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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]
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XthA (exonuclease III, a DNA repair enzyme) and KatE (catalase) are known to play important roles in the defense against oxidative stress but KatF regulon genes are not induced by oxidative stress. [2] There is an overlap between oxidative stress response and other regulatory networks like heat shock response, SOS response.
Lipid peroxidation, or lipid oxidation, is a complex chemical process that leads to oxidative degradation of lipids, [1] resulting in the formation of peroxide and hydroperoxide derivatives. [2] It occurs when free radicals , specifically reactive oxygen species (ROS), interact with lipids within cell membranes , typically polyunsaturated fatty ...
Pro-oxidants are chemicals that induce oxidative stress, either by generating reactive oxygen species or by inhibiting antioxidant systems. [1] The oxidative stress produced by these chemicals can damage cells and tissues, for example, an overdose of the analgesic paracetamol (acetaminophen) can fatally damage the liver, partly through its production of reactive oxygen species.
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.
But under oxidative stress conditions, excessive ROS can damage cellular proteins, lipids and DNA, leading to fatal lesions in the cell that contribute to carcinogenesis. Cancer cells exhibit greater ROS stress than normal cells do, partly due to oncogenic stimulation, increased metabolic activity and mitochondrial malfunction.
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