The effect of methylmercury contamination and feed composition on the total DNTB (dithiobis (2-nitrobenzoic) acid)-reductase and thioredoxin reductase activities and on the expression of some genes involved in redox processes in the liver of the European Seabass (Dicentrarchus labrax)

Mercury (Hg) is a ubiquitous pollutant which accumulates in aquatic systems. Methylmercury (MeHg) is the most common form of organic mercury which bioaccumulates and biomagnifies in the food chain. Top predatory fish species, such as tuna, have been considered some of the major contributors to dietary MeHg exposure. The toxicity of MeHg is attributed to its high specificity for selenium (Se) and its activity as an irreversible inhibitor of selenoenzymes: due to its high binding affinity for Se, the amount of this element available for the synthesis of selenoproteins is diminished. In this study, the effect of MeHg contamination and feed composition was assessed through the activity of DNTB-reductase and thioredoxin reductase (TrxR) activities as well as through the expression levels of the redox genes txn1, gpx1, txnrd1 and txnrd2 in the liver of Dicentrarchus labrax. In the first part of the experiment, Phase A, the results showed that the ingestion during 14 days of feeds polluted with 0, 0.5, 5 and 10 ppm MeHg, did not significantly affect either the total DNTB-reductase and TrxR activities or the expression level of the redox genes. In the second, and longer exposure experiment, Phase B, that lasted 53 days, there were no significant differences either in the total DNTB-reductase activity between the groups of D. labrax fed with a substitution of 20% of the feed with fish (both thawed hake and canned albacore) and the corresponding groups that also received 10 ppm MeHg in the diet. The inhibition of TrxR activity was only prevented by the substitution with thawed hake; however, the substitution with canned albacore failed to counteract the effect of MeHg and resulted in the lowest TrxR activity registered. On the other hand, the substitution with fish under exposure to MeHg did affect the expression of redox genes. Thus, perhaps the activity of selenoenzymes may not have a direct relationship with the expression levels of their corresponding selenogenes. It can therefore be concluded that TrxR is a toxicological target of MeHg and it has the potential to be a biomarker of MeHg exposure. Moreover, the expression levels of selenogenes may not be an appropriate measure of MeHg exposure, instead it is possible that the expression of the genes together with the efficiency of the translation process may be the determinants of the MeHg toxicity.