Dawson P A, Filipe M I
Histochem J. 1983 Jan;15(1):3-13. doi: 10.1007/BF01006067.
The uptake of [35S]sodium sulphate, as a sulphomucin precursor, was studied at the ultrastructural level as part of our investigation into alterations in glycoprotein synthesis occurring in colonic mucosa adjacent to carcinoma ('transitional' mucosa). The sulphate labelling was analysed statistically after incorporation and pulse labelling studies to show the amount of uptake into cellular organelles and the rate of transport through the cells. Uptake studies showed the following changes in the 'transitional' mucosa as compared with normal mucosa. (1) In the middle crypt, sulphate incorporation from the Golgi apparatus into the mucin droplets of the goblet cells was reduced in contrast with an increased uptake into the vesicles of the absorptive and 'intermediate' cells. (2) In the upper crypt, more sulphate was incorporated in the goblet cells. These results correlate well with previous histochemical findings of a larger proportion of sulphomucins in the vesicles of columnar cells and a predominance of sialomucins in the goblet cells in the colonic mucosa associated with carcinoma. The pulse labelling studies revealed that in the middle crypt region of the 'transitional' mucosa, the rate of movement of label was faster through the Golgi body but less labelling was reaching the mucin droplets. The data suggest that either an inadequate supply of acceptor molecules was available at the Golgi level or a blockage in the attachment mechanism of the free sulphate to the completing glycoproteins was occurring at this level. Alternatively both mechanisms may be operating simultaneously.
作为我们对癌旁结肠黏膜(“过渡性”黏膜)中发生的糖蛋白合成改变研究的一部分,我们在超微结构水平上研究了[35S]硫酸钠作为硫黏蛋白前体的摄取情况。在掺入和脉冲标记研究后,对硫酸盐标记进行了统计学分析,以显示细胞器的摄取量和通过细胞的转运速率。摄取研究表明,与正常黏膜相比,“过渡性”黏膜有以下变化。(1)在隐窝中部,杯状细胞黏液滴中从高尔基体掺入的硫酸盐减少,而吸收性细胞和“中间”细胞的小泡摄取增加。(2)在隐窝上部,杯状细胞中掺入的硫酸盐更多。这些结果与先前的组织化学研究结果很好地相关,即在与癌相关的结肠黏膜中,柱状细胞小泡中硫黏蛋白的比例更大,杯状细胞中唾液黏蛋白占优势。脉冲标记研究表明,在“过渡性”黏膜的隐窝中部区域,标记物通过高尔基体的移动速率更快,但到达黏液滴的标记物较少。数据表明,要么在高尔基体水平上受体分子供应不足,要么在这个水平上游离硫酸盐与完成的糖蛋白的附着机制存在障碍。或者,这两种机制可能同时起作用。