With an annual catch of 35,000 – 50,000 tons and a commercial value of roughly €100 million, common shrimp is one of the most valuable European fisheries and aquaculture commodities. Since the late 1960s, European landings strongly decreased until 1990, due to a strongly reduced shrimp abundance and reproduction. In the Wadden Sea, the shrimp stock and hence landed volumes recovered slowly after 1990 to record landings in 2010. In the Southern Bight (i.e. Northern France to Dutch Delta), one of the busiest international shipping lanes, the stock only recovered after 2003. Until now, no explanation was found for these abnormal long-term trends in the shrimp stock.
The use of TBT as antifouling agent began in the 1960s, leading to exuberant TBT concentrations in the 1970s and 1980s, especially nearby recreational marinas, shipping lanes, and industrial harbours. At the end of the 1980s, the use of TBT on smaller ship ( 25 m) was only accepted in 2003 and finally entered-into-force in 2008. In 2004, Nishikawa et al. (2004) proved that TBT mimics vertebrate hormone signalling by activating the retinoid-X-receptor (RXR). As this receptor is strongly conserved in the animal kingdom, an identical mode of action (MOA) was generally accepted to have caused the observed reproductive and developmental defects in marine shellfish and gastropods. RXR is a nuclear receptor (NR) believed to directly modulate (i.e. by heterodimerization) the activity of many other NRs. NRs are the major targets of lipophilic hormones (e.g. steroids), and directly induce tissue specific expression of genes involved in development, reproduction, immune response, etc.
Within this PhD-thesis, three main research questions were addressed. (1) Does TBT affect the functionality of the shrimp RXR receptor?, (2) what is the temporal and spatial distribution of TBT in North Sea shrimp, and finally (3) do the TBT concentrations observed in the North Sea disrupt shrimp endocrine functioning
