Altered thyroid status in lake trout ( Salvelinus namaycush) exposed to co-planar 3,3′,4,4′,5-pentachlorobiphenyl

Abstract

Recent studies indicate that co-planar 3,3′,4,4′,5-pentachlorobiphenyl (PCB) congeners or their metabolites may disrupt thyroid function in fishes. Although co-planar PCB have been detected at microgram per kilogram levels in fish from contaminated areas, few studies have examined mechanisms whereby, co-planar PCBs may alter thyroid function in fish. We treated immature lake trout by intraperitoneal (i.p.)-injection or dietary gavage with vehicle containing 0, 0.7, 1.2, 25 or 40 μg 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) per kg BW. Blood and tissue samples were collected at various times up to 61 weeks following exposure. The treatments produced sustained dose-dependent elevations of tissue (PCB 126) concentrations. Thyroid epithelial cell height (TECH), plasma thyroxine (T 4) and 3,3′,5-triiodo- l-thyronine (T 3) concentrations, hepatic 5′-monodeiodinase, hepatic glucuronidation of T 4 and T 3, as well as plasma T 4 kinetics and fish growth were analyzed. Exposure to the highest doses of PCB 126 caused increased TECH, plasma T 4 dynamics and T 4-glucuronidation (T 4-G). PCB 126 did not affect 5′-monodeiodinase and T 3-glucuronidation (T 3-G) and there were no effects on fish growth or condition. Because T 3 status and growth were unaffected, the thyroid system was able to compensate for the alterations caused by the PCB 126 exposure. It is clear that concentrations of co-planar PCBs similar to those found in predatory fish from contaminated areas in the Great Lakes are capable of enhancing metabolism of T 4. These changes may be of significance when T 4 requirements are high for other reasons (e.g. periods of rapid growth, warm temperatures, metamorphosis, and parr-smolt transformation).