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Reactive oxygen species in the activation and regulation of intracellular signaling events.
Oxygen/nitrogen radicals: lung injury and disease (Lung biology in health and disease). Vallyathan V, Castranova V, Shi X, eds. New York: Marcel Dekker, 2004 Apr; 187:59-90
All aerobic cells are capable of producing reactive oxygen species (ROS) due to incomplete reduction of molecular oxygen to water under both physiological and pathological conditions. As unstable free radicals containing an unpaired electron in their outer orbital, ROS are extremely active in reaction with other cellular components, such as lipids, proteins, and DNA through electron capturing. Terminologically, ROS include both fee radicals, such as superoxide anion (02), hydroperoxyl radical (HO2), and hydroxyl radical (OH), and non-free radicals, mainly H2O2. Although H202 by itself is not a free radical, in the presence of reduced transition n1etals (e.g., ferrous or cuprous ions), it can be transformed into the highly reactive -OH and related oxidants through the Fenton reaction (2). Cellular sources of ROS include membrane-associated NADPH oxidase, cytosolic Xanthine oxidase, peroxisomal oxidases, endoplasmic reticular oxidases, and mitochondriaa. Among. these cellular sources, both NADPH oxidase and mitochondria are considered to be the major sources of ROS production in response to specific circumstances. In addition, a number of environmental hazards, such as chemical toxicants, carcinogenic metals, and fibrotic mineral dusts, can serve as either powerful exogenous sources of ROS or stimulate the production of ROS from cells (1).
Cell-function; Cellular-structures; Lipids; Proteins; Free-radicals; Environmental-hazards
Vallyathan-V; Castranova-V; Shi-X
Oxygen/nitrogen radicals: lung injury and disease (Lung biology in health and disease)
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