Exposure to manganese (II) chloride induces developmental toxicity, oxidative stress and inflammatory response in Marine medaka (Oryzias melastigma) embryos

Abstract

Manganese (Mn) is an essential metal for organisms, but high levels can induce serious toxicity. To date, the toxic mechanism of Mn to marine fish is still poorly understood. In the present study, Oryzias melastigma embryos were exposed to different concentrations of MnCl2 (0–152.00 mg/L) to investigate its effect on early development. The results showed that exposure to MnCl2 caused developmental toxicity to embryos, including increased heart rate, delayed hatching time, decreased hatching rate and increased malformation rate. MnCl2 exposure could induce oxidative stress in O. melastigma embryos, as indicated by increased the contents of malondialdehyde (MDA) and the activities of the antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT)). The heart might be an important target organ for MnCl2 because of cardiac malformations and disruption in the expression of cardiac development-related genes (ATPase, epo, fg8g, cox1, cox2, bmp4 and gata4). In addition, the expression levels of stress- (omTERT and p53) and inflammation-related genes (TNFα and il1β) were significantly up-regulated, suggesting that MnCl2 can trigger stress and inflammatory response in O. melastigma embryos. In conclusion, this study demonstrated that MnCl2 exposure can induce developmental toxicity, oxidative stress and inflammatory response in O. melastigma embryos, providing insights into the toxic mechanism of Mn to the early development of marine fish.