Zambrano F, Canelo E
Departamento de Biología, Facultad de Ciencias, Universidad de Chile, Santiago, Chile.
Toxicon. 1996 Apr;34(4):451-8. doi: 10.1016/0041-0101(95)00145-x.
Several partial reactions of the Na(+)-K+ pump enzyme were studied in a microsomal fraction derived from the gill of carp (Cyprinus carpio Linneo). We tested the effect of three toxins [(i) microcystin-LR, (ii) microcystin-LR-like toxin component isolated from Microcystis aeruginosa culture and (iii) okadaic acid] on the phosphorylation, ouabain binding and ATPase activity of the Na(+)-K+ pump. The K(+)-dependent hydrolysis of the Na(+)-dependent phosphorylation of Na(+)-K+ pump, as well the release of bound ouabain were inactivated in direct proportion to the amount of each toxin treatment. These results indicate that these toxins not only block the hydrolysis of phosphorylated protein at serine and threonine residues, but also inhibit the aspartic dephosphorylation step of the sodium pump enzymes. This inactivation could disrupt the ion homeostasis of the internal medium by blocking the gill function. The blockage of gill activity could be the cause of the massive fish death during blooms of M. aeruginosa.
在源自鲤鱼（鲤科鲤属林奈种）鳃的微粒体部分中研究了钠钾泵酶的几种部分反应。我们测试了三种毒素[（i）微囊藻毒素-LR，（ii）从铜绿微囊藻培养物中分离出的微囊藻毒素-LR样毒素成分，以及（iii）冈田酸]对钠钾泵的磷酸化、哇巴因结合和ATP酶活性的影响。钠钾泵的钠依赖性磷酸化的钾依赖性水解以及结合的哇巴因的释放与每种毒素处理的量成比例失活。这些结果表明，这些毒素不仅阻断丝氨酸和苏氨酸残基处磷酸化蛋白的水解，还抑制钠泵酶的天冬氨酸去磷酸化步骤。这种失活可能通过阻断鳃功能破坏内部介质的离子稳态。鳃活动的阻断可能是铜绿微囊藻水华期间大量鱼类死亡的原因。
