Associations between organohalogen concentrations and transcription of thyroid-related genes in a highly contaminated gull population.

A number of studies have reported altered circulating thyroid hormone levels in birds exposed either in controlled settings or in their natural habitat to ubiquitous organohalogen compounds including organochlorines (OCs) and polybrominated diphenyl ether (PBDE) flame retardants. However, limited attention has been paid to underlying homeostatic mechanisms in wild birds such as changes in the expression of genes in the hypothalamic-pituitary-thyroid (HPT) axis. The objective of the present study was to investigate the relationships between hepatic concentrations of major organohalogens (PBDEs and OCs), and circulating thyroid hormone (free and total thyroxine (T4) and triiodothyronine (T3)) levels and transcription of 14 thyroid-related genes in three tissues (thyroid, brain, and liver) of an urban-adapted bird exposed to high organohalogen concentrations in the Montreal area (QC, Canada), the ring-billed gull (Larus delawarensis). Positive correlations were found between liver concentrations of several polychlorinated biphenyls (PCBs), PBDEs as well as chlordanes and total plasma T4 levels. Hepatic concentrations of several PBDEs were negatively correlated with mRNA levels of deiodinase type 3, thyroid peroxidase, and thyroid hormone receptor β (TRβ) in the thyroid gland. Liver PCB (deca-CB) correlated positively with mRNA levels of sodium-iodide symporter and TRα. In brain, concentrations of most PBDEs were positively correlated with mRNA levels of organic anion transporter protein 1C1 and transthyretin, while PCBs positively correlated with expression of TRα and TRβ as well as deiodinase type 2. These multiple correlative linkages suggest that organohalogens operate through several mechanisms (direct or compensatory) involving gene transcription, thus potentially perturbing the HPT axis of this highly organohalogen-contaminated ring-billed gull population.