT3 ratio was higher both in CRF (18 +/- 5) and in ESND (23 +/- 18) as compared to controls (10 +/- 4). Serum inorganic sulfate was increased and correlated positively with T3S values in CRF patients. In conclusion, the results of this study in a large series of patients confirm that patients with systemic non-thyroidal illness have increased serum T3S levels. The mechanisms responsible for these changes appear to be different in ESND and CRF patients. In ESND the increase in serum T3S levels is mainly related to reduced degradation of the hormone by type I MD, whereas in CRF it might be driven by the enhanced sulfate ion concentration, and could be partially dependent on the impaired renal excretion of T3S. Because T3S can be reconverted to T3, it is possible that increased T3S concentrations contribute to maintenance of the euthyroid state in systemic non-thyroidal disease.sulfur--T3 sulfate high in hyperT.doc
Thyroid follicle cells from various mammalian species incorporate 35-SO4(2-). Light and electron microscopic autoradiographs show that the Golgi complex is the predominant site of sulfate incorporation and that the secretory product accumulating in the follicle lumen is sulfated. In order to determine which components of the luminal content carry the sulfate residues, inside-out follicles from pig thyroid glands were incubated in the presence of 35-SO4(2-) and the secretory product released into the culture medium was analyzed by polyacrylamide gel electrophoresis. The observations show that the secretory product consists of sulfated thyroglobulin and that approximately 13 sulfate residues are bound covalently to 1 molecule of dimeric thyroglobulin. Digestion of 35-SO4(2-)-thyroglobulin with endoglycosidase H removes 20 to 30% of the radioactivity, indicating that the high mannose carbohydrate side chains carry sulfate residues. The complex carbohydrate side chains are apparently free of sulfate since treatment with endoglycosidase D did not alter the sulfate content. About 2/3 of the sulfate is cleaved by hydrolysis with 1 M HCl (5 min, 95 degrees C) indicating the presence of tyrosine sulfate. Part of the sulfate is exposed and presumably located on the surface of the thyroglobulin molecule as suggested by the direct accessibility of 35-SO4(2-)-thyroglobulin to digestion with sulfatases. The sulfate residues contribute to the anionic state of thyroglobulin. It is postulated that the sulfate residues operate in the regulation of thyroglobulin transport in the cell and in the tight packaging of thyroglobulin in the follicle lumen.sulfated thyroglobulin.doc
Mammalian thyroglobulin is released by thyroid follicle cells as a sulfated glycoprotein; the sulfate residues are mostly linked to tyrosine, but they are also attached to the high-mannose carbohydrate side-chains. To decide whether sulfation of thyroglobulin is confined to mammals, representatives of other vertebrate classes were analyzed for the presence of sulfated thyroglobulin: fish (trout), amphibians (clawed toad) and birds (chicken). Mini-organs were prepared from thyroid tissue and suspended in a 35SO4-(-)-containing culture medium. Light- and electron-microscope autoradiographs prepared from the mini-organs showed that thyroid follicle cells from all species examined incorporate 35SO4-(-) and synthesize a sulfated secretory product which accumulates in the follicle lumen. The Golgi complex was detected as the primary intracellular site of sulfate organification. The 35SO4-(-)-radiolabeled secretory product of all species was shown by polyacrylamide-gel-electrophoretic analyses to consist of thyroglobulin, identified by comparison with biosynthetically 125I-labeled thyroglobulin. The results indicate that the sulfation of thyroglobulin is a ubiquitous post-translational modification observed already in the thyroglobulin of lower vertebrates. Our observations suggest that sulfation of thyroglobulin was acquired in the early stages of thyroid evolution.sulfation of thyroglobulin in all vetebrates.doc
The metabolism of methionine was studied in rainbow trout fed diets containing different levels of methionine and cystine. Growth data indicated that methionine requirement was between 0.5 and 1% dry diet in the absence of dietary cystine, but 0.5% was adequate when dietary cystine was 2%. In fish fed diets deficient in sulfur-containing amino acids, elevated hepatic activities of glutathione reductase were found, whereas glutathione peroxidase and glutathione levels were unaffected. Plasma and liver concentrations (18 hours after feeding) of methionine and cystine were affected by dietary methionine, but dietary cystine had little effect. Cystine appeared to be converted to taurine in the liver. In fish injected intraperitoneally with [14COOH]- and [14CH3]methionine, over 24 hours the carboxyl group was oxidized more than the methyl group and more was incorporated into protein. However, much more of the methyl group was incorporated into the lipid fraction. The results suggest the operation of the transsulfuration pathway of methionine catabolism. Oxidation of methionine was related to its concentration in the tissues, and little affected by dietary cystine. A 28-day experiment on the metabolism of injected [14COOH]methionine showed that its turnover was slow, and much of the radioactivity was associated with protein.sulfur deficiency--methionine metabolism.doc
The effect of a sulfur deficiency on the metabolism of selenium and sulfur was investigated in eight merino wethers. The sheep were fed high-sulfur (2 g S/kg) or low-sulfur (0.5 g S/kg) diets for two periods of 35 days each, and received selenium as selenomethionine at dietary concentrations of 0.02, 0.06, 0.09 and 0.67 mg Se/kg. Sheep fed the low-sulfur diet had reduced feed intake, reduced nitrogen, sulfur and selenium balance, but elevated plasma and wool selenium concentrations. Selenium concentrations in organs and tissues of slaughtered animals paralleled the selenium intake of the animal, with the renal cortex containing the highest concentration and bone the lowest. The effect of the 0.5 g S/kg diet on feed intake is in contrast with the results from the previous experiment (White and Somers 1977) using 0.7 g S/kg. It is this difference in fed intake which was responsible for many of the effects on selenium metabolism observed in this experiment. Once the feed intake effects are accounted for, the implications for sulfur--selenium interactions remain as before, i.e. more selenium is incorporated into wool and plasma protein when dietary sulfur is limiting than when it is not.sulfur-selenium interactions.doc
This is an interesting note for anyone suffering for low thyroid. I have low thyroid, and LOVE your site, it's one of my favs, as I am a firm believer in nutrition/supplements being the backbone of thyroid disease.
I'll get to the point: Before I started nutritional supplementation, etc. I developed a rash from my hot tub (a reaction to bromine). Many people may get rashes for many different reasons, but the difference is that my rash would not heal, instead, it seemed to be out of control. I tried EVERYTHING, and I mean EVERYTHING!! and my dr. finally recommended a steroid cream. I did not want to do this. I began researching on my own, and on a guy feeling, I tried a SULPHUR cream for my rash. (in fact, I obtained it in a mexican store, sold as a sulphur acne cream)..
The healing was nothing short of miraculous, and if anyone out there suffers from hypothyroid and finds themselves plagued with any type of rash/ skin problem that is NOT responding to conventional treatments, perhaps they might want to try a sulphur ointment (this was 10% sulphur, put into a petroleum base and NOTHING else in the ointment).
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