Effects of fluoride on the ultrastructure and expression of Type I collagen in rat hard tissue.

Effects of fluoride on the ultrastructure and expression of Type I collagen in rat hard tissue.
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DOI:
10.1016/j.chemosphere.2014.12.090
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发表时间:
2015-06
期刊:
影响因子:
8.8
通讯作者:
Xiaoyan Yan;Xianhui Hao;Qingli Nie;C. Feng;Hongwei Wang;Zilong Sun;R. Niu;Jundong Wang
Xiaoyan Yan;Xianhui Hao;Qingli Nie;C. Feng;Hongwei Wang;Zilong Sun;R. Niu;Jundong Wang
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Xiaoyan Yan;Xianhui Hao;Qingli Nie;C. Feng;Hongwei Wang;Zilong Sun;R. Niu;Jundong Wang

文献摘要

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长期过量的氟(F)摄入会破坏骨沉积和重塑活动的平衡,并与氟骨症有关。I型胶原蛋白,这是负责骨的稳定性和细胞的生物功能,可以被破坏过量的F摄入。在这项研究中,氟化钠(NaF)以150 mg L-1口服给大鼠60和120 d。用透射电镜观察了过量氟摄入对大鼠骨超微结构和胶原形态的影响。此外,我们还采用定量真实的时间(qRT)-PCR技术研究了氟摄入对大鼠骨组织中COL 1A 1和COL 1A 2表达水平的影响,以阐明氟诱导胶原蛋白损伤的分子机制。结果表明,氟影响了骨组织中Ⅰ型胶原的排列,并引起了骨组织超微结构的改变。同时,氟中毒组COL 1A 1和COL 1A 2 mRNA表达降低,COL I蛋白水平降低。我们的结论是,过量的F摄入对I型胶原的排列产生不利影响,并引起骨组织超微结构的变化。COL 1A 1 mRNA表达的降低和COL I蛋白水平的改变可能是氟暴露导致骨骼损伤的原因之一。
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−1for 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 ofCOL1A1andCOL1A2in 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 ofCOL1A1andCOL1A2were 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. ReducedCOL1A1mRNA expression and altered COL I protein levels may contribute to the skeletal damage resulting from F exposure.