## Abstract Previous studies have shown that mediated Cl^β^ transport which occurs by at least two processes (Cl^β^βdependent cation cotransport and Cl^β^ selfβexchange) becomes progressively inhibited when extracellular Cl^β^ exceeds about 60 mM (Hoffmann et al., 1979). To account for this type of
The transport of chloride in ehrlich ascites tumor cells
β Scribed by Charles Levinson; Mitchel L. Villereal
- Publisher
- John Wiley and Sons
- Year
- 1976
- Tongue
- English
- Weight
- 785 KB
- Volume
- 88
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
The steady state transport and distribution of chloride between the intracellular and extracellular phases was investigated when the extracellular chloride concentration was varied by isosmotic replacement with nitrate, bromide and acetate. The results of these experiments show that chloride transport, measured by uptake of ^36^Cl, is sensitive to the replacement anion. In the presence of nitrate, chloride transport is a linear function of the extracellular chloride concentration. The relationship between chloride transport and extracellular chloride in the presence of bromide is concave upward which suggests that this anion inhibits chloride movement. However, when acetate replaces chloride, the relationship between chloride transport and extracellular chloride is concave downward. The chloride distribution ratio of cells incubated in 145β155 mM chloride medium is 0.386 and is not effected by the replacement of chloride with nitrate, bromide or acetate.
These findings are consistent with the assertion that chloride transport is composed of two parallel pathways, a diffusional plus a saturating, mediated component. Of the total chloride flux (9.1 mmoles Clβ/kg dry weight per minute) measured in chloride medium (145β155 mM Cl β), the mediated component represents 40% and the diffusional component 60%.
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