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Oxidative stress and reduced glutamine synthetase activity in the absence of inflammation in the cortex of mice with experimental allergic encephalomyelitis.

Abstract：

:Pathological changes occur in areas of CNS tissue remote from inflammatory lesions in multiple sclerosis (MS) and its animal model experimental allergic encephalomyelitis (EAE). To determine if oxidative stress is a significant contributor to this non-inflammatory pathology, cortex tissues from mice with clinical signs of EAE were examined for evidence of inflammation and oxidative stress. Histology and gene expression analysis showed little evidence of immune/inflammatory cell invasion but reductions in natural antioxidant levels and increased protein oxidation that paralleled disease severity. Two-dimensional oxyblots and mass-spectrometry-based protein fingerprinting identified glutamine synthetase (GS) as a particular target of oxidation. Oxidation of GS was associated with reductions in enzyme activity and increased glutamate/glutamine levels. The possibility that this may cause neurodegeneration through glutamate excitotoxicity is supported by evidence of increasing cortical Ca(2+) levels in cortex extracts from animals with greater disease severity. These findings indicate that oxidative stress occurs in brain areas that are not actively undergoing inflammation in EAE and that this can lead to a neurodegenerative process due to the susceptibility of GS to oxidative inactivation.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Castegna A,Palmieri L,Spera I,Porcelli V,Palmieri F,Fabis-Pedrini MJ,Kean RB,Barkhouse DA,Curtis MT,Hooper DC

doi

10.1016/j.neuroscience.2011.04.041

subject

Has Abstract

pub_date

2011-06-30 00:00:00

pages

97-105

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(11)00459-3

journal_volume

185

pub_type

杂志文章

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