Abstract

Highlights

  • Zebrafish embryonic fluoride exposure affect bone formation process of osteogenesis and osteoclastogenesis.
  • Low fluoride exposure promoted bone mineralization and increases bone density.
  • High fluoride exposure inhibited bone mineralization and decreases bone density.
  • Bone damage may be related to the loss of DLAV angiogenesis

In this study, we aimed to investigate the mechanism by which fluoride exposure causes bone damage and the relationship with the loss of dorsal longitudinal anastomotic vessel (DLAV) formation in zebrafish larvae to further understanding of skeletal fluorosis. We assessed the development of chondrogenesis, osteogenesis, and DLAV angiogenesis, and reactive oxygen species (ROS) in zebrafish larvae subjected to blank control group (Con), low-fluoride group (LF), and high-fluoride group (HF). Abnormal development of the cartilage area, bone mineralization accompanied with abnormal mRNA expression of osteoblast-related OC, ALP, and Runx2b genes and osteoclast-related OPG and RANKL genes, and abnormal DLAV angiogenesis and ROS levels in zebrafish larvae were affected to varying degrees with the increase of fluoride exposure. We concluded that exposure of zebrafish embryos to fluoride can affect bone development process of chondrogenesis and osteogenesis, and that bone damage might be related to the loss of DLAV angiogenesis.

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FULL-TEXT STUDY ONLINE AT
https://www.sciencedirect.com/science/article/pii/S0147651324014428

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