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Interaction of two mechanisms regulating alkali cations in hela cells
Author(s) -
Cook John S.,
Vaughan Gerald L.,
Proctor William R.,
Brake Emily Tate
Publication year - 1975
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1040860108
Subject(s) - ouabain , cycloheximide , hela , biophysics , intracellular , stimulation , chemistry , ion transporter , electrolyte , cell , alkali metal , cell culture , microbiology and biotechnology , biochemistry , sodium , biology , endocrinology , protein biosynthesis , membrane , electrode , genetics , organic chemistry
Abstract The alkali cation content of HeLa cells is independent of culture density and of whether the cells are grown in suspension or attached to the culture vessel. With a cell doubling time of 28 hours, the cell K content turns over approximately once per hour. Following partial blockade of the alkali‐cation transport system with ouabain, two distinct but interrelated mechanisms operate in the cellular response: (a) an increase in intracellular Na stimulates the pump so that the short‐term alteration in electrolyte composition is less than would be expected from the fraction of pump sites inhibited, and (b) there is a cyclo‐heximide‐sensitive recovery in transport capacity reflecting a restoration of functional transport sites to their normal density on the cell surface. Experimental manipulations that mimic the effect of ouabain lead to a stimulation of transport, but they do not result in an increase in the number of ouabain‐binding sites on the surface. The data are consistent with a four‐to‐six‐hour turnover of transport sites at the surface, but there is no evidence for a specific induction of the transport system within this short‐term recovery period.