Effect of experimental 3,5,3<i>'</i>-triiodothyronine hyperthyroidism on thyroid hormone deiodination in brain regions and liver of rainbow trout,<i>Oncorhynchus mykiss</i>

Abstract

We studied the effect of 3,5,3'-triiodothyronine (T 3 ) hyperthyroidism, induced by 12 ppm T 3 in food for 10 days, on the low-K m activities of thyroxine (T 4 ) outer-ring deiodination (ORD) to form T 3 , T 4 inner-ring deiodination (IRD) to form 3,3',5'-triiodothyronine (reverse T 3 (rT 3 )), T 3 ORD to form 3,5-diiodothyronine (3,5-T 2 ), and T 3 IRD to form 3,3'-diiodothyronine (3,3'-T 2 ) in six brain regions and in liver of immature rainbow trout (Oncorhynchus mykiss) at 12°C. Throughout the brain, T 4 ORD activity of control trout was uniformly low and T 3 ORD activity was negligible. T 4 IRD and T 3 IRD activities were about 5-fold and 50-fold greater, respectively, than T 4 ORD activity and were higher in the optic lobes, hypothalamus, and telencephalon/olfactory bulbs than in the medulla or cerebellum. T 3 treatment doubled the plasma T 3 level with no change in plasma T 4 level and reduced T 4 ORD and T 4 IRD activities in all brain regions but did not alter T 3 IRD activity or the negligible T 3 ORD activity. Relative to controls, T 3 treatment reduced liver T 4 ORD activity 6-fold, increased T 4 IRD activity 8-fold, and increased T 3 IRD activity 12-fold. We conclude that (i) there are regional differences in trout brain T 4 IRD and T 3 IRD activities but not in T 4 ORD activity, indicating spatial variation in brain T 4 and T 3 catabolism, (ii) in response to a mild T 3 challenge the brain deiodination pathways do not undergo the same autoregulatory adjustments as those in liver, and (iii) a T 3 challenge reduces brain T 4 IRD activity with no change in T 3 IRD activity, which suggests that the two IRDs may be controlled by separate deiodinases.