Habermann E
Naunyn Schmiedebergs Arch Pharmacol. 1983 Jul;323(3):269-75. doi: 10.1007/BF00497673.
Palytoxin in concentrations as low as 10(-11) to 10(-12) M promotes the outflow of the lipophilic [3H]tetraphenylphosphonium ion from particulate brain cortex of guinea-pigs and rats, and from preloaded crude synaptosomes of rats, which indicates depolarization. The outflow is not influenced by tetrodotoxin or the calcium channel blocker nimodipin, or by substitution of choline for Na+ ions. It is increased by Ca2+ and by borate, the latter interacting with the toxin itself. To assess the fixation of palytoxin to biological membranes, a binding step was installed before the depolarization step. Palytoxin binds to membranes from rat brain, liver, kidney, human and dog erythrocytes, and to a lesser degree to liposomes made from rat brain or erythrocyte lipids. Binding is reversible. It is decreased by mild physical pretreatments of crude synaptosomes. Palytoxin binding is increased in the presence of micromolar concentrations of Ca2+ or borate. It is concluded that the potentiation of palytoxin actions by Ca2+ or borate is at least partially due to the promotion of its binding.
浓度低至10⁻¹¹至10⁻¹² M的刺尾鱼毒素可促进亲脂性[³H]四苯基鏻离子从豚鼠和大鼠的脑皮质颗粒以及大鼠预先加载的粗制突触体中流出，这表明发生了去极化。这种流出不受河豚毒素或钙通道阻滞剂尼莫地平的影响，也不受用胆碱替代钠离子的影响。钙离子和硼酸盐可使其增加，后者与毒素本身相互作用。为了评估刺尾鱼毒素与生物膜的结合情况，在去极化步骤之前设置了一个结合步骤。刺尾鱼毒素可与大鼠脑、肝、肾、人及犬红细胞的膜结合，与由大鼠脑或红细胞脂质制成的脂质体的结合程度较低。结合是可逆的。粗制突触体经过温和的物理预处理后，其结合能力下降。在微摩尔浓度的钙离子或硼酸盐存在的情况下，刺尾鱼毒素的结合能力增强。得出的结论是，钙离子或硼酸盐对刺尾鱼毒素作用的增强至少部分是由于促进了其结合。
