Abstract

The redox cycling of heavy metals as well as their interactions with organic pollutants is a major contributor to the oxidative stress resulting from aquatic pollution. Therefore, in order to evaluate β-naphthoflavone (BNF), Cu and BNF/Cu-induced oxidative stress with single and subsequent exposures, research was carried out in European eel ( Anguilla anguilla L.). Eel gill and kidney oxidative stress biomarker responses such as lipid peroxidation (LPO), glutathione peroxidase (GPX), catalase (CAT), glutathione S-transferase (GST) and total reduced glutathione (GSH) to a single 24 h exposure to two copper concentrations (Cu-1 μM, 2.5 μM) and BNF (2.7 μM) with or without 24 h BNF (2.7 μM) pre-exposure were investigated. Cu exposure alone showed a significant gill GST increase at the lowest concentration and GSH content decrease for the highest concentration. Double BNF exposure in gill demonstrated a significant increase in LPO, CAT, GPX and GST, as well as a decrease in GSH content. However, in sequential BNF/Cu exposures, only the highest Cu concentration exhibited a significant increase in LPO and GSH as well as a decrease in GPX (vs. BNF + CW). In kidney, Cu exposure alone showed a significant CAT and GSH contents decrease for both concentrations, and at highest concentration in GPX; as well as GST increase at the lowest concentration. Double BNF exposure showed a significant increase in LPO and GST. Nevertheless, in sequential BNF/Cu exposures, both concentrations exhibited a significant increase in LPO and decrease in GSH contents. Moreover, LPO was also increased significantly in comparison to BNF + CW and the equivalent Cu exposures without BNF pre-exposure. Concerning GPX, a significant increase was observed at highest Cu concentration. In GST, a significant decrease at the lowest Cu concentration and increase at the highest Cu concentration was observed. Summarizing, a simple copper or BNF exposures have no ability to induce LPO in both gill and kidney. However, double BNF exposure induced LPO in both organs and sequential BNF/Cu exposures potentiated the risk of peroxidative damage occurrence in both organs. BNF/Cu interference on antioxidant responses differs between the studied organs. In gill, antagonistic effects were denoted with probable reflex in terms of peroxidative damage increase. In kidney, BNF pre-exposure prevented CAT and GPX inhibition by copper; though, no advantage of this effect was perceptible as defence against LPO generation. Considering BNF as a surrogate for a PAH and the detected interactions with copper, as well as the likelihood that these effects would be observed in polluted ecosystems, current results demonstrate their relevance to actual ecological exposures contributing to a better knowledge on oxidative stress mechanisms in fish.

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