Transition from a hatchery to a laboratory environment induces inner-ring monodeiodination pathways for thyroid hormones in liver of rainbow trout, Oncorhynchus mykiss

Abstract

In laboratory-acclimated rainbow trout (Oncorhynchus mykiss) the main hepatic deiodination pathway for thyroid hormones is L-thyroxine (T4) outer-ring deiodination (T4ORD), which produces biologically active 3,5,3′-triiodo-L-thyronine (T3); T4 inner-ring deiodination (T4IRD) as well as T3ORD and T3IRD activities are low or undetectable. Surprisingly, trout transported 48 h previously from a local hatchery to the laboratory demonstrated not only low T4ORD activity but also significant T4IRD and T3IRD activities. To test if the transition from hatchery to laboratory environment had induced the unexpected inner-ring deiodinations, we measured hepatic deiodinase activities over the same time frame in trout recently transported to the laboratory and also in trout retained undisturbed at the hatchery. Undisturbed hatchery trout showed typical hepatic deiodinase function: T4ORD activity predominated, while T3IRD, T4IRD, and T3ORD activities were basal. However, after 1–3 days in the laboratory, hepatic T4ORD activity was reduced and T4IRD and T3IRD activities were increased. By 5 days, deiodinase activities of laboratory trout reverted to the levels of hatchery trout. We conclude that physical disturbance can temporarily depress thyroidal status by simultaneously decreasing hepatic production of biologically active T3 and inducing degradation of T4 and T3.