Ontogeny of UDP-GT activity in Japanese quail and effects of PCB 126 on UDP-GT activity in chicken embryos

MCCLEARY, R.J.R.*; MCFARLAND, E.C.; GRASMAN, K.A.; MCNABB, F.M.A.: Ontogeny of UDP-GT activity in Japanese quail and effects of PCB 126 on UDP-GT activity in chicken embryos.

Uridinediphosphate-glucuronosyltransferases (UDP-GTs) are important phase II liver biotransformation enzymes responsible for conjugation of many endogenous and exogenous substances in vertebrates. Induction of UDP-GTs has been shown in birds exposed to pollutant chemicals such as PCBs and TCDD. Because UDP-GTs are responsible for the removal of thyroxine from the circulation, their induction can cause a concomitant decrease in circulating thyroid hormones (THs). To investigate the development of UDP-GT activity in precocial bird embryos, we examined the pattern of enzyme activity during different stages of embryonic (d12, 14, 16 and 17 of incubation) and post-hatch (d<1, 1 and 7) development in Japanese quail. To elucidate the effects of pollutant chemicals on UDP-GT induction in developing bird embryos, we dosed chicken eggs with the coplanar PCB 126 (0, .0512 to .80 ng/g egg) and sampled on d20 of the 21 day incubation period. We validated a colorimetric assay for UDP-GT activity in quail and chicken liver homogenate with para-nitrophenol as substrate. Plasma THs were determined by RIA. The development of quail UDP-GT activity shows low, stable activity pre-hatch, increasing activity during the peri-hatch period and further increases in activity from d1 to 7 post-hatch. In PCB-dosed chickens, there were no significant differences from controls in UDP-GT activity, plasma thyroxine, thyroid gland weights or thyroid gland THs. Thus, embryonic exposure to PCB 126 did not cause thyroid disruption at sub-lethal concentrations. However, additional congeners and PCB mixtures need to be evaluated for their effects on thyroid function. Supported by EPA grant #827400-01-0 and a Sigma Xi Grant-in-Aid of Research.

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