Oxidatively Modified GST and MRP1 in Alzheimer’s Disease Brain: Implications for Accumulation of Reactive Lipid Peroxidation Products

@article{Sultana2004OxidativelyMG,
  title={Oxidatively Modified GST and MRP1 in Alzheimer’s Disease Brain: Implications for Accumulation of Reactive Lipid Peroxidation Products},
  author={Rukhsana Sultana and David Allan Butterfield},
  journal={Neurochemical Research},
  year={2004},
  volume={29},
  pages={2215-2220}
}
Alzheimer disease (AD) is a neurodegenerative disorder characterized pathologically by intracellular inclusions including neurofibrillary tangles (NFT) and senile plaques. Several lines of evidence implicate oxidative stress with the progression of AD. 4-hydroxy-2-trans-nonenal (HNE), an aldehydic product of membrane lipid peroxidation, is increased in AD brain. The alpha class of glutathione S-transferase (GST) can detoxify HNE and plays an important role in cellular protection against… 
View on Springer
chem.uky.edu
157 Citations
Highly Influential Citations
1
Background Citations
56
Methods Citations
5
Results Citations
11

157 Citations

Role of by-products of lipid oxidation in Alzheimer's disease brain: a focus on acrolein.
TLDR
Interestingly, data indicates that lipid peroxidation occurs in the brain of MCI and also in preclinical AD patients suggesting that oxidative damage may play an early role in the pathogenesis of AD.
Involvements of the lipid peroxidation product, HNE, in the pathogenesis and progression of Alzheimer's disease.
Oxidative modification and down-regulation of Pin1 in Alzheimer's disease hippocampus: A redox proteomics analysis
Alterations in brain antioxidant enzymes and redox proteomic identification of oxidized brain proteins induced by the anti-cancer drug adriamycin: implications for oxidative stress-mediated chemobrain
Lipid peroxidation triggers neurodegeneration: a redox proteomics view into the Alzheimer disease brain.
Protein oxidation and lipid peroxidation in brain of subjects with Alzheimer's disease: insights into mechanism of neurodegeneration from redox proteomics.
TLDR
The role of protein oxidation and lipid peroxidation in the pathogenesis of AD is focused on and particular attention is given to the current knowledge about the redox proteomics identification of oxidatively modified proteins in AD brain.
Redox proteomics identification of oxidatively modified proteins in Alzheimer's disease brain and in vivo and in vitro models of AD centered around Abeta(1-42).
Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer’s Disease
TLDR
It is opine that targeting altered pathways secondary to oxidative damage in brain from persons with AD, aMCI, or Down syndrome with AD may provide strategies to slow or perhaps one day, prevent, progression or development of this devastating dementing disorder.
Nitrosative stress, cellular stress response, and thiol homeostasis in patients with Alzheimer's disease.
TLDR
The data support a role for nitrative stress in the pathogenesis of AD and indicate that the stress-responsive genes, such as HO-1 and TRXr, may represent important targets for novel cytoprotective strategies.
Redox proteomic identification of 4-Hydroxy-2-nonenal-modified brain proteins in amnestic mild cognitive impairment: Insight into the role of lipid peroxidation in the progression and pathogenesis of Alzheimer's disease
...
...

References

SHOWING 1-10 OF 38 REFERENCES
Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer’s disease brain contribute to neuronal death
Oxidative Alterations in Alzheimer's Disease
TLDR
Overall these studies indicate that oxidative stress and the inflammatory cascade, working in concert, are important in the pathogenetic cascade of neurodegeneration in AD, suggesting that therapeutic efforts aimed at both of these mechanisms may be beneficial.
Decreased glutathione transferase activity in brain and ventricular fluid in Alzheimer's disease
TLDR
Reduced levels of GST, a protective mechanism against HNE, may have a role in the pathogenesis of neuron degeneration in AD, particularly in areas severely affected in the disease.
Proteomic identification of oxidatively modified proteins in Alzheimer's disease brain. Part I: creatine kinase BB, glutamine synthase, and ubiquitin carboxy-terminal hydrolase L-1.
Carbonyl toxicology and Alzheimer's disease.
TLDR
This review examines the role that carbonyls may play in the development of Alzheimer's disease and the evidence for their involvement in AD, and the potential mechanisms that the brain utilizes to detoxify carbonyl species and possible therapeutic interventions based oncarbonyl detoxification.
Acrolein, a product of lipid peroxidation, inhibits glucose and glutamate uptake in primary neuronal cultures.
Increased oxidative stress in Alzheimer's disease as assessed with 4-hydroxynonenal but not malondialdehyde.
TLDR
Increased production of 4-HNE indicates increased oxidative stress (lipid peroxidation), which is not evident using the more common marker MDA, and was related to the degree of cognitive impairment (MMSE).
Four-Hydroxynonenal, a Product of Lipid Peroxidation, is Increased in the Brain in Alzheimer’s Disease
A Role for 4‐Hydroxynonenal, an Aldehydic Product of Lipid Peroxidation, in Disruption of Ion Homeostasis and Neuronal Death Induced by Amyloid β‐Peptide
TLDR
The data suggest that HNE mediates Aβ‐induced oxidative damage to neuronal membrane proteins, which, in turn, leads to disruption of ion homeostasis and cell degeneration.
Expression of glutathione-S-transferase isozyme in the SY5Y neuroblastoma cell line increases resistance to oxidative stress.
...
...