User:EAGMIL/Osmotic shock
Recovery and tolerance mechanisms
[edit]For hyper-osmotic stress
[edit]Calcium plays a large role in the recovery and tolerance for both hyper and hypo-osmotic stress situations. Under hyper-osmotic stress conditions, increased levels of intracellular calcium are exhibited. This may play a crucial role in the activation of second messenger pathways.[1]
Specifically, MAP Kinase Hog-1 is a second messenger molecule that is activated under hyper-osmotic stress conditions.[2] It is responsible for an increase in the production of glycerol within the cell succeeding osmotic stress.[2]
For hypo-osmotic stress
[edit]Hypo-osmotic stress recovery is largely mediated by the influx and efflux of several ions and molecules. After hypo-osmotic stress, cell recovery has shown to be consistent with an influx of extracellular Calcium.[3] This influx of calcium may alter the cell's permeability[3]. Recovery may also be mediated by 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%.
Additionally, some organisms have been shown to use phenothiazines to regulate and prevent the efflux of amino acids. Changes in the cell's permeability allows the efflux of amino acids during recovery[3].
Hypo-osmotic stress is correlated with extracellular ATP release. ATP is used to activate purinergic receptors[4]. These receptors regulate sodium and potassium levels on either side of the cell membrane.
This is the sandbox page where you will draft your initial Wikipedia contribution.
If you're starting a new article, you can develop it here until it's ready to go live. If you're working on improvements to an existing article, copy only one section at a time of the article to this sandbox to work on, and be sure to use an edit summary linking to the article you copied from. Do not copy over the entire article. You can find additional instructions here. Remember to save your work regularly using the "Publish page" button. (It just means 'save'; it will still be in the sandbox.) You can add bold formatting to your additions to differentiate them from existing content. |
Article Draft
[edit]Lead
[edit]Article body
[edit]References
[edit]- ^ "Hyper-osmotic stress induces volume change and calcium transients in chondrocytes by transmembrane, phospholipid, and G-protein pathways".
{{cite web}}
: CS1 maint: url-status (link) - ^ a b "MAP Kinase Hog1 Regulates Metabolic Changes Induced by Hyperosmotic Stress".
{{cite web}}
: CS1 maint: url-status (link) - ^ a b c "A ca2+ Influx in Response to Hypo-Osmotic Stress May Alter Osmolyte Permeability by a Phenothiazine-Sensitive Mechanism".
{{cite web}}
: CS1 maint: url-status (link) - ^ "Hyposmotic Stress Causes ATP Release and Stimulates Na,K‐ATPase Activity in Porcine Lens".
{{cite web}}
: CS1 maint: url-status (link)
Peer Reviews
[edit]- This is probably part of a different article, but maybe you could include definitions of isotonic, hypertonic, and hypotonic. Or just link them to the articles that define them.
- This is a great idea! I'll be sure to include links to those articles. I want those concepts to be understood, but don't want them to take over this article.
- Maybe explain what role glycerol plays in helping the cell overcome osmotic stress (in the For hyper-osmotic stress section). Bizzers03 (talk) 19:12, 28 November 2021 (UTC)
- Also a good idea. I'm looking into this.