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S-Nitrosylation in Regulation of Inflammation and Cell Damage

[ Vol. 19 , Issue. 15 ]

Author(s):

Subhajit Dasgupta*, Jenny- Jaramillo Gomez, Inderjit Singh and Mushfiquddin Khan   Pages 1831 - 1838 ( 8 )

Abstract:


Background: Cell signaling through nitric oxide (NO) is a multifaceted mechanism, which regulates metabolic activities and fate in different tissues. The peroxynitrite (ONOO-) formed as reaction product of nitric oxide radical and superoxide interacts with cell membrane phospholipids and proteins causing damage.

Objective: The reaction kinetics to form nitrotyrosine (ONOO-tyrosine) and/or nitrosylated cysteine (ONOO-cysteine) in protein molecules during posttranslational modification and nitration of lipids are therefore critical in determining cells’ signaling mechanism for survival or apoptosis.

Results: The nitrosylation was found to modulate GPCRs and activation of guanylate cyclase as well as regulate NF-κB activation. The recent findings have shown the neuroprotective effects of S- nitrosylation, though mechanism is unclear.

Conclusion: While keeping the background in mind, we address here the biological function of NO derivatives in medicine. We target four known compounds: SNAP, SIN- 1 chloride, SNP and GSNO to understand the effect of NO in different tissues. Here we analyze the existing findings to assess therapeutic relevance of NO-signaling during inflammation, vasodilation and tolerance.

Keywords:

Nitric oxide, nitrosylation, G- protein coupled receptor, inflammation, neurodegeneration.

Affiliation:

Medical University of South Carolina, Charleston, SC 29425, Medical University of South Carolina, Charleston, SC 29425, Medical University of South Carolina, Charleston, SC 29425, Medical University of South Carolina, Charleston, SC 29425

Graphical Abstract:



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