Alterations in monovalent cation transport in Sindbis virus-infected chick cells.

Alterations in monovalent cation transport in Sindbis virus-infected chick cells.
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辛德比斯病毒感染的鸡细胞中单价阳离子转运的变化。

DOI:
10.1016/0042-6822(84)90096-5
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发表时间:
1984
期刊:
影响因子:
3.7
通讯作者:
BoseJr,HR
BoseJr,HR
中科院分区:
医学3区
文献类型:
--
作者:
Ulug,ET;Garry,RF;Waite,MR;BoseJr,HR

文献摘要

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用钾示踪剂86Rb+进行的内流实验表明,由于Sindbis病毒感染禽类成纤维细胞,Na+K+ATPase或钠泵的活性降低了40%-50%。这种哇巴因敏感的主动转运系统的抑制与细胞内K+浓度的降低和细胞蛋白质合成的终止在时间上相关。相比之下,速尿敏感的(Na+K+Cl−)共转运系统促进的内流速率仅略有下降。外流实验表明,感染Sindbis病毒的雏鸡细胞的非特异性通透性的相对速率或K+的“泄漏”没有发生变化。与Sindbis病毒感染细胞结合的[~3H]哇巴因的量与Na+K+ATPase活性的降低平行。这些结合研究表明,Na+泵部位的数量没有差异。然而,在感染病毒的细胞中,哇巴因结合的Kmof增加了大约3.5倍。Na+泵对K+的表观亲和力未见改变,但哇巴因敏感K+转运的Vmax降低。这些实验表明,在感染Sindbis病毒的鸡细胞中,Na+K+ATPase周转率的降低导致细胞内单价阳离子水平的改变。
Influx experiments using the potassium tracer86Rb+indicated that the activity of the Na+K+ATPase, or sodium pump, was reduced 40–50% as a consequence of Sindbis virus infection of avian fibroblasts. The inhibition of this ouabain-sensitive, active transport system temporally correlated with a decrease in the intracellular K+concentration and the termination of cellular protein synthesis. By contrast, the rate of influx facilitated by the furosemide-sensitive (Na+K+Cl−) cotransport system was only slightly depressed. Efflux experiments indicated that no alterations in the relative rate of nonspecific permeability or “leakage” of K+could be detected in chick cells infected by Sindbis virus. The amount of [3H]ouabain bound to Sindbis virus-infected cells paralleled the reduction in Na+K+ATPase activity. These binding studies revealed no difference in the number of Na+pump sites. TheKmof ouabain binding, however, increased approximately 3.5-fold in the virus-infected cells. No change in the apparent affinity of the Na+pump for K+could be detected, yet theVmaxfor ouabain-sensitive K+transport was decreased. These experiments suggest that a reduction in Na+K+ATPase turnover results in the altered intracellular monovalent cation levels found in Sindbis virus-infected chick cells.