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Inhibition of Na+, K+-ATPase activates swelling-induced taurine efflux in a human neuroblastoma cell line.

Basavappa, S, Mobasheri, A, Errington, R, Huang, CC, Al-Adawi, S and Ellory, JC (1998) Inhibition of Na+, K+-ATPase activates swelling-induced taurine efflux in a human neuroblastoma cell line. J Cell Physiol, 174 (2). pp. 145-153.

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The Na+ pump (Na+, K+-ATPase) has been implicated in the regulation of many cellular functions, including cell volume regulation. The effects of inhibiting Na+ pump activity on cell volume and taurine efflux were evaluated in the human neuroblastoma cell line CHP-100. Cell volume changes monitored with the Coulter Multisizer technique and confocal microscopy showed that neuroblastoma cells exposed to ouabain swelled by 22 +/- 4% (n = 5). The rapid cell swelling was followed by regulatory volume decrease (RVD). In cells treated with ouabain, 14C-taurine efflux increased by 183 +/- 11% compared with controls. However, cells exposed simultaneously to ouabain and hypoosmotic solution resulted in a 14C-taurine efflux of 207 +/- 18%. Western blot and immunofluorescence microscopy with specific monoclonal antibodies for the catalytic alpha isoforms of Na+, K+-ATPase demonstrated high levels of the ubiquitously expressed alpha1 and the neuronal-specific alpha3. Ouabain-binding data showed that CHP-100 cells express approximately 3 x 10(5) pump units/cell. The present data indicate that efflux of taurine may be involved during volume recovery subsequent to blockade of Na+, K+-ATPase in CHP-100 cells.

Item Type: Article
Divisions : Surrey research (other units)
Authors :
Basavappa, S
Errington, R
Huang, CC
Al-Adawi, S
Ellory, JC
Date : February 1998
DOI : 10.1002/(SICI)1097-4652(199802)174:2<145::AID-JCP1>3.0.CO;2-O
Uncontrolled Keywords : Biological Transport, Brain Neoplasms, Cell Size, Humans, Neuroblastoma, Sodium-Potassium-Exchanging ATPase, Taurine, Tumor Cells, Cultured
Related URLs :
Depositing User : Symplectic Elements
Date Deposited : 17 May 2017 10:17
Last Modified : 24 Jan 2020 18:54

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