Selenomethionine alleviated fluoride-induced toxicity in zebrafish (Danio rerio) embryos by restoring oxidative balance and rebuilding inflammation homeostasis.

Abstract

Fish are target organisms that are extremely susceptible to fluoride pollution, and an increase in fluoride load will damage multiple systems of fish. Selenomethionine (Se-Met) at low levels has been reported to alleviate oxidative damage and inflammation caused by toxic substances, but whether it can alleviate fluoride-induced toxicity in zebrafish embryos has not been elucidated. In this study, the intervention effects of Se-Met on developmental toxicity, oxidative stress and inflammation in zebrafish embryos exposed to fluoride were determined. Our results showed that fluoride accumulated in larvae and induced developmental toxicity in zebrafish embryos, caused oxidative damage and apoptosis, increased significantly the MPO and LZM activities and the levels of the inflammation-related genes IL-1β, IL-6, TNF-α, IL-10 and TGF-β. Moreover, fluoride significantly increased the levels of ERK2, JNK, p38 and p65 in MAPKs and NF-κB pathways. Se-Met-treatment alleviated the adverse effects induced by fluoride, and all of the above indicators induced by fluoride returned to near control levels with increasing concentrations and time. However, treatment with Se-Met-alone also markedly increased the levels of IL-6, TNF-α, IL-10, TGF-β, ERK2 and JNK. In short, these data demonstrated that Se-Met-could alleviate fluoride-induced toxicity in zebrafish embryos by restoring oxidative balance and rebuilding inflammation homeostasis, although low levels of Se-Met-alone had certain toxic effects on zebrafish embryos. Taken together, Se-Met-plays an important role in preventing toxic damage induced by fluoride in zebrafish embryos, although it has certain toxic effects.