Shock caused by a sudden change in the solute concentration around a cell
Tonicity concept related to the transport of water towards the more concentrated aqueous solution (osmotic transport): In isotonic solutions, water flows equally into and out of the cell (equilibrium). In hypertonic solutions water flows out of the cell and the cell shrinks (plasmolysis). In hypotonic solutions, water flows into the cell and the cell swells (turgescence).
Osmotic shock or osmotic stress is physiologic dysfunction caused by a sudden change in the solute concentration around a cell, which causes a rapid change in the movement of water across its cell membrane. Under hypertonic conditions - conditions of high concentrations of either salts, substrates or any solute in the supernatant - water is drawn out of the cells through osmosis. This also inhibits the transport of substrates and cofactors into the cell thus “shocking” the cell. Alternatively, under hypotonic conditions - when concentrations of solutes are low - water enters the cell in large amounts, causing it to swell and either burst or undergo apoptosis.[1]
All organisms have mechanisms to respond to osmotic shock, with sensors and signal transduction networks providing information to the cell about the osmolarity of its surroundings;[2] these signals activate responses to deal with extreme conditions.[3] Cells that have a cell wall tend to be more resistant to osmotic shock because their cell wall enables them to maintain their shape.[4] Although single-celled organisms are more vulnerable to osmotic shock, since they are directly exposed to their environment, cells in large animals such as mammals still suffer these stresses under some conditions.[5] Current research also suggests that osmotic stress in cells and tissues may significantly contribute to many human diseases.[6]
In eukaryotes, calcium acts as one of the primary regulators of osmotic stress. Intracellular calcium levels rise during hypo-osmotic and hyper-osmotic stresses.
^Lang KS, Lang PA, Bauer C, Duranton C, Wieder T, Huber SM, Lang F (2005). "Mechanisms of suicidal erythrocyte death". Cellular Physiology and Biochemistry. 15 (5): 195–202. doi:10.1159/000086406. PMID 15956782.
^Kültz D, Burg M (November 1998). "Evolution of osmotic stress signaling via MAP kinase cascades". The Journal of Experimental Biology. 201 (Pt 22): 3015–21. doi:10.1242/jeb.201.22.3015. PMID 9787121.
^Kültz D (November 2007). "Osmotic stress sensing and signaling in animals". The FEBS Journal. 274 (22): 5781. doi:10.1111/j.1742-4658.2007.06097.x. PMID 17944944.
^"Unique Characteristics of Prokaryotic Cells".
^Ho SN (January 2006). "Intracellular water homeostasis and the mammalian cellular osmotic stress response". Journal of Cellular Physiology. 206 (1): 9–15. doi:10.1002/jcp.20445. PMID 15965902. S2CID 21178769.
^Brocker C, Thompson DC, Vasiliou V (August 2012). "The role of hyperosmotic stress in inflammation and disease". Biomolecular Concepts. 3 (4): 345–364. doi:10.1515/bmc-2012-0001. PMC 3438915. PMID 22977648.
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(September 1965). "The release of enzymes from Escherichia coli by osmoticshock and during the formation of spheroplasts". The Journal of Biological...
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