Exposure to magnesium oxide nanoparticles induces mitochondrial dysfunction and apoptosis in fish Megalobrama amblycephala by disrupting magnesium homeostasis

Abstract

The widespread use of magnesium oxide nanoparticles (MgO NPs) presents a potential biological effect and toxicity to both aquatic ecosystems and human well-being. However, the potential toxicity of MgO NPs has been barely investigated. In this study, the toxicological evaluation of MgO NPs was systematically determined by using fish Megalobrama amblycephala as a model in both in vivo and in vitro studies. In vivo, fish were exposed to three concentrations of MgO NPs in water (0, 50 and 100 mg/L). In vitro, primary hepatocytes were exposed to three concentrations (0, 16 and 32 mM) of MgO NPs in the medium. Our results demonstrated that MgO NPs impaired Mg homeostasis leading to mitochondrial dysfunction, and triggered apoptosis in both in vivo and in vitro. This was evidenced by the elevated mitochondrial Mg content and Trpm7 and Mrs2 protein expression, a loss of MMP, the impaired activities of mitochondrial complexes IV and V, an upregulation of Cyt-c and caspase 3, and a downregulation of Bcl-2. Overall, MgO NP exposure disrupts the Mg homeostasis, thereby leading to mitochondrial dysfunction and apoptosis.

Keywords: Apoptosis; Magnesium homeostasis; Magnesium oxide nanoparticle; Mitochondrial function; Toxicological evaluation.