Oxygen, reactive oxygen species and tissue damage.

By C. Bergamini, Stefania Gambetti, A. Dondi, C. Cervellati. Current pharmaceutical design, 2004

653 citations recorded by the source corpus.

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Oxidative Stress and Diabetic Retinopathy (2007, background): “Mitochondrial superoxide production initiates a cascade of damaging events via the production of more superoxide, hydrogen peroxide, hydroxyl radicals, and peroxynitrite which injure macromolecules either at or near the site of their formation [80].”
Molecular mediators of hepatic steatosis and liver injury. (2004, neutral): “Some of the consequences of increased ROS include depletion of ATP and nicotinamide dinucleotide, DNA damage, alterations in protein stability, the destruction of mem - branes via lipid peroxidation, and the release of proinflammatory cytokines (62, 67).”
Photophysics and photochemistry of photodynamic therapy: fundamental aspects (2009, background): “Since damage set by H2O2 is not restricted to one cellular compartment, hydrogen peroxide is quite relevant in producing cellular damage [21, 22].”
Antioxidant mechanism of tea polyphenols and its impact on health benefits (2020, background): “The species mainly include superoxide anion free radicals (O2 ), hydroxyl free radicals (OH ), hydrogen peroxide (H2O2), and others (Bergamini et al., 2004; Kim et al., 2009).”