Selenoenzyme activities in selenium-and iodine-deficient sheep

dc.contributor.author	Voudouri, AE	en
dc.contributor.author	Chadio, SE	en
dc.contributor.author	Menegatos, JG	en
dc.contributor.author	Zervas, GP	en
dc.contributor.author	Nicol, F	en
dc.contributor.author	Arthur, JR	en
dc.date.accessioned	2014-06-06T06:45:36Z
dc.date.available	2014-06-06T06:45:36Z
dc.date.issued	2003	en
dc.identifier.issn	01634984	en
dc.identifier.uri	http://dx.doi.org/10.1385/BTER:94:3:213	en
dc.identifier.uri	http://62.217.125.90/xmlui/handle/123456789/2534
dc.subject	I	en
dc.subject	Se	en
dc.subject	Selenoenzymes	en
dc.subject	Sheep	en
dc.subject.other	glutathione peroxidase	en
dc.subject.other	iodide peroxidase	en
dc.subject.other	iodine	en
dc.subject.other	isoenzyme	en
dc.subject.other	liothyronine	en
dc.subject.other	phospholipid	en
dc.subject.other	phospholipid derivative	en
dc.subject.other	selenium	en
dc.subject.other	thyroid hormone	en
dc.subject.other	thyrotropin	en
dc.subject.other	thyroxine	en
dc.subject.other	animal experiment	en
dc.subject.other	animal model	en
dc.subject.other	animal tissue	en
dc.subject.other	article	en
dc.subject.other	artificial diet	en
dc.subject.other	blood level	en
dc.subject.other	brain	en
dc.subject.other	cerebellum	en
dc.subject.other	comparative study	en
dc.subject.other	controlled study	en
dc.subject.other	cytosol	en
dc.subject.other	enzyme activity	en
dc.subject.other	enzyme analysis	en
dc.subject.other	enzyme blood level	en
dc.subject.other	erythrocyte	en
dc.subject.other	iodine deficiency	en
dc.subject.other	kidney	en
dc.subject.other	lamb	en
dc.subject.other	liothyronine blood level	en
dc.subject.other	liver	en
dc.subject.other	male	en
dc.subject.other	nonhuman	en
dc.subject.other	selenium deficiency	en
dc.subject.other	sheep	en
dc.subject.other	thyroid function	en
dc.subject.other	thyroid gland	en
dc.subject.other	thyroid hormone blood level	en
dc.subject.other	thyrotropin blood level	en
dc.subject.other	thyroxine blood level	en
dc.subject.other	tissue slice	en
dc.subject.other	Animals	en
dc.subject.other	Brain	en
dc.subject.other	Erythrocytes	en
dc.subject.other	Glutathione Peroxidase	en
dc.subject.other	Iodide Peroxidase	en
dc.subject.other	Iodine	en
dc.subject.other	Kidney	en
dc.subject.other	Liver	en
dc.subject.other	Male	en
dc.subject.other	Selenium	en
dc.subject.other	Sheep	en
dc.subject.other	Thyroid Gland	en
dc.subject.other	Thyroid Hormones	en
dc.subject.other	Thyrotropin	en
dc.subject.other	Thyroxine	en
dc.subject.other	Triiodothyronine	en
dc.subject.other	Animalia	en
dc.subject.other	lamb	en
dc.subject.other	Ovis aries	en
dc.title	Selenoenzyme activities in selenium-and iodine-deficient sheep	en
heal.type	journalArticle	en
heal.identifier.primary	10.1385/BTER:94:3:213	en
heal.publicationDate	2003	en
heal.abstract	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 preservation 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.	en
heal.journalName	Biological Trace Element Research	en
dc.identifier.issue	3	en
dc.identifier.volume	94	en
dc.identifier.doi	10.1385/BTER:94:3:213	en
dc.identifier.spage	213	en
dc.identifier.epage	224	en