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Nitric Oxide and Nitroxidative Stress in Alzheimer's Disease
Abstract
Nitric oxide is a signaling molecule produced by neurons and endothelial cells in the brain. NO is synthesized from L-arginine and oxygen by nitric oxide synthase: neuronal (nNOS), endothelial (eNOS), and inducible (iNOS). The endothelial NO acts as a vasorelaxant in the vasculature and as a neurotransmitter when produced by neurons (under the pathological conditions of Alzheimer's disease). NO can be scavenged in a rapid reaction with superoxide (O2-) to generate peroxynitrite (ONOO-), with a half-life of < 1 s. ONOO- is a potent oxidant and the primary component of nitroxidative stress. At high concentrations (> 100 nM), ONOO- can undergo homolytic or heterolytic cleavage to produce NO2+, NO2, and OH., highly reactive oxidative species and secondary components of nitroxidative stress. The high nitroxidative stress can initiate a cascade of redox reactions which can trigger apoptosis and evoke cytotoxic effects on neurons and endothelial cells. This article reviews the functions of NO and the potential role of NO/O2-/ONOO- induced nitroxidative stress in neuronal and endothelial degeneration observed in Alzheimer's disease.
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In the citing paper
“Given the sensitivity of CM-H2DCFDA to oxidation by ONOO−, in combination with the propensity of ONOO− formation attributable to Aβ-induced stress, we reasoned that the primary RS detected in our paradigm was ONOO− (Setsukinai et al., 2003; Malinski, 2007).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Malinski, 2007
In the citing paper
“Tyrosine nitration provides a footprint for free radical-mediated damage involving oxidation of NO· to ONOO− or products of its subsequent decomposition and the formation of a tyrosyl radical intermediate (Halliwell and Gutteridge, 2007; Malinski, 2007).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Malinski, 2007
In the citing paper
“An imbalance between protective • NO and highly cytotoxic ONOO -may be crucial in the initial step of the development of several vascular and neuronal diseases, including AD (Malinski, 2007).”
From Multi-target neuroprotective effects of herbal medicines for Alzheimer's disease (2022) · cites this paper as Malinski, 2007
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Metadata
- Authors
- Malinski, T.
- Affiliations
- Department of Chemistry and Biochemistry Ohio University, 350 W. State Street, Athens, OH 45701, USA. Tel.: ; E-mail: malinski@ohio.edu
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2007-05-08
- Volume
- 11
- Issue
- 2
- Pages
- 207-218
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W1690235847
- Cited by
- 220
- References
- 86
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 8 · 2023: 14 · 2022: 17 · 2021: 12 · 2020: 13 · 2019: 13 · 2018: 15 · 2017: 9 · 2016: 8 · 2015: 9 · 2014: 10 · 2013: 14 · 2012: 10
- FWCI
- 9.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- nitric oxide, nitro-oxidative stress
- MeSH terms
- Alzheimer Disease, Humans, Neurons, Nitric Oxide, Amyloid beta-Peptides, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Dexfenfluramine, Peroxynitrous Acid, Endothelial Cells
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