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短期铝暴露对脱矿骨基质诱导骨形成的影响。

Influence of short-term aluminum exposure on demineralized bone matrix induced bone formation.

作者信息

Severson A R, Haut C F, Firling C E, Huntley T E

机构信息

Department of Anatomy and Cell Biology, University of Minnesota-Duluth 55812.

出版信息

Arch Toxicol. 1992;66(10):706-12. doi: 10.1007/BF01972621.

DOI:10.1007/BF01972621
PMID:1290403
Abstract

The effects of aluminum exposure on bone formation employing the demineralized bone matrix (DBM) induced bone development model were studied using 4-week-old Sprague-Dawley rats injected with a saline (control) or an aluminum chloride (experimental) solution. After 2 weeks of aluminum treatment, 20-mg portions of rat DBM were implanted subcutaneously on each side in the thoracic region of the control and experimental rats. Animals were killed 7, 12, or 21 days after implantation of the DBM and the developing plaques removed. No morphological, histochemical, or biochemical differences were apparent between plaques from day 7 control and experimental rats. Plaques from day 12 control and experimental rats exhibited cartilage formation and alkaline phosphatase activity localized in osteochondrogenic cells, chondrocytes, osteoblasts, and extracellular matrix. Unlike the plaques from control rats that contained many osteoblastic mineralizing fronts, the plaques from the 12-day experimental group had a preponderance of cartilaginous tissue, no evidence of mineralization, increased levels of alkaline phosphatase activity, and a reduced calcium content. Plaques developing for 21 days in control animals demonstrated extensive new bone formation and bone marrow development, while those in the experimental rats demonstrated unmineralized osteoid-like matrix with poorly developed bone marrow. Alkaline phosphatase activity of the plaques continued to remain high on day 21 for the control and experimental groups. Calcium levels were significantly reduced in the experimental group. These biochemical changes correlated with histochemical reductions in bone calcification.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

利用脱矿骨基质(DBM)诱导骨发育模型,研究了铝暴露对骨形成的影响。实验采用4周龄的斯普拉格-道利大鼠,分别注射生理盐水(对照组)或氯化铝(实验组)溶液。铝处理2周后,将20毫克大鼠DBM分别皮下植入对照组和实验组大鼠胸部两侧。植入DBM后7、12或21天处死动物,取出发育中的骨块。7天的对照组和实验组骨块之间在形态学、组织化学或生物化学方面均无明显差异。12天的对照组和实验组骨块均表现出软骨形成,碱性磷酸酶活性定位于骨软骨生成细胞、软骨细胞、成骨细胞和细胞外基质中。与含有许多成骨矿化前沿的对照组骨块不同,12天实验组的骨块软骨组织占优势,无矿化迹象,碱性磷酸酶活性水平升高,钙含量降低。对照组动物中发育21天的骨块显示出广泛的新骨形成和骨髓发育,而实验组大鼠的骨块则显示出未矿化的类骨质样基质,骨髓发育不良。对照组和实验组骨块在第21天的碱性磷酸酶活性持续保持较高水平。实验组的钙水平显著降低。这些生化变化与骨钙化的组织化学减少相关。(摘要截断于250字)

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本文引用的文献

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Aluminum localization in bone from hemodialyzed patients: relationship to matrix mineralization.血液透析患者骨骼中铝的定位:与基质矿化的关系。
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