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锶会导致慢性肾衰竭大鼠出现骨软化症。

Strontium causes osteomalacia in chronic renal failure rats.

作者信息

Schrooten I, Cabrera W, Goodman W G, Dauwe S, Lamberts L V, Marynissen R, Dorriné W, De Broe M E, D'Haese P C

机构信息

Department of Nephrology, University of Antwerp, Belgium.

出版信息

Kidney Int. 1998 Aug;54(2):448-56. doi: 10.1046/j.1523-1755.1998.00035.x.

Abstract

BACKGROUND

We recently reported an association between increased bone strontium (Sr) levels and osteomalacia in dialysis patients.

METHODS

To delineate whether or not Sr acts as a causal factor in the development of osteomalacia, we devised the following study: four groups of chronic renal failure (CRF) rats were given Sr, aluminum (Al), both of these compounds or none of the elements (controls).

RESULTS

Administration of Sr and/or A1 resulted in increased bone levels of the respective elements. Histological examination revealed impairment of mineralization in the Sr group and to a lesser extent in the Al group as compared to the control group. There was also a significant increase in osteoid area in the Sr group, but not in the Al group. No differences in bone surface or erodic perimeter were noted between the various study groups. Histochemically, Sr could be localized in calcified bone, mainly in new bone close to the osteoid/calcification front, a critical site of bone mineralization. Histochemical findings were confirmed by electron probe X-ray microanalysis.

CONCLUSIONS

These findings indicate that Sr accumulation in chronic renal failure rats resulted in the development of osteomalacic lesions, in contrast to the Al group where adynamic bone disease was induced in the present set-up. Further studies are required to define the mechanism by which way Sr causes osteomalacia in chronic renal failure rats.

摘要

背景

我们最近报道了透析患者骨锶(Sr)水平升高与骨软化症之间的关联。

方法

为了确定Sr是否是骨软化症发生的因果因素,我们设计了以下研究:将四组慢性肾衰竭(CRF)大鼠分别给予Sr、铝(Al)、这两种化合物或不给予任何元素(对照组)。

结果

给予Sr和/或Al导致相应元素在骨中的水平升高。组织学检查显示,与对照组相比,Sr组矿化受损,Al组受损程度较轻。Sr组类骨质面积也显著增加,而Al组没有。各研究组之间在骨表面或侵蚀周长方面没有差异。组织化学分析显示,Sr可定位于钙化骨中,主要在靠近类骨质/钙化前沿的新骨中,这是骨矿化的关键部位。电子探针X射线微分析证实了组织化学结果。

结论

这些发现表明,慢性肾衰竭大鼠体内Sr的蓄积导致了骨软化性病变的发生,这与在本实验中诱导出现动力缺失性骨病的Al组形成对比。需要进一步研究来确定Sr导致慢性肾衰竭大鼠骨软化症的机制。

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