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多聚抗凝血酶原刺激物诱导的血管内凝块形成是该毒素对大鼠/大鼠组织致死性的主要机制。

Intravascular plug formation induced by poly-APS is the principal mechanism of the toxin's lethality in rats/rat tissues.

作者信息

Bunc Matjaz, Sarc Lucija, Rozman Janez, Turk Tom, Sepcic Kristina, Suput Dus

机构信息

Institute of Pathophysiology, Medical Faculty, Ljubljana, Slovenia.

出版信息

Cell Mol Biol Lett. 2002;7(1):106-8.

Abstract

Toxic water soluble polymeric 3-alkylpyridinium salts isolated from the sponge Raniera sarai strongly inhibited AChE in vitro. In vivo, experimental animals died due to plugs formed in microcirculation. The mechanism of this plug formation is unknown. In vitro, the toxin did not affect the coagulation rate, but the rate of platelet aggregation was accelerated in a dose-dependent manner. The hemolytic activity of poly-APS was diminished by the addition of serum proteins in a dose-dependent manner. These results support the conclusion that non-specific binding to proteins is the underlying mechanism of the lethality of poly APS.

摘要

从海绵拉涅拉氏海绵中分离出的有毒水溶性聚合物3-烷基吡啶盐在体外强烈抑制乙酰胆碱酯酶。在体内,实验动物因微循环中形成血栓而死亡。这种血栓形成的机制尚不清楚。在体外,该毒素不影响凝血速率,但血小板聚集速率以剂量依赖的方式加快。添加血清蛋白后,聚APS的溶血活性以剂量依赖的方式降低。这些结果支持以下结论:与蛋白质的非特异性结合是聚APS致死性的潜在机制。

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