Abstract

Present investigation was carried out to study toxicological damages of copper exposure and mitigation of its adverse effects with β-glucan administration in IgM + B cells which processes multiple roles similar to macrophages in Nile tilapia ( Oreochromis niloticus ). IgM + B cells were pretreated with β-glucan (25 μg/mL) for 24 h before exposed to cupric oxide nanoparticles (CuO NPs) or cupric chloride (Cu ions) at the doses of 0, 5, 10, and 20 μg/mL for 24 h, respectively. Our results demonstrated that β-glucan increased reduced glutathione (GSH) to against oxidative damage from CuO NPs and Cu ions exposure in IgM + B cells. The apoptosis process through mitochondrial signaling pathway was depressed in IgM + B cells since the mitochondrial membrane potential (ΔΨm) was protected from copper exposure by β-glucan treatment. Furthermore, the inhibition on phagocytic abilities of IgM + B cells caused by copper exposure could be enhanced with β-glucan treatment via evaluation of microspheres and bioparticles uptake and LPS-induced NO production. Importantly, β-glucan might participate in immunomodulation in IgM + B cells through B cell antigen receptor (BCR) to suppress toxicological effect derived from copper exposure. Taken together, this study provides more information on the toxicological damages in IgM + B cells upon copper exposure and explains the molecular mechanism to reverse adverse effects caused by copper exposure with β-glucan administration.