Aquatic organisms may suffer from exposure to high Cu concentrations, since this
metal is widely used in feed supplementation, in
pesticide formulation and as antifouling. Chronic exposure to Cu, even at sub-lethal doses, may strongly affect fish physiology. To date, several
biomarkers have been used to detect Cu exposure in fish producing contrasting results. Therefore, we used a proteomic approach to clarify how Cu exposure may affect the serum
proteome of gilthead sea bream (Sparus aurata), since serum could be considered a good source of early-
biomarkers of Cu toxicosis. For this purpose we exposed juvenile gilthead sea bream to waterborne Cu (0.5 mg/L). Our results indicate that fish tightly regulate circulating Cu levels, which are not affected by
metal exposure. This homeostatic control is mainly achieved by the liver, able to excrete high amounts of the
metal via bile. Cu exposure caused differential expression of several
serum proteins, 10 of which were identified by Mascot and BLAST search. All these
proteins, with the exception of
growth hormone receptor and γ-
glutamyl-carboxylase, can be related to: 1) Cu-induced hepatotoxicity (
cytochrome oxidase subunit I,
alanine aminotransferase,
glutathione S-transferase); 2) potential immunosuppression due to interference of Cu with the
inflammation/immunity network (α-1 antitrypsin,
angiotensinogen,
complement component C3, recombination-activating
protein-1 and warm temperature acclimation-related 65 kDa
protein).