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Cited by 31Ion Transport and Channel RegulationCancer, Hypoxia, and MetabolismATP Synthase and ATPases Research

H+ Transport and the Regulation of Intracellular pH in Ehrlich Ascites Tumor Cells

Bowen, Jesse W., Levinson, Charles·1984·The Journal of Membrane Biology
DOI 10.1007/bf01868522
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Abstract

The intracellular pH (pHi) of Ehrlich ascites tumor cells, both in the steady state and under conditions of acid loading or recovery from acid loading, was investigated by measuring the transmembrane flux of H+ equivalents and correlating this with changes in the distribution ratio of dimethyloxazolidine-2,4-dione (DMO). The pHi of cells placed in an acidic medium (pHo below 7.15) decreases and reaches a steady-state value that is more alkaline than the outside. For example when pHo is acutely reduced to 5.5, pHi falls exponentially from 7.20 +/- 0.06 to 6.29 +/- 0.04 with a halftime of 5.92 +/- 1.37 min, suggesting a rapid influx of H+. The unidirectional influx of H+ exhibits saturation kinetics with respect to extracellular [H+]; the maximal flux is 15.8 +/- 0.05 mmol/(kg dry wt X min) and Km is 0.74 +/- 0.09 X 10(-6) M. Steady-state cells with pHi above 6.8 continuously extrude H+ by a process that is not dependent on ATP but is inhibited by anaerobiosis. Acid-loaded cells (pHi 6.3) when returned to pHo 7.3 medium respond by transporting H+, resulting in a rapid rise in pHi. The halftime for this process is 1.09 +/- 0.22 min. The H+ efflux measured under similar conditions increases as the intracellular acid load increases. An ATP-independent as well as an ATP-dependent efflux contributes to the restoration of pHi to its steady-state value.

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  • pH-buffering mechanisms such as Na+/H+ antiporters or histone deacetylation consume cellular energy and can alter gene transcription and reduce cellular growth through changes in the acetylation state of chromatin.

    “However, such mechanisms (e.g., Na+/H+ antiporters or histone deacetylation) consume cellular energy and can alter gene transcription and reduce cellular growth through changes in the acetylation state of chromatin (Boron and Russell, 1983; Bowen and Levinson, 1984; Boron, 2004).”

    From Toward Best Practices for Controlling Mammalian Cell Culture Environments (2022) · cites this paper as Bowen and Levinson, 1984

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Authors
Bowen, J. W., & Levinson, C.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
Venue
The Journal of Membrane Biology
Publisher
Springer Science and Business Media LLC
Published
1984-02
Volume
79
Issue
1
Pages
7-18
ISSN
  • 0022-2631 (ISSN-L)
  • 1432-1424
DOI
10.1007/bf01868522
OpenAlex
W2070229124
Cited by
31
References
27
Citations by year
2022: 1 · 2021: 1
FWCI
2.37
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • The Journal of Membrane Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
Keywords
intracellular pH regulation, proton transport, H+ efflux, acid load, Ehrlich ascites tumor cells, saturation kinetics, anaerobic conditions, acid-base balance
MeSH terms
Adenosine Triphosphate, Animals, Biological Transport, Carcinoma, Ehrlich Tumor, Cell Membrane Permeability, Cells, Cultured, Dimethadione, Hydrogen, Hydrogen-Ion Concentration, Mice

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