Horiguchi Y, Uemura T, Kozaki S, Sakaguchi G
Biochim Biophys Acta. 1986 Oct 31;889(1):65-71. doi: 10.1016/0167-4889(86)90009-1.
We investigated the role of extracellular Ca2+ in the Clostridium perfringens enterotoxin-induced alteration of the permeability of the plasma membrane. Enterotoxin released 86Rb and 51Cr from the Vero cells preloaded with the isotope. In the presence of EGTA, however, it released 86Rb but not 51Cr. The binding of enterotoxin to the cells was not influenced by Ca2+ or Mg2+. The effects of various cations on the enterotoxin-induced 51Cr release was also studied. The release depended on extracellular Ca2+ but not on Mg2+; it was inhibited by each of Zn2+, La3+ and Co2+. Zn2+ and Co2+ also inhibited 51Cr release caused by the enterotoxin previously bound to the cell membrane. In contrast, antibody against enterotoxin did not neutralize the toxin once it was bound to the Vero cells. When the cells were treated with enterotoxin, 45Ca influx occurred and reached the plateau in a few minutes, as did 86Rb release.
我们研究了细胞外钙离子在产气荚膜梭菌肠毒素诱导的质膜通透性改变中的作用。肠毒素从预先加载同位素的Vero细胞中释放出⁸⁶Rb和⁵¹Cr。然而,在EGTA存在的情况下,它释放出⁸⁶Rb但不释放⁵¹Cr。肠毒素与细胞的结合不受钙离子或镁离子的影响。还研究了各种阳离子对肠毒素诱导的⁵¹Cr释放的影响。这种释放依赖于细胞外钙离子而不是镁离子;它受到锌离子、镧离子和钴离子的抑制。锌离子和钴离子也抑制先前与细胞膜结合的肠毒素引起的⁵¹Cr释放。相比之下,抗肠毒素抗体一旦与Vero细胞结合就不能中和毒素。当细胞用肠毒素处理时,⁴⁵Ca内流发生并在几分钟内达到平台期,⁸⁶Rb释放也是如此。