Thyroid dysfunction in sea bass (Dicentrarchus labrax): Underlying mechanisms and effects of polychlorinated biphenyls on thyroid hormone physiology and metabolism

peer reviewedaudience: researcher, professional, student, popularization, otherThe current study examines the effect of subchronic exposure to a mixture of Aroclor standards on thyroid hormone physiology and metabolism in juvenile sea bass. The contaminant mixture was formulated to reflect the persistent organic pollution to which the European sea bass population could conceivably be exposed (0.3, 0.6 and 1.0 g 7PCBs per g food pellets) and higher (10 g 7PCBs per g food pellets). After 120 days of exposure, histomorphometry of thyroid tissue, muscular thyroid hormone concentration and activity of enzymes involved in metabolism of thyroid hormones were assessed. Mean concentrations of 8, 86, 142, 214 and 2279 ng g−1 ww ( 7 ICES PCB congeners) were determined after 120 days exposure. The results show that the effects of PCB exposures on the thyroid system are dose-dependent. Exposure to environmentally relevant doses of PCB (0.3–1.0 g 7PCBs per g food pellets) induced a larger variability of the follicle diameter and stimulated hepatic T4 outer ring deiodinase. Muscular thyroid hormone levels were preserved thanks to the PCB induced changes in T4 dynamics. At 10 times higher concentrations (10 g 7PCBs per g food pellets) an important depression of T3 and T4 levels could be observed which are apparently caused by degenerative histological changes in the thyroid tissue

Environmental factors affecting thyroid function of wild sea bass (Dicentrarchus labrax) from European coasts

Thyroid functional status of wild fish in relation with the contamination of their environment deserves further investigation. We here applied a multi-level approach of thyroid function assessment in 87 wild sea bass collected near several estuaries: namely the Scheldt, the Seine, the Loire, the Charente and the Gironde. Thyroxine (T4) and triiodothyronine (T3) concentrations in muscle were analyzed by radioimmunoassay. The activity of hepatic enzymes involved in extrathyroidal pathways of thyroid hormone metabolism, viz. deiodination, glucuronidation and sulfatation were analyzed. Last, follicle diameter and epithelial cell heights were measured. We observed changes that are predicted to lead to an increased conversion of T4–T3 and lowered thyroid hormone excretion. The changes in the metabolic pathways of thyroid hormones can be interpreted as a pathway to maintain thyroid hormone homeostasis. From all compounds tested, the higher chlorinated PCBs seemed to be the most implicated in this perturbation

Anammox bacteria in different compartments of recirculating aquaculture systems

Contains fulltext : 91560.pdf (publisher's version ) (Open Access)5 p

A physiological role for glucuronidated thyroid hormones: Preferential uptake by H9c2(2-1) myotubes

Contains fulltext : 35115.pdf (publisher's version ) (Closed access)Conjugation reactions are important pathways in the peripheral metabolism of thyroid hormones. Rat cardiac fibroblasts produce and secrete glucuronidated thyroxine (T4G) and 3,3',5-triiodothyronine (T3G). We here show that, compared to fibroblasts from other anatomical locations, the capacity of cardiofibroblasts to secrete T4G and T3G is highest. H9c2(2-1) myotubes, a model system for cardiomyocytes, take up T4G and T3G at a rate that is 10-15 times higher than that for the unconjugated thyroid hormones. T3 and T4, and their glucuronides, stimulate H9c2(2-1) myoblast-to-myotube differentiation. A substantial beta-glucuronidase activity was measured in H9c2(2-1) myotubes, and this confers a deconjugating capacity to these cells, via which native thyroid hormones can be regenerated from glucuronidated precursors. This indicates that the stimulatory effects on myoblast differentiation are exerted by the native hormones. We suggest that glucuronidation represents a mechanism to uncouple local thyroid hormone action in the heart from that in other peripheral tissues and in the systemic circulation. This could represent a mechanism for the local fine-tuning of cardiac thyroid hormone action