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      The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.

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          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.

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          Author and article information

          Mol. Neurobiol.
          Molecular neurobiology
          Sep 2016
          : 53
          : 7
          [1 ] Tir Na Nog, Bryn Road seaside 87, Llanelli, SA152LW, Wales, UK.
          [2 ] Metabolic Research Unit, Deakin University, Geelong, Australia.
          [3 ] Department of Medicine, Hammersmith Hospital, Imperial College London, London, W12 0HS, UK.
          [4 ] Orygen, The National Centre of Excellence in Youth Mental Health and the Centre of Youth Mental Health, Poplar Road 35, Parkville, 3052, Australia.
          [5 ] The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville, 3052, Australia.
          [6 ] Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Level 1 North, Main Block, Parkville, 3052, Australia.
          [7 ] IMPACT Strategic Research Center, School of Medicine, Deakin University, P.O. Box 291, Geelong, 3220, Australia.
          [8 ] IMPACT Strategic Research Center, School of Medicine, Deakin University, P.O. Box 291, Geelong, 3220, Australia. dr.michaelmaes@hotmail.com.
          [9 ] Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.
          [10 ] Health Sciences Graduate Program, Health Sciences Center, State University of Londrina, Londrina, Brazil. dr.michaelmaes@hotmail.com.

          Chronic fatigue,Cytokines,Depression,Inflammation,Metabolism,Oxidative and nitrosative stress


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