Thyroid endocrine disruption in situ and in vivo experiments reveals compensatory mechanisms

We compared effects of in situ and in vivo exposure of EDC on teleost thyroid system in order to get a complete picture of the putative interactions. A 120-day experimental exposure was designed in combination to in situ measurements of persistent organic pollutants in 87 wild sea bass (Dicentrarchus labrax) form European estuaries. Seventy-five individuals were exposed to doses of PCB (0.3 to 1.0 µg Σ7PCBs per g food pellets) that reflects the persistent organic pollution to which the European sea bass population could conceivably be exposed. We applied a series of recommended measurement endpoints in these studies. The centrally controlled thyroidal secretion of T4 was monitored adequately from the muscular T4 levels and from thyroid histological appearance. Muscular T3 levels and enzymatic deiodinase and sulfatase activities in liver were measured.

Observations made in experimental exposure to environmental relevant doses of PCB were consistent with those made in our field study. In both studies the muscular T4 levels were unaffected and no multivariate relationship with contaminant exposure could be revealed. Measurements of follicular diameter and epithelial cell heights showed no significant differences. Our findings revealed an increase of the hepatic T4ORD activity by higher chlorinated PCB congeners and DDTs. In both studies, we observed a general decrease the thyroid hormone conjugation by sulfatases that increases their solubility and facilitates their excretion. The muscular T3 levels were well preserved. These changes likely represent compensatory responses to disrupting effects that might otherwise have depressed T3 levels. This approach permitted us to interpret the causes and implications of alterations of the teleost thyroid system.