Polychlorinated biphenyl effects on avian hepatic enzyme induction and thyroid function

Abstract

Polychlorinated biphenyls (PCBs) decrease thyroid function in laboratory rodents by inducing activity of a liver enzyme, uridine diphosphate-glucuronosyltransferase (UDP-GT), thereby increasing thyroxine (T 4) clearance. This loss of T 4 can lead to hypothyroidism. In this study, an assay was validated for measuring UDP-GT activity toward T 4 in Japanese quail. UDP-GT induction by Aroclor 1254 was evaluated in quail, and responses of quail and mice were compared. In Experiment 1, Japanese quail and Balb/c mice were dosed orally with vehicle or Aroclor 1254 (250 or 500 mg/kg) and sacrificed 5 days later. In Experiment 2, Japanese quail were dosed orally with vehicle or Aroclor 1254 (500 mg/kg) and sacrificed 5 or 21 days later. UDP-GT capacity (pmol T 4 glucuronidated by the liver/min per g body weight) increased with PCB exposure with all doses and exposure times in both species. Plasma T 4 tended to decrease (not significant) with both PCB doses and exposure times in quail and was significantly decreased with both doses in mice. Quail did not become hypothyroid at either dose or exposure time. In contrast, mice did become hypothyroid after a 5-day exposure. It is unclear how PCBs affect the hypothalamic–pituitary–thyroid (HPT) axis in quail, but activation of the HPT axis appears to be inhibited in mice. We believe this is the first demonstration of a T 4-specific, avian UDP-GT response to PCBs. However, this avian response was less than that in mice with equivalent doses of PCBs. Thus, thyroid function in birds appears to be less vulnerable to PCBs than in mammals.