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Oxidative stress may damage cellular proteins and cause myocyte apoptosis and necrosis.
ROS may damage cellular components and trigger a cascade of events leading to cell death [ 15].
Because oxidative stress may damage cellular contents such as DNA, lipids and proteins, organisms developed various antioxidant defense mechanisms [ 52, 53].
Free divalent iron ions participate in the Fenton reaction, producing highly reactive hydroxyl radicals, which may damage cellular components, including DNA, and impair DNA repair [ 43].
Two potential mechanisms by which benzene metabolites may damage cellular macromolecules to induce toxicity include the covalent binding of reactive metabolites of benzene and the capacity of benzene metabolites to induce oxidative damage.
Similar(55)
Oxidative stress induced by reactive oxygen species (ROS) may directly damage cellular membranes via lipid peroxidation.
The elevated level of ROS may damage the cellular membranes, proteins and nucleic acids.
Metal ions released into the oral cavity from dental prosthesis alloys may damage the cellular metabolism or proliferation and cause hypersensitivity or allergies.
These stressful conditions may damage important cellular structures and interfere with essential functions of the parasites.
Reactive oxygen species (ROS) are a family of compounds that can oxidatively damage cellular macromolecules and may influence lifespan.
Excessive ROS could damage cellular components.
More suggestions(15)
may stimulate cellular
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may inhibit cellular
may underlie cellular
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may involve cellular
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may sequester cellular
may exhaust cellular
may compromise cellular
may increase cellular
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