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镉诱导发育中大鼠牙釉质晶体缺陷的机制。

Mechanism of cadmium induced crystal defects in developing rat tooth enamel.

机构信息

Division of Oral Anatomy, Meikai University School of Dentistry, Saitama 350-0283, Japan.

出版信息

Proc Jpn Acad Ser B Phys Biol Sci. 2009;85(10):500-7. doi: 10.2183/pjab.85.500.

Abstract

It is well known that exposure to environmental cadmium causes itai-itai (ouch-ouch) disease. However, the exact mechanism underlying this bone disease remains unresolved. By focusing on the calcification mechanism, we examined developing tooth enamel in rats exposed to cadmium to test the hypothesis that cadmium exposure may cause defects in crystal formation. Electron microscopy revealed the presence of perforated crystals in developing tooth enamel, indicating that the process of crystal nucleation may have been interrupted by cadmium exposure. Furthermore, biochemical analyses revealed that the catalytic activity of carbonic anhydrase in the immature enamel matrix declined remarkably despite the fact that quantitative reduction of this enzyme was insignificant, suggesting that the decline of catalytic activity may have resulted from the replacement of zinc with cadmium ions. Therefore, we concluded that the poor catalytic activity of cadmium-binding carbonic anhydrase might hinder the nucleation process, leading to an impairment in mineralization that causes itai-itai disease.

摘要

众所周知,接触环境镉会导致痛痛病。然而,这种骨病的确切机制仍未解决。通过关注钙化机制,我们检查了暴露于镉的大鼠发育中的牙釉质,以检验镉暴露可能导致晶体形成缺陷的假设。电子显微镜显示发育中的牙釉质中存在穿孔晶体,表明晶体成核过程可能被镉暴露打断。此外,生化分析表明,尽管这种酶的定量减少并不显著,但不成熟牙釉质基质中碳酸酐酶的催化活性显著下降,表明催化活性的下降可能是由于锌被镉离子取代所致。因此,我们得出结论,镉结合碳酸酐酶的催化活性差可能会阻碍成核过程,导致矿化受损,从而导致痛痛病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5501/3621555/c1238e56f8cc/pjab-85-500-g001.jpg

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