## Abstract The way in which the lectins concanavalin A (Con A) and __Ricinus communis__ agglutinin (Ricin) alter the K^+^ content of Ehrlich ascites tumor cells was investigated. Unidirectional and net fluxes were determined in unwashed cells during a time course following lectin addition. Total i
Lanthanum-induced alterations of cellular electrolytes in Ehrlich ascites tumor cells: A new view
✍ Scribed by Charles Levinson; Thomas C. Smith; Terry M. Mikiten
- Publisher
- John Wiley and Sons
- Year
- 1972
- Tongue
- English
- Weight
- 317 KB
- Volume
- 80
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
We have shown previously that Ehrlich ascites tumor cells maintained at room temperature under an oxygen atmosphere lose Na^+^, K^+^ and Cl^−^ isosmotically when exposed to La^+++^ (0.1 to 1.0 mM). Concomitant with these changes there is an increase in the recorded membrane potential (increasing intracellular negativity). The present studies further characterize the effect of La^+++^ on electrolyte distribution. Ehrlich ascites tumor cells were maintained at 0.5° C to permit Na^+^ gain and K^+^ loss. The addition of 1 mM La^+++^ to low temperature cells induces rapid loss of Na^+^, K^+^ and Cl^−^. This net loss of cellular electrolytes occurs even in cells depleted of ATP content using 2‐deoxyglucose (5 mM) and rotenone (10^−6^ M). Analysis of the appearance of tracer ^22^Na in the environment of cells preloaded with the radioisotope shows that La^+++^‐induced changes in membrane permeability or in active ion transport mechanisms are not responsible for the dramatic loss of electrolytes from experimental cells. The electrolyte loss occurs only when the cells are resuspended mechanically during the washing procedure used to prepare the cells for electrolyte determination.
We conclude that the results of La^+++^ interaction with Ehrlich ascites tumor cells are twofold. As we have previously reported, La^+++^ stabilizes and causes a hyperpolarization of the membrane potential. Secondly, La^+++^ predisposes the cell membrane to become highly permeable when subjected to mechanical stress.
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