Abstract
Oxidative stress may be a hallmark of several neurodegenerative disorders, including Alzheimer’s disease (AD), Huntington’s disease (HD), and Parkinson’s disease (PD), as well as Creutzfeldt-Jakob disease (CJD), frontotemporal dementia, and amyotrophic lateral sclerosis (ALS) (1). Oxidative stress occurs when the formation of reactive oxygen species (ROS) increases, or when scavenging of ROS or repair of oxidatively modified molecules decreases (2,3). ROS are highly reactive, toxic oxygen moieties, such as hydroxyl radical, peroxyl radical, superoxide anion, and hydrogen peroxide. Collectively, ROS can lead to oxidation of proteins and DNA, peroxidation of lipids, and, ultimately, cell death. To counteract these damaging radicals, antioxidant systems have been developed. Among these are enzymes, such as glutathione peroxidase, glutathione reductase, superoxide dismutase (SOD), and catalase, among others; and small, nonprotein, cellular antioxidants such as, glutathione, vitamin C, vitamin E, and uric acid.
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© 2003 Humana Press Inc.,Totowa, NJ
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Castegna, A., Drake, J., Pocernich, C., Butterfield, D.A. (2003). Protein Carbonyl Levels—An Assessment of Protein Oxidation. In: Hensley, K., Floyd, R.A. (eds) Methods in Biological Oxidative Stress. Methods in Pharmacology and Toxicology. Humana Press. https://doi.org/10.1385/1-59259-424-7:161
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DOI: https://doi.org/10.1385/1-59259-424-7:161
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Print ISBN: 978-0-89603-815-8
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