Please use this identifier to cite or link to this item:
|Title:||Chlorinative stress: An under appreciated mediator of neurodegeneration?||Authors:||Yap, Y.W.
|Issue Date:||2007||Citation:||Yap, Y.W., Whiteman, M., Cheung, N.S. (2007). Chlorinative stress: An under appreciated mediator of neurodegeneration?. Cellular Signalling 19 (2) : 219-228. ScholarBank@NUS Repository. https://doi.org/10.1016/j.cellsig.2006.06.013||Abstract:||Oxidative stress has been implicated as playing a role in neurodegenerative disorders, such as ischemic stroke, Alzheimer's, Huntington's, and Parkinson's disease. Persuasive evidences have shown that microglial-mediated oxidative stress contributes significantly to cell loss and accompanying cognitive decline characteristic of the diseases. Based on the facts that (i) levels of catalytically active myeloperoxidase are elevated in diseased brains and (ii) myeloperoxidase polymorphism is associated with the risk of developing neurodegenerative disorders, HOCl as a major oxidant produced by activated phagocytes in the presence of myeloperoxidase is therefore suggested to be involved in neurodegeneration. Its association with neurodegeneration is further showed by elevated level of 3-chlorotyrosine (bio-marker of HOCl in vivo) in affected brain regions as well as HOCl scavenging ability of neuroprotectants, desferrioxamine and uric acid. In this review, we will summary the current understanding concerning the association of HOCl and neuronal cell death where production of HOCl will lead to further formation of reactive nitrogen and oxygen species. In addition, HOCl also causes tissue destruction and cellular damage leading cell death. © 2006.||Source Title:||Cellular Signalling||URI:||http://scholarbank.nus.edu.sg/handle/10635/28738||ISSN:||08986568||DOI:||10.1016/j.cellsig.2006.06.013|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Aug 3, 2020
WEB OF SCIENCETM
checked on Jul 27, 2020
checked on Aug 4, 2020
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.