Effect of selenium deficiency on hepatic type I 5-iodothyronine deiodinase activity and hepatic thyroid hormone levels in the rat

Author:

Beckett G J1,Russell A2,Nicol F3,Sahu P1,Wolf C R2,Arthur J R3

Affiliation:

1. University Department of Clinical Chemistry, Royal Infirmary, Edinburgh EH3 9YW

2. ICRF Molecular Pharmacology Group, Hugh Robson Building, George Square, Edinburgh EH8 9XD

3. Division of Biochemical Sciences, Rowett Research Institute, Greenburn Road, Aberdeen AB2 9SB, U.K.

Abstract

Selenium deficiency in rats for a period of up to 6 weeks inhibited both the production of 3,3′, 5-tri-iodothyronine (T3) from thyroxine (T4) (5′-deiodination) and also the catabolism of T3 to 3,3′-di-iodothyronine (5-deiodination) in liver homogenates. The hepatic stores of T3 were decreased by only 8% in selenium deficiency, despite the T3 production rate from T4 being only 7% of the rate found in selenium-supplemented rats. Hepatic glutathione S-transferase (GST) activity was increased in both hypothyroidism and selenium deficiency, but apparently by different mechanisms, since mRNA expression for this family of enzymes was lowered by hypothyroidism and increased in selenium deficiency. It is concluded that, since both T3 production and catabolism are inhibited by selenium deficiency, there is little change in hepatic T3 stores, and therefore the changes in the activity of certain hepatic enzymes, such as GST, that are found in selenium deficiency are not the result of tissue hypothyroidism.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry

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