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Altered proton extrusion in cells adapted to growth at low extracellular pH
Author(s) -
Owen Charles S.,
Pooler Patricia M.,
Wahl Miriam L.,
Coss Ronald A.,
Leeper Dennis B.
Publication year - 1997
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/(sici)1097-4652(199712)173:3<397::aid-jcp12>3.0.co;2-9
Subject(s) - extracellular , extrusion , proton , chemistry , biophysics , microbiology and biotechnology , biochemistry , chemical engineering , materials science , biology , metallurgy , physics , quantum mechanics , engineering
Intracellular pH (pH i ) homeostasis is crucial to cell survival. Cells that are chronically exposed to a low pH environment must adapt their hydrogen ion extrusion mechanisms to maintain their pH i in the physiologic range. An important component of the adaptation to growth at low pH is the upregulation of pH i relative to the extracellular pH (pH e ). To test the ability of low pH e adapted cells to respond to a pH i lowering challenge, a fluorescence assay was used that directly monitors proton removal as the rate of change of pH i during recovery from cytosolic acidification. Two cell lines of Chinese hamster origin (ovarian carcinoma and ovary fibroblastoid cells) were compared, both of which showed altered proton extrusion after adaptation to growth at low pH e = 6.70. In the ovarian carcinoma (OvCa) cell line, the pattern was consistent with an upregulation by means of an increase in the number of functional proton transporters in the plasma membrane. In the ovary fibroblastoid (CHO‐10B) cell line, pH i was consistently elevated in adapted cells as compared with cells grown at normal pH e = 7.30 without an increase in maximum extrusion rate. This upregulation was consistent with a shift in the activating pH i of proton transporters without an increase in the number of transporters, i.e., a change in substrate affinity of the transporter. In OvCa cells, recovery from acidification could be blocked by amiloride, an inhibitor of Na + /H + exchange. In contrast, a more modest effect of amiloride on CHO cells was observed but a complete inhibition was seen with the Cl − /HCO − 3 exchange inhibitor 4,4′‐diisothiocyanatostilbene‐2,2′‐disulfonic acid (DIDS). These data indicate that the two cell lines rely to different degrees on the two major pathways for pH regulation during recovery from cytosolic acidification. J. Cell. Physiol. 173:397–405, 1997. © 1997 Wiley‐Liss, Inc.