Singlet oxygen-mediated damage to proteins and its consequences.
By M. Davies. Biochemical and Biophysical Research Communications - BBRC, 2003
887 citations recorded by the source corpus.
Subfields: Biophysics, Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/a18ffe0674ef3adc4a7289675b4abef6d9dccb79
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Citations in the corpus
- Protein oxidation in muscle foods: a review. (2011, background): “Alzheimer) [1, 2] whereas the occurrence of Pox in food systems has been largely unexplored.”
- Cadmium toxicity causes oxidative stress and induces response of the antioxidant system in cucumber seedlings (2007, background): “…conditions, their formation might be in excess of antioxidant scavenging capacity, thus creating oxidative stress by reaction and damage to all biomolecules, especially proteins, due to the higher rate constants of the reaction of the superoxide anion with amino acid side chains (Davies, 2003).”
- Protein oxidation and peroxidation (2016, background): “High yields of endo-and hydro-peroxides can also be formed by singlet oxygen ( 1 g; 1 O 2 ) (reviewed [9,25,145].”
- Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal (2014, background): “2 )(1) can react with amino acid, and proteins resulting in multiple effects including oxidation of side-chains, backbone fragmentation, dimerization/aggregation, unfolding or conformational changes, enzymatic inactivation, and alterations in cellular handling and turnover of proteins [69, 70].”
- Gum Arabic: More Than an Edible Emulsifier (2012, neutral): “9 and 10 (Davies, 2003; Bisby et al., 1999).”
- Antimicrobial strategies centered around reactive oxygen species--bactericidal antibiotics, photodynamic therapy, and beyond. (2013, background): “…and in regulatory mechanisms, has meant that defense against excessive ROS has needed to evolve to deal with the harmful effects of ROS, such as lipid peroxidation (damaging cell membranes), oxidative damage to proteins (Davies, 2003), mutations to DNA, and activation of procell-death factors.”