Thyroid Hormone Deiodination in Brain, Liver, Gill, Heart and Muscle of Atlantic Salmon (Salmo salar) during Photoperiodically-Induced Parr-Smolt Transformation. II. Outer- and Inner-Ring 3,5,3′-Triiodo-l-Thyronine and 3,3′,5′-Triiodo-l-Thyronine (Reverse T3) Deiodination

Abstract

Outer-ring deiodinase (ORD) and inner-ring deiodinase (IRD) pathways for 3,5,3′-triiodo-l-thyronine (T3) and 3,3′,5′-T3 (reverse T3, rT3) were examined in microsomal fractions of liver, heart, gill, brain, and skeletal muscle of 20-month-old Atlantic salmon induced to undergo parr-smolt transformation (PST) in late February and March by imposing a 16-hr photoperiod. All tissues showed negligible T3ORD activity. T3IRD activity was detected in both the liver (Km = 0.65 nM; Vmax = 15.5 pmol T3 deiodinated · hr-1 · mg microsomal protein-1) and brain of smolts, but not in gill, heart, or skeletal muscle. rT3ORD was detected in liver, brain, and muscle, and at very low levels in gill and heart. rT3IRD activity occurred to some extent in all tissues except brain. T3IRD activity changed in brain during PST, and was low in brain and liver of post-smolts examined in late October. We conclude that (i) deiodination of T3 proceeds exclusively through an IRD pathway, which may permit regulation of T3 degradation independently of the ORD pathway responsible for T3 formation; (ii) deiodination of rT3 proceeds mainly through an ORD pathway but rT3IRD activity does occur in some tissues; and (iii) the altered brain T3IRD activity during PST suggests regulation of T3 turnover in the brain at this time.