20/10/2020 Osmotic shock - Wikipedia

Osmotic shock
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 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, at low concentrations of
solutes, 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] 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.[4] Current research also
suggests that osmotic stress in cells and tissues may significantly contribute to many human
diseases.[5]

In eukaryotes, calcium acts as one of the primary regulators of osmotic stress. Intracellular calcium
levels rise during hypo-osmotic and hyper-osmotic stresses.

Contents
Recovery and tolerance mechanisms
For hyper-osmotic stress
For hypo-osmotic stress
Osmotic damage in humans
See also
References

Recovery and tolerance mechanisms

For hyper-osmotic stress

extracellular sequestering of Calcium by blood Albumin.

Transient intracellular Ca2+ increase.

For hypo-osmotic stress

intracellular Ca2+ increase and Extracellular ATP Release[6]

Calcium dependent efflux of the osmolyte Taurine. Extracellular calcium removal was found to
prevent Taurine efflux by 50%, and removal of extracellular Ca2+ and simultaneous depletion of
intracellular Ca2+ stores with thapsigargin decreased it by 85%.[7]

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Osmotic damage in humans

See also
Osmolyte
Myo-Inositol
Taurine and Taurine-transporting ATPase
Creatine
Betaines
Trimethylglycine – A Betaine and metabolite of Choline
Sorbitol
Glycerophosphocholine

References
1. Lang KS, Lang PA, Bauer C, et al. (2005). "Mechanisms of suicidal erythrocyte death" (https://doi.
org/10.1159%2F000086406). Cell. Physiol. Biochem. 15 (5): 195–202. doi:10.1159/000086406 (h
ttps://doi.org/10.1159%2F000086406). PMID 15956782 (https://pubmed.ncbi.nlm.nih.gov/159567
82).
2. Kültz D, Burg M (1 November 1998). "Evolution of osmotic stress signaling via MAP kinase
cascades" (http://jeb.biologists.org/cgi/reprint/201/22/3015). J. Exp. Biol. 201 (Pt 22): 3015–21.
PMID 9787121 (https://pubmed.ncbi.nlm.nih.gov/9787121).
3. Kültz D (2007). "Osmotic stress sensing and signaling in animals". FEBS Journal. 274 (22):
5781–5781. doi:10.1111/j.1742-4658.2007.06097.x (https://doi.org/10.1111%2Fj.1742-4658.2007.
06097.x). PMID 17944944 (https://pubmed.ncbi.nlm.nih.gov/17944944).
4. Ho SN (2006). "Intracellular water homeostasis and the mammalian cellular osmotic stress
response". J. Cell. Physiol. 206 (1): 9–15. doi:10.1002/jcp.20445 (https://doi.org/10.1002%2Fjcp.
20445). PMID 15965902 (https://pubmed.ncbi.nlm.nih.gov/15965902).
5. Brocker, C; Thompson, DC; Vasiliou, V (August 2012). "The role of hyperosmotic stress in
inflammation and disease" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3438915).
Biomolecular Concepts. 3 (4): 345–64. doi:10.1515/bmc-2012-0001 (https://doi.org/10.1515%2Fb
mc-2012-0001). PMC 3438915 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3438915).
PMID 22977648 (https://pubmed.ncbi.nlm.nih.gov/22977648).
6. Hélène Ollivier; Karine Pichavant-Rafini; Eneour Puill-Stephan; Patrick Calvès; Liliane Nonnotte;
Guy Nonnotte (2006). "Effects of hypo-osmotic stress on ATP release in isolated turbot
(Scophthalmus maximus) hepatocytes". Biol. Cell. 98 (7): 427–437. doi:10.1042/BC20050077 (htt
ps://doi.org/10.1042%2FBC20050077). PMID 16519627 (https://pubmed.ncbi.nlm.nih.gov/165196
27).
7. Olivero P, Stutzin A (2004). "Calcium modulates osmosensitive taurine efflux in HeLa cells".
Neurochem. Res. 29 (1): 169–76. doi:10.1023/B:NERE.0000010446.50158.8d (https://doi.org/10.
1023%2FB%3ANERE.0000010446.50158.8d). PMID 14992276 (https://pubmed.ncbi.nlm.nih.go
v/14992276).

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