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. 1973 Apr;51(4):620–625. doi: 10.1104/pp.51.4.620

Loss of Membrane Transport Ability in Leaf Cells and Release of Protein as a Result of Osmotic Shock

Lea Amar 1, Leonora Reinhold 1
PMCID: PMC366318  PMID: 16658382

Abstract

Osmotic shock severely reduces the ability of aged strips of Phaseolus vulgaris leaves to take up α-aminoisobutyric acid, an amino acid analogue which is known to be transported by a specific mechanism. Cold osmotic shock, i.e., transfer from 0.5 m sucrose at 25 C to H2O at 2 C, decreases α-aminoisobutyric acid uptake almost to zero. Substitution of 10−3m ethylenediaminetetraacetate for the sucrose, i.e., treatment which does not involve plasmolysis, produces a similar, but less severe, effect.

About 3.5% of the total cell protein is released as a result of cold osmotic shock, by far the greater proportion being liberated into the water during the second stage of the shock treatment. Ethylenediaminetetraacetate and other shock treatments also bring about protein release, and the amount released is correlated with degree of depression of subsequent α-aminoisobutyric acid uptake.

Shock tissue is capable of recovering a large proportion of its uptake capacity during subsequent immersion in 10−4m CaSO4.

Separate estimation of α-aminoisobutyric acid influx and efflux showed that the marked effect of shock on net flux is largely attributable to a reduction in influx, and not to an increase in efflux. This and other results indicate that the shock effect on net flux is not due to nonspecific damage to membranes bringing about “leakiness.”

The fact that α-aminoisobutyric acid uptake is reduced to near zero by treatment which allows the cells to retain over 95% of their protein suggests that the shock phenomenon is analogous to that in bacteria, and that the small fraction of protein lost may be closely involved in the transport mechanism.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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