发育中的海胆胚胎中的碳酸酐酶活性，特别涉及骨针的钙化

Carbonic anhydrase activity in developing sea urchin embryos with special reference to calcification of spicules.

作者信息

Mitsunaga K, Akasaka K, Shimada H, Fujino Y, Yasumasu I, Numanoi H

出版信息

Cell Differ. 1986 Jun;18(4):257-62. doi: 10.1016/0045-6039(86)90057-6.

Abstract

Eggs and embryos of the sea urchins Anthocidaris crassispina and Hemicentrotus pulcherrimus did not exhibit significant changes in carbonic anhydrase activity during early development. Acetazolamide inhibited enzyme activity in homogenates of embryos and inhibited the formation of calcified spicules in a culture of micromeres at concentrations between 40 and 100 microM. Acetazolamide allowed intact embryos to develop to quasi-normal plutei but inhibited calcium deposition in the spicules. It is suggested that carbonic anhydrase contributes to CaCO3 deposition in the spicule.

摘要

厚刺海胆和马粪海胆的卵及胚胎在早期发育过程中碳酸酐酶活性未表现出显著变化。乙酰唑胺抑制胚胎匀浆中的酶活性，并在浓度为40至100微摩尔时抑制小分裂球培养物中钙化骨针的形成。乙酰唑胺使完整胚胎发育为准正常的长腕幼虫，但抑制骨针中的钙沉积。表明碳酸酐酶有助于骨针中碳酸钙的沉积。