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强心苷的糖部分对于抑制从红细胞中由岩沙海葵毒素诱导的钾离子释放的作用至关重要。

Sugar moiety of cardiac glycosides is essential for the inhibitory action on the palytoxin-induced K+ release from red blood cells.

作者信息

Ozaki H, Nagase H, Urakawa N

出版信息

FEBS Lett. 1984 Jul 23;173(1):196-8. doi: 10.1016/0014-5793(84)81045-5.

Abstract

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.

摘要

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。

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