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首页> 美国卫生研究院文献>The Journal of Clinical Investigation >Effect of diphenylhydantoin on synaptosome sodium-potassium-ATPase
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Effect of diphenylhydantoin on synaptosome sodium-potassium-ATPase

机译：二苯乙内酰脲对突触体钠钾ATP酶的影响

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Previous studies have demonstrated that electrically induced seizures in rat result in an increased brain intracellular sodium which can be decreased by treatment with sodium diphenylhydantoin (DPH). The correlation of cation transport with membrane-oriented sodium-potassium-adenosine triphosphatase (Na-K-ATPase) prompted an investigation of the effect of DPH upon ATPase enzyme activity.Rat cerebral cortical synaptosomes isolated in Ficoll gradients were employed as the source for Na-K-ATPase. With 50 mM Na, 10 mM K, 7.5 mM Mg, and 1.8 mM ATP, the specific activity of the preparation was 70 μmoles Pi released/mg synaptosomal protein per 30 min. The ionic and substrate concentrations yielding one-half maximal velocity were 0.5 mM K, 5 mM Na, and 8.5 × 10-5 M ATP, respectively.At 50 mM Na and 0.2 mM K, DPH produced an average of 92% stimulation of Pi release above control. The ratio of Na:K rather than the absolute levels of the ions was critical in determining the effect of DPH. DPH produced significant stimulation of enzyme activity under conditions of a high Na:K ratio (25-50:1). At ratios of 5-10:1, DPH produced little or no effect, and at low Na:K ratios (less than 5:1), DPH was inhibitory. Under all ionic conditions examined, DPH produced no apparent change in enzyme affinity for ATP.Assuming the proposed association of Na-K-ATPase with cation transport in brain, the data suggest the possibility that DPH may control seizures by its stimulation of Na-K-ATPase activity.
机译：先前的研究表明，大鼠的电诱发癫痫发作可导致脑内细胞内钠增加，而二苯乙内酰脲钠（DPH）可以降低脑内钠的含量。阳离子运输与膜导向的钠钾-腺苷三磷酸酶（Na-K​​-ATPase）的相关性促使人们研究了DPH对ATPase酶活性的影响。 -K-ATP酶。用50 mM Na，10 mM K，7.5 mM Mg和1.8 mM ATP，制剂的比活性为每30分钟释放70μmol的Pi释放/ mg突触体蛋白。产生最大速度一半的离子和底物浓度分别为0.5 mM K，5 mM Na和8.5×10 -5 M ATP。在50 mM Na和0.2 mM K下，DPH产生Pi释放的平均刺激高于控制水平的92％。 Na：K的比例而不是离子的绝对含量对确定DPH的效果至关重要。 DPH在高Na：K比（25-50：1）的条件下产生了明显的酶活性刺激。在5-10：1的比例下，DPH几乎没有产生作用，而在Na：K较低的比例（小于5：1）下，DPH具有抑制作用。在所有离子条件下，DPH对ATP的酶亲和力均未产生明显变化。假设Na-K-ATPase与大脑中阳离子运输的拟议关联，数据表明DPH可能通过刺激Na-K来控制癫痫发作-ATP酶活性。

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