EFFECT OF T3 OR T4 CHALLENGE ON INNER-RING AND OUTER-RING DEIODINATION OF T3 AND T4 IN THE LIVER, KIDNEY, AND GILL OF RAINBOW-TROUT, ONCORHYNCHUS-MYKISS

Citation
Dl. Maclatchy et Jg. Eales, EFFECT OF T3 OR T4 CHALLENGE ON INNER-RING AND OUTER-RING DEIODINATION OF T3 AND T4 IN THE LIVER, KIDNEY, AND GILL OF RAINBOW-TROUT, ONCORHYNCHUS-MYKISS, The Journal of experimental zoology, 265(6), 1993, pp. 637-645
Citations number
28
ISSN journal
0022104X
Volume
265
Issue
6
Year of publication
1993
Pages
637 - 645
Database
ISI
SICI code
0022-104X(1993)265:6<637:EOTOTC>2.0.ZU;2-F
Abstract
The effects of feeding 3,5,3'-triiodo-L-thyronine (T3)- and L-thyroxin e (T4)-supplemented diets for 3 days on the plasma T3 and T4 concentra tions and on the plasma outer-ring (5'D) and inner-ring (5D) deiodinat ion of T4 and T3 were studied in vitro for the liver, gill, and kidney of rainbow trout (Oncorhynchus mykiss) at 12-degrees-C. Trout were sa mpled 24 hr after their last meal. T3 treatment increased plasma T3 bu t did not alter plasma T4. T4 treatment did not alter plasma T3 or T4. In untreated trout, T(4)5'D activity to form T3 occurred in all 3 tis sues; T(4)5D activity to form 3,3',5'-T3 (rT3) was not significant, T( 3)5D activity to form 3,3'-T2 (diiodo-L-thyronine) was low, and T(3)5' D activity to form 3,5-T2 was barely detectable. A low-K(m) T(4)5'D (T 4 concentration = 0.65 nM) was confirmed in liver and gill, and a high -Km T(4)5'D (T4 concentration = 12 nM) was confirmed in liver and kidn ey. For liver, T3 feeding depressed both low-K(m) and high-K(m) T(4)5' D isozymes, but induced T(4)5D and T(3)5D; T4 feeding depressed only t he high-K(m) T(4)5'D and increased T(3)5'D slightly. For gill, T3 feed ing depressed the low-K(m) T(4)5'D and induced T(4)5D; T4 feeding incr eased T(3)5'D. For kidney, T3 feeding depressed the high-K(m) T(4)5'd and induced T(3)5'D; T4 feeding depressed the high-K(m) T(4)5'D and in creased T(3)5'D. We conclude that in response to either a T3 or a T4 c hallenge, trout tissues employ several T3 homeostatic mechanisms. Resp onses to a T3 challenge included (1) depression of both low-K. and hig h-K(m) T(4)5'D activities to decrease production of T3, (2) elevation of T(4)5D activity to direct T4 substrate to rT3, and (3) elevation of T(3)5D activity to degrade T3 to 3,3'-T2. In contrast, responses to a 4-fold greater dietary T4 challenge were restricted primarily to depr ession of high-K(m) T(4)5'D activity in the liver and kidney.