Ozaki H, Nagase H, Urakawa N
FEBS Lett. 1984 Jul 23;173(1):196-8. doi: 10.1016/0014-5793(84)81045-5.
Palytoxin (PTX), a highly toxic and sugar-containing substance isolated from Palythoa tuberculosa, caused K+ release from rabbit red blood cells. Cardiac glycosides, such as ouabain, convallatoxin, cymarin, digoxin and digitoxin, inhibited the PTX-induced K+ release. Their corresponding aglycones did not inhibit the K+ release, but antagonized the inhibitory effect of the glycosides. All these cardiotonic steroids equally inhibited the activity of (Na+ + K+)-ATPase prepared from hog cerebral cortex. These results suggest that the sugar moiety of the cardiac glycosides is important for the inhibitory effect on the K+ release induced by PTX and that the inhibition is not related to their inhibitory potency on the (Na+ + K+)-ATPase activity.
刺尾鱼毒素（PTX）是一种从瘤海葵中分离出的剧毒含糖物质，可导致兔红细胞释放钾离子。强心苷，如哇巴因、铃兰毒苷、海葱苷、地高辛和洋地黄毒苷，可抑制PTX诱导的钾离子释放。它们相应的苷元不抑制钾离子释放，但能拮抗强心苷的抑制作用。所有这些强心甾体均同等程度地抑制从猪大脑皮层制备的（钠+钾）-ATP酶的活性。这些结果表明，强心苷的糖部分对于抑制PTX诱导的钾离子释放很重要，并且这种抑制作用与其对（钠+钾）-ATP酶活性的抑制效力无关。
