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
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
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.