LAUSR

Copper (Cu), as an essential micronutrient in human and animal metabolism, easily spreads and excessively accumulates in rearing water, which make it more susceptible to fish farms and threatens the health of aquatic animals. In this issue, the protective effect of vitamin C against oxidative damage caused by copper exposure was studied in monocytes/macrophages (MO/MФ) and IgM+ B cells of Nile tilapia (Oreochromis niloticus), the cell types possessing phagocytic activities. The significant increase of ROS level and up-regulation of proinflammatory factors accompanied by depletion of GSH and down-regulation of antioxidative molecules in MO/MФ and IgM+ B cells, when stressed with CuO NPs or Cu ions, indicated the induction of oxidative damage due to the toxicological effects with copper exposure. Copper induced cell apoptosis through mitochondrial-dependent pathway in these two cell populations was demonstrated with disruption of mitochondrial membrane potential (ΔΨm) and activation of apoptosis factor. Furthermore, the phagocytic abilities for microspheres and bioparticle uptake significantly decreased in these two cell populations upon CuO NPs or Cu ions; meanwhile, antigen presentation of MO/MФ and antibody production of IgM+ B cells were also inhibited. However, vitamin C supplementation reversed all these biochemical indices, as well as cell apoptosis and phagocytic abilities in MO/MФ and IgM+ B cells that were induced by CuO NPs or Cu ions. In conclusion, these results revealed that vitamin C exerts cytoprotective effects against oxidative damage through its antioxidant properties and may be of therapeutic use in preventing toxicological effects caused by copper exposure.