(udp-gt) Ontogeny and Pcb Effects in Galliform Birds

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. This research was supported by funding from the U. S. Environmental Protection Agency, Sigma Xi, the Biology Department at Virginia Tech and the Graduate Student Association of Virginia Tech.