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. During hyper-osmotic stress extracellular albumin binds calcium.

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]

Osmotic damage in humans

See also

References

  1. ↑ Lang KS, Lang PA, Bauer C, et al. (2005). "Mechanisms of suicidal erythrocyte death". Cell. Physiol. Biochem. 15 (5): 195–202. doi:10.1159/000086406. PMID 15956782.
  2. ↑ Kültz D, Burg M (1 November 1998). "Evolution of osmotic stress signaling via MAP kinase cascades". J. Exp. Biol. 201 (Pt 22): 3015–21. PMID 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. PMID 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. PMID 15965902.
  5. ↑ Brocker, C; Thompson, DC; Vasiliou, V (August 2012). "The role of hyperosmotic stress in inflammation and disease.". Biomolecular Concepts. 3 (4): 345–64. doi:10.1515/bmc-2012-0001. PMC 3438915Freely accessible. PMID 22977648.
  6. ↑ Hélène Ollivier, Karine Pichavant-Rafini, Eneour Puill-Stephan, Patrick Calvès, Liliane Nonnotte and 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. PMID 16519627.
  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. PMID 14992276.


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