Ascorbate oxidation by Cu(Amyloid-β) complexes: determination of the intrinsic rate as function of alterations in the peptide sequence reveals key residues for ROS production
Explore this paper's citation graph
Summary
By examination of the dependence of the intrinsic rate of ascorbate oxidation, followed by UV-Vis spectroscopy, for several altered peptides, some of the key residues that influence ROS production are determined.
- Type
- article
- Published
- 2018-04-03
- Cited by
- 44
- References
- 50
- Access
- Open access
- OpenAlex
- https://openalex.org/W2795843933
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:4792453
Keywords
Chemistry, Peptide, Reactive oxygen species, Ascorbic acid, Oxidative stress
References
- Mechanisms for copper acquisition, distribution and regulation.
- Structure and spectroscopy of copper-dioxygen complexes.
- Exploring the structural details of Cu(I) binding to α-synuclein by NMR spectroscopy.
- Coordination of redox active metal ions to the amyloid precursor protein and to amyloid-β peptides involved in Alzheimer disease. Part 1: An overview
- Insights on the interaction of alpha-synuclein and metals in the pathophysiology of Parkinson's disease.
- A new water-soluble Cu(II) chelator that retrieves Cu from Cu(amyloid-β) species, stops associated ROS production and prevents Cu(II)-induced Aβ aggregation.
- An integrated study of the affinities of the Aβ16 peptide for Cu(I) and Cu(II): implications for the catalytic production of reactive oxygen species.
- Affinity of copper and zinc ions to proteins and peptides related to neurodegenerative conditions (Aβ, APP, α-synuclein, PrP)
- Treatment of Wilson's disease with tetrathiomolybdate: V. Control of free copper by tetrathiomolybdate and a comparison with trientine.
- Copper in the brain and Alzheimer’s disease
- Methods and techniques to study the bioinorganic chemistry of metal–peptide complexes linked to neurodegenerative diseases
- Amyloid beta-Cu2+ complexes in both monomeric and fibrillar forms do not generate H2O2 catalytically but quench hydroxyl radicals.
- Importance of dynamical processes in the coordination chemistry and redox conversion of copper amyloid-β complexes
- Oxidative Stress and Neurodegenerative Disorders
- Copper(I) targeting in the Alzheimer's disease context: a first example using the biocompatible PTA ligand.
- Bioinorganic chemistry of Parkinson's disease: structural determinants for the copper-mediated amyloid formation of alpha-synuclein.
- Electrochemical and homogeneous electron transfers to the Alzheimer amyloid-β copper complex follow a preorganization mechanism
- Copper, zinc and iron in neurodegenerative diseases (Alzheimer's, Parkinson's and prion diseases)
- Zn impacts Cu coordination to amyloid-β, the Alzheimer's peptide, but not the ROS production and the associated cell toxicity.
- Structure and mechanism of copper, zinc superoxide dismutase
Cited by
- Cu and Zn coordination to amyloid peptides: From fascinating chemistry to debated pathological relevance
- Mutations of Histidine 13 to Arginine and Arginine 5 to Glycine Are Responsible for Different Coordination Sites of Zinc(II) to Human and Murine Peptides.
- Structural Insight into Redox Dynamics of Copper Bound N-Truncated Amyloid-β Peptides from in Situ X-ray Absorption Spectroscopy.
- Copper reduction and dioxygen activation in Cu-amyloid beta peptide complexes: insight from molecular modelling.
- A catalytic antioxidant for limiting amyloid-beta peptide aggregation and reactive oxygen species generation
- Structural analysis of copper(I) interaction with amyloid β peptide.
- Role of PTA in the prevention of Cu(Amyloid-β) induced ROS formation and Amyloid-β oligomerisation in the presence of Zn
- Cu(II) Binding to the N-Terminal Model Peptide of the Human Ctr2 Transporter at Lysosomal and Extracellular pH.
- His6, His13, and His14 residues in Aβ 1–40 peptide significantly and specifically affect oligomeric equilibria
- CuII Binding Properties of N-Truncated Aβ Peptides: In Search of Biological Function.
- Alzheimer's Disease And Retinal Degeneration: A Glimpse At Essential Trace Metals In Ocular Fluids And Tissues.
- A β-sheet-targeted theranostic agent for diagnosing and preventing aggregation of pathogenic peptides in Alzheimer’s disease
- Binding and Reactivity of Copper to R1 and R3 Fragments of tau Protein.
- Mechanistic approaches for chemically modifying the coordination sphere of copper–amyloid-β complexes
- Molecular dynamics simulations of copper binding to N-terminus mutants of amyloid-β
- Copper Transporters? Glutathione Reactivity of Products of Cu–Aβ Digestion by Neprilysin
- Both metal-chelating and free radical-scavenging synthetic pentapeptides as efficient inhibitors of reactive oxygen species generation.
- The aroylhydrazone INHHQ prevents memory impairment induced by Alzheimer’s-linked amyloid-β oligomers in mice
- On the propagation of the OH radical produced by Cu-amyloid beta peptide model complexes. Insight from molecular modelling.
- N-truncated Aβ peptides impact on Cu and Cu(Aβ)-generated ROS: Cu(I) matters !
Related papers
- Mitochondrial Reactive Oxygen Species and Their Contribution in Chronic Kidney Disease Progression Through Oxidative Stress
- Oxidative Stress in Diabetes and Periodontitis
- Review Article: Oxidative Stress as Molecular Mechanism in Environmntal Stress
- [The role of reactive oxygen species (ROS) in arrhythmogenesis].
- Role of reactive oxygen species in cervical carcinoma
- Detection of oxidative stress in neurodegenerative diseases