Toxicological damages on copper exposure to IgM+ B cells of Nile tilapia (Oreochromis niloticus) and mitigation of its adverse effects by β-glucan administration. (June 2022)

• Record Type: Journal Article
• Authors: Chen, Jianlin; Lei, Yang; Dong, Zijiong; Fu, Shengli; Li, Lan; Gao, Along; Wu, Liting; Ye, Jianmin
• Is Part Of: Toxicology in vitro. Volume 81(2022)
• Publication Date: 2022-06
• Subjects: Heavy metals -- IgM+ B cells -- Oxidative damage -- Toxicological mechanism -- β-Glucan administration -- Cytoprotective effects; Toxicity testing -- In vitro -- Periodicals; Toxicology -- Periodicals; 615.9
• DOI: 10.1016/j.tiv.2022.105334
• Languages: English
• ISSNs: 0887-2333

Abstract

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. Highlights: CuO NPs and Cu ions produced significant pro-inflammation in IgM + B cells. Copper depressed phagocytosis and promoted apoptosis in IgM + B cells. Adverse effects elicited by CuO NPs was more obvious than those of Cu ions exposure. β-glucan administration reversed adverse effects derived from copper exposure.