Department of Endemic Diseases, Jilin University, 1163 Xinmin Street, Changchun 130021, People's Republic of China.
Biol Trace Elem Res. 2011 Oct;143(1):446-56. doi: 10.1007/s12011-010-8881-0. Epub 2010 Oct 23.
Exposure to excessive fluoride poses a threat to human health, including increased susceptibility to developing the skeletal fluorosis. Despite its recognized importance as an endemic disease, little is known about how fluoride directly impacts on osteoblasts. We previously reported that fluoride-stimulating monolayer-cultured osteoblast proliferation or inhibiting cell viability depended on fluoride-exposure concentration and period, both accompanied with active oxidative stress. The purpose of this study was to provide extra insight into skeletal fluorosis by comparing their regulation of oxidative stress in rats and OS732 cells (a human osteoblast-like cell line) cultured in the three-dimensional approach. Our in vivo and in vitro studies proved that exposure to fluoride promoted varying extents of oxidative stress. Three-dimensional cultured OS732 cells revealed the action of fluoride on cell viability from excitatory to inhibitory trend according to fluoride-exposure concentration and time. The study provided insight into the mechanism of skeletal fluorosis. Also, this study distinguished itself by identifying oxidative stress as a potential modulator of osteogenesis in skeletal fluorosis.
过量氟化物暴露会对人类健康造成威胁,包括增加患氟骨症的易感性。尽管氟化物被认为是一种地方病,但人们对氟化物如何直接影响成骨细胞知之甚少。我们之前的报告表明,氟化物刺激单层培养的成骨细胞增殖或抑制细胞活力取决于氟化物暴露浓度和时间,同时伴有活跃的氧化应激。本研究旨在通过比较氟化物在大鼠和三维培养的 OS732 细胞(一种人成骨样细胞系)中对氧化应激的调节作用,为氟骨症提供更多的认识。我们的体内和体外研究证明,暴露于氟化物会促进不同程度的氧化应激。三维培养的 OS732 细胞根据氟化物暴露浓度和时间,揭示了氟化物对细胞活力的作用从兴奋到抑制的趋势。该研究深入了解了氟骨症的发病机制。此外,本研究还将氧化应激确定为氟骨症成骨作用的一个潜在调节剂。