Uridinediphosphate-glucuronosyltransferase (UDP-GT) Ontogeny and PCB Effects in Galliform Birds

Abstract

Hepatic UDP-GTs are partly responsible for metabolism of the thyroid hormone, thyroxine (T4), in mammals, but little is known of UDP-GT activity in birds. To determine the ontogenic pattern of UDP-GT activity in precocial birds, we measured activity in Japanese quail (Coturnix japonica) liver at days 12 and 14 of the 16.5-day incubation, 3 perihatch stages and <1, 1, 4, 6, 7, 20 and 42 days posthatch. We used an enzymatic reaction with para-nitrophenol (pNP) as substrate that was validated for quail tissue. The pattern of UDP-GT development included low embryonic activity, increased activity beginning in the perihatch period, a peak in activity at day 4 posthatch and a return to lower activity levels from day 6 to adults. The profile of UDP-GT activity, in relation to the ontogeny of circulating T4 and triiodothyronine (T3) in quail, is consistent with UDP-GT playing a role in regulating circulating T4 and with the perihatch peak in T3 stimulating the posthatch peak in UDP-GT activity. To examine the effects of polychlorinated biphenyls (PCBs) on UDP-GT in developing precocial birds, we dosed chicken (Gallus domesticus) eggs with concentrations of PCB 126 from 0 to 0.80 ng/g egg (in sunflower oil) prior to incubation. Tissues were sampled at day 20 of the 21-day incubation and assayed for plasma hormones and UDP-GT activity. Eggs also were dosed with 0 or 0.25 ng PCB 126/g egg or with 0 or 0.64 ng/g egg of the coplanar PCB 77, allowed to hatch, and sampled at 42 days posthatch. There was no consistent pattern of altered thyroid hormones or UDP-GT activity in developing chickens exposed to either of these coplanar PCBs although previous studies indicated developmental alterations from exposure to the higher doses.