Protein Oxidation

By E. Stadtman, R. Levine. Annals of the New York Academy of Sciences, 2000

876 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/c6af89e64fb974a35d70c1f007f566b642f50785

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Citations in the corpus

Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases (2014, background): “Most importantly, the excess ROS can damage the integrity of various biomolecules including lipids [13], proteins [14] and DNA [15] leading to increased oxidative stress in various human diseases such as diabetes mellitus, neurodegenerative diseases, rheumatoid arthritis, cataracts, cardiovascular d”
Relationship between lipid and protein oxidation in fish (2019, positive): “…react further with amino groups (Schaich & K. M., 1976) or for unsaturated lipid aldehydes reacting with Cys, His, or Lys through Michael addition (Stadtman & Levine, 2000). b Some products of lipid oxidation (hydroperoxides, lipid free radi‐ cals and volatile secondary oxidation products) can…”
Potential Role of Carotenoids as Antioxidants in Human Health and Disease (2014, background): “They are capable of irreversible oxidation of fundamental biological macromolecules: proteins, lipids, nucleic acids and carbohydrates [41,42].”
Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives (2022, background): “, itrosylat on might decrease the activi y of enzymes a d also reduces the production of growth facto s that might result in cellular dysfunction [33].”
Cellular response to hyperosmotic stresses. (2007, background): “Carbonylation affects protein stability and function, notably inhibiting enzyme activity (279).”
Oxygen Toxicity and Reactive Oxygen Species: The Devil Is in the Details (2009, background): “For example, protein oxidation and nitrosylation (carbonyl, nitration, and nitrotyrosine formation) can impair a wide variety of enzymatic processes and growth factors that can result in marked cellular dysfunction (12).”
Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review (2014, background): “which indiscriminately target proteins [5], lipids [6], polysaccharides [7] and DNA [8,9], and trigger the intrinsic pathway of apoptosis.”
Reactive oxygen species, antioxidants, and the mammalian thioredoxin system. (2001, background): “As the term ROS implies, intracellular production of those oxygen intermediates threatens the integrity of various biomolecules including proteins [1], lipids as well as lipoproteins involved in atherosclerosis [2], and DNA [3].”
Molecular biomarkers of oxidative stress in aquatic organisms in relation to toxic environmental pollutants. (2006, neutral): “…free radical of biological and toxicological importance, because of its potent oxidative potential and indiscriminate reactivity with cellular components, such as lipids of biological membranes, proteins of enzymes, and DNA (Stadtman and Levine, 2000; Richter, 1987; Jackson and Loeb, 2001).”
Role of oxidative carbonylation in protein quality control and senescence (2005, background): “The increase in protein carbonyls during aging in animals is quite substantial (Levine, 2002) eventually reaching a level of one out of every third protein molecule carrying this modification (Stadtman and Levine, 2000).”