# ANION TRANSPORT IN EHRLICH CARCINOMA CELLS

> **NIH NIH R01** · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 1989 · $12,664

## Abstract

The overall objective of our research is the characterization of the
inorganic anion permeability pathways of the Ehrlich mouse ascites
carcinoma cell.  The kinetic characteristics of chloride, sulfate, and
inorganic phosphate transport across the plasma membrane suggest that in
order for these anions to enter the cell they must first interact with
specific membrane carrier systems. Previous studies have provided evidence
consistent with the view that chloride and sulfate utilize a single carrier
system possessing two reactive sites, while phosphate utilizes an entirely
separate system.  Recent studies have shown that chloride utilizes three
separate permeability pathways:  nonmediated diffusion (10%), co-transport
with potassium and sodium (40%), and mediated self-exchange through the
anion transporter (50%).  During the past year, we have investigated the
co-transport pathway in some detail.  Our results show that in order for
chloride to be transported by this mechanism both potassium and sodium are
required.

In cells under steady state (physiological) conditions, the anion/cation
stoichiometry at 37~C is:  2Cl:1Na:1K.  Chloride transport mediated by the
anion exchanger (Cl self-exchange) exhibits self-inhibition at high
extracellular chloride which is abolished when pHo is lowered to 5.5.  This
finding suggests that H+ interacts at a modifier (inhibitory) site on the
anion transporter and in so doing relieves inhibition.  In contrast to
chloride, about 85% of phosphate transport depends on the presence of
sodium in the extracellular medium.  We have shown that monovalent
phosphate is the predominate, if not exclusive, species transported and
that a decrease in intracellular pH results in inhibition of transport.  In
the next year of this project, we plan to further characterize the cation
requirements of the chloride-cation co-transport pathway.  We are
particularly interested in the mechanism by which this transport system
switches from a bi-directional exchange during the physiological steady
state (constant cell volume) to a net transport pathway when the tumor cell
volume regulates.  (A)

## Key facts

- **NIH application ID:** 3170797
- **Project number:** 3R01CA032927-06S2
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
- **SAM.gov UEI:** C3KXNLTAAY98
- **Principal Investigator:** CHARLES LEVINSON
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $12,664
- **Award type:** 3
- **Project period:** 1982-07-01 → 1989-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3170797

## Citation

> US National Institutes of Health, RePORTER application 3170797, ANION TRANSPORT IN EHRLICH CARCINOMA CELLS (3R01CA032927-06S2). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3170797. Licensed CC0.

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