Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.6.1 (sulfatase)
 3,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study tested the effects of different iodine intakes on thyroid ultrastructure and function in thyroid remnants after subtotal thyroidectomy (sub-tx). Removal of most of the thyroid gland causes an elevation of endogenous TSH, which chronically stimulates the residual tissue. Male Sprague-Dawley rats were divided into three groups; Low Iodine Group (LIG), Moderate Iodine Group (MIG), and High Iodine Group (HIG). There was no significant difference among total thyroid weights removed by sub-tx, but thyroid remnant weights and TSH levels were higher at death (6 weeks after sub-tx) in LIG than in MIG and HIG. Total specific activities of cathepsin D and of arylsulfatase A in the sedimentable and nonsedimentable subcellular fractions were at least 38% lower in LIG than in MIG and HIG. The ratio between relative follicular volume and colloid volume determined by morphometry was higher in LIG than in MIG and lower in HIG than in MIG. Ultrastructurally, the relative volume occupied by secondary lysosomes was higher in HIG than in MIG, whereas the number of secondary lysosomes was not higher in LIG than in controls. Autoradiographic studies with 125I revealed that a large part of the radioactivity was in thyroid cell secondary lysosomes in MIG and HIG when radioiodine was injected 3 weeks before death. It is concluded that after sub-tx, iodine 1) regulates the weight of thyroid remnants, perhaps only indirectly through TSH, 2) modulates the number of secondary lysosomes in thyroid cells, and 3) slows down the turnover of secondary lysosomes. An iodine-deficient regimen impedes the secondary lysosomes to increase. Because of these findings, we postulate that chronic TSH stimulation along with a possible toxic role of iodine after sub-tx could induce an accumulation of lysosomal bodies.
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PMID:Effects of iodine intake on thyroid secondary lysosomes after subtotal thyroidectomy. 338 83

Subtotal thyroidectomies were performed in rats to increase the level of endogenous TSH, creating a condition of chronic TSH stimulation. The activities of various classes of lysosomal enzymes (cathepsin D, beta-glucuronidase, and aryl sulfatase A) were studied in thyroid tissue remaining in situ at various time intervals after subtotal thyroidectomy (sub-tx). These alterations were correlated with morphometric and ultrastructural changes in tissue lysosomes and with serum T4 and TSH. Specific activities of all three lysosomal enzymes were elevated in the residual tissue as compared with those in control tissue during 7 weeks after sub-tx in the first experiment. In the second experiment, the activities of all three enzymes were elevated both 3 and 6 weeks after sub-tx, and the activities of cathepsin D and aryl sulfatase A in the postnuclear homogenate (S2) were significantly elevated. Plasma TSH was elevated and T4 was decreased both 3 and 6 weeks after sub-tx. The results of the third experiment determined that there were significant alterations in nuclear cytoplasmic ratios as well as in the number, area, and volume density of lysosomes in both groups compared with respective control values. In addition, both lysosomal area and volume density in animals 6 weeks after sub-tx were significantly larger than those in animals 3 weeks after sub-tx. We conclude that chronic stimulation of residual thyroid tissue 6 weeks after sub-tx causes alterations in lysosomal ultrastructure as well as in lysosomal enzyme activity.
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PMID:Thyroid lysosomal enzyme activity and ultrastructure after subtotal thyroidectomy. 614 15

Several steady state indices of thyroid hormone distribution, metabolism, excretion, and absorption were measured in intact hypothyroid and euthyroid rats, to explore the role of intestines and enterohepatic pathways in the dynamic regulation of whole-body thyroid hormone in these two states. Ten rats were studied, 5 normal control (N) and 5 rendered hypothyroid (3.48 vs. 19.8 ng/ml TSH) by surgical thyroidectomy 3.5 weeks earlier (HYPO). High specific activity 125I-labeled T3 (T3*) was infused at the same constant rate for 7 days from osmotic minipumps implanted sc. Daily urine and feces, and seventh-day cardiac and portal venous blood, bile, and whole intestinal contents were assessed. Bowel and feces were homogenized, extracted, and chromatographed, along with serum, bile, and urine samples. Bile, bowel, and fecal extract samples were also hydrolyzed with aryl-sulfatase and/or beta-glucuronidase and chromatographed to identify conjugates and determine total T3* in all fluid and tissue samples. In the N group, the bowel contained 21.2 +/- 1.22 (SD) times more T3* (mass) than plasma (199 ng vs. 9.39 ng), this ratio falling to 9.03 +/- 1.78 in the HYPO group (30.4 ng vs. 3.37 ng), a shift to relatively more T3* in blood. Urinary T3* was zero in both groups. But fecal excretion was 34 +/- 4.43% of total T3* infused (production) in N and only 20.3 +/- 3.05% in HYPO rats, closely paralleling reduced fecal bulk flow, and thus providing more time for T3* absorption. Endogenous T3 and T4 concentrations measured in portal plasma were 15-31% greater in normals and 69-95% greater in HYPO rats than in corresponding systemic plasma samples, a direct indication of absorption of endogenous T3 and T4 in both groups, with greater absorption in the HYPO group. About 66% total T3* was metabolically degraded in N rats, rising to approximately 80% in HYPO rats. Plasma clearance rates of T3 fell more than 50% in HYPO rats, and total T3 production fell to about 20% of normal. It appears that HYPO rats compensate for low T3 by fecally excreting a much smaller fraction of total T3 production, absorbing more T3 and T4, and leaving a larger fraction for T3 action and degradative metabolism.
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PMID:Enterohepatic regulation and metabolism of 3,5,3'-triiodothyronine in hypothyroid rats. 846 66