Long-term excessive fluoride (F) intake disrupts the balance of bone deposition and remodeling activities and is linked to skeletal fluorosis. Type I collagen, which is responsible for bone stability and cell biological functions, can be damaged by excessive F ingestion. In this study, Sodium fluoride (NaF) was orally administrated to rat at 150 mg L(-1) for 60 and 120 d. We examined the effects of excessive F ingestion on the ultrastructure and collagen morphology of bone in rats by using transmission electron microscopy (TEM). Furthermore, we investigated the effect of F consumption on the expression levels of COL1A1 and COL1A2 in the bone tissues of rats by using quantitative real time (qRT)-PCR, to elucidate the molecular mechanisms of F-induced collagen protein damage. Our results showed that F affected collagen I arrangement and produced ultrastructural changes in bone tissue. Meanwhile, the mRNA expression of COL1A1 and COL1A2 were reduced and the COL I protein levels decreased in the fluorosis group. We concluded that excessive F ingestion adversely affected collagen I arrangement and caused ultrastructural changes in bone tissue. Reduced COL1A1 mRNA expression and altered COL I protein levels may contribute to the skeletal damage resulting from F exposure.
Keywords: Fluoride; Hard tissue; Rat; Type I collagen; Ultrastructure.
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