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Oxidation response is stimulated by a disturbance in the balance between the production of reactive oxygen species and antioxidant responses, known as oxidative stress. Active species of oxygen naturally occur in aerobic cells and have both intracellular and extracellular sources.
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. [1]
Antioxidants are reducing agents, and limit oxidative damage to biological structures by passivating them from free radicals. [ 4 ] Strictly speaking, the free radical theory is only concerned with free radicals such as superoxide ( O 2 − ), but it has since been expanded to encompass oxidative damage from other reactive oxygen species (ROS ...
Glutathione peroxidase (GPx) (EC 1.11.1.9) is the general name of an enzyme family with peroxidase activity whose main biological role is to protect the organism from oxidative damage. [2] The biochemical function of glutathione peroxidase is to reduce lipid hydroperoxides to their corresponding alcohols and to reduce free hydrogen peroxide to ...
Glutathione reductase (GR) also known as glutathione-disulfide reductase (GSR) is an enzyme that in humans is encoded by the GSR gene.Glutathione reductase (EC 1.8.1.7) catalyzes the reduction of glutathione disulfide to the sulfhydryl form glutathione (), which is a critical molecule in resisting oxidative stress and maintaining the reducing environment of the cell.
The activated NADPH oxidase generates superoxide which has roles in animal immune response and plant signalling. [9] Superoxide can be produced in phagosomes which have ingested bacteria and fungi, or it can be produced outside of the cell. [10] In macrophages, superoxide kills bacteria and fungi by mechanisms that are not yet fully understood.
The oxidation of estradiol by lactoperoxidase is a possible source of oxidative stress in breast cancer. [ 15 ] [ 17 ] The ability of lactoperoxidase to propagate a chain reaction leading to oxygen consumption and intracellular hydrogen peroxide accumulation could explain the hydroxyl radical-induced DNA base lesions recently reported in female ...
Study of a rat model of premature aging found increased oxidative stress, reduced antioxidant enzyme activity and substantially greater DNA damage in the brain neocortex and hippocampus of the prematurely aged rats than in normally aging control rats. [52] The DNA damage 8-OHdG is a product of ROS interaction with DNA.