The deleterious effects of oxidative and nitrosative stress on palmitoylation, membrane lipid rafts and lipid-based cellular signalling : new drug targets in neuroimmune disorders

Morris, Gerwyn, Walder, Ken, Puri, Basant K., Berk, Michael and Maes, Michael 2016, The deleterious effects of oxidative and nitrosative stress on palmitoylation, membrane lipid rafts and lipid-based cellular signalling : new drug targets in neuroimmune disorders, Molecular neurobiology, vol. 53, no. 7, pp. 4638-4658, doi: 10.1007/s12035-015-9392-y.

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Title The deleterious effects of oxidative and nitrosative stress on palmitoylation, membrane lipid rafts and lipid-based cellular signalling : new drug targets in neuroimmune disorders
Author(s) Morris, Gerwyn
Walder, KenORCID iD for Walder, Ken orcid.org/0000-0002-6758-4763
Puri, Basant K.
Berk, MichaelORCID iD for Berk, Michael orcid.org/0000-0002-5554-6946
Maes, Michael
Journal name Molecular neurobiology
Volume number 53
Issue number 7
Start page 4638
End page 4658
Total pages 21
Publisher Springer
Place of publication New York, N.Y.
Publication date 2016-09
ISSN 0893-7648
1559-1182
Keyword(s) chronic fatigue
cytokines
depression
inflammation
metabolism
oxidative and nitrosative stress
Summary Oxidative and nitrosative stress (O&NS) is causatively implicated in the pathogenesis of Alzheimer’s and Parkinson’s disease, multiple sclerosis, chronic fatigue syndrome, schizophrenia and depression. Many of the consequences stemming from O&NS, including damage to proteins, lipids and DNA, are well known, whereas the effects of O&NS on lipoprotein-based cellular signalling involving palmitoylation and plasma membrane lipid rafts are less well documented. The aim of this narrative review is to discuss the mechanisms involved in lipid-based signalling, including palmitoylation, membrane/lipid raft (MLR) and n-3 polyunsaturated fatty acid (PUFA) functions, the effects of O&NS processes on these processes and their role in the abovementioned diseases. S-palmitoylation is a post-translational modification, which regulates protein trafficking and association with the plasma membrane, protein subcellular location and functions. Palmitoylation and MRLs play a key role in neuronal functions, including glutamatergic neurotransmission, and immune-inflammatory responses. Palmitoylation, MLRs and n-3 PUFAs are vulnerable to the corruptive effects of O&NS. Chronic O&NS inhibits palmitoylation and causes profound changes in lipid membrane composition, e.g. n-3 PUFA depletion, increased membrane permeability and reduced fluidity, which together lead to disorders in intracellular signal transduction, receptor dysfunction and increased neurotoxicity. Disruption of lipid-based signalling is a source of the neuroimmune disorders involved in the pathophysiology of the abovementioned diseases. n-3 PUFA supplementation is a rational therapeutic approach targeting disruptions in lipid-based signalling.
Language eng
DOI 10.1007/s12035-015-9392-y
Field of Research 111799 Public Health and Health Services not elsewhere classified
Socio Economic Objective 929999 Health not elsewhere classified
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2015, Springer
Persistent URL http://hdl.handle.net/10536/DRO/DU:30078520

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
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