Reactive oxygen species sources

One of the important consequences of neuronal stimulation is increased neuronal aerobic metabolism which produces reactive oxygen species (ROS). ROS can oxidize several biomoiecules (carbohydrates, DNA, lipids, and proteins). Thus, even oxygen, which is essential for aerobic life, may be potentially toxic to cells. Addition of one electron to molecular oxygen (O,) generates a free radical [O2)) the superoxide anion. This is converted through activation of an enzyme, superoxide dismurase, to hydrogen peroxide (H-iO,), which is, in turn, the source of the hydroxyl radical (OH). Usually catalase... 

At the present time it is difficult to single out any one factor that could be held ultimately responsible for cell death after cerebral ischaemia. Recent studies, however, have provided us with sufficient evidence to conclude that free radical damage is at least one component in a chain of events that leads to cell death in ischaemia/reperfiision injury. As noted earlier in this review, much of the evidence for free radicals in the brain and the sources of free radicals come from studies in animals subjected to cerebral ischaemia. Perhaps the best evidence for a role for free radicals or reactive oxygen species in cerebral ischaemia is derived from studies that demonstrate protective effects of antioxidants. Antioxidants and inhibitors of lipid peroxidation have been shown to have profound protective effects in models of cerebral ischaemia. Details of some of these studies will be mentioned later. Several reviews have been written on the role of oxygen radicals in cerebral ischaemia (Braughler and HaU, 1989 Hall and Btaughler, 1989 Kontos, 1989 Floyd, 1990 Nelson ef /., 1992 Panetta and Clemens, 1993). 

Inside the dark box main sockets and automation port ensure integration of special probe requirements like incubators. There is provision to insert a fiberoptic-guided light source that accept filters for fluorescent work. The sensitivity of the NightOWL is claimed to enable direct detection of reactive oxygen species, even without enhancers like luminol. 

Xanthine oxidase is not the only source of reactive species in ischemia-reoxygenation injury. Another source of oxygen radicals is NADPH oxidase. For example, it has been shown that endothelial NADPH oxidase produced reactive oxygen species in lungs exposed to ischemia [13]. (The role of NADPH oxidase as a producer of oxygen radicals in tissue is considered below.)... 

Mitochondria, nitric oxide synthase and arachidonic acid metabolism are sources of reactive oxygen species during ischemia—reperfusion injury 568... 

Mitochondria, nitric oxide synthase and arachidonic acid metabolism are sources of reactive oxygen species during ischemia-reperfusion injury. ROS generation during ischemia-reperfusion may come from several sources, including NOS activity, mitochondrial electron transport, multiple steps in the metabolism of arachidonic... 

XOR is a cytoplasmic enzyme and a ready source of electrons for transfer to molecular oxygen to form reactive oxygen species such as superoxide and peroxide. It is therefore thought to be involved in free radical-generated tissue injury and has been implicated in the pathogenesis of ischemia-reperfusion damage. Moreover, it has recently been implicated in the production of peroxynitrite (89), and carbonate radical anion (92), both potent biological oxidants. Its exact role in lipid peroxidation, inflammation, and infection needs... 

As the power house of the cell, the mitochondrion is essential for energy metabolism. As the motor of cell death (1), this organelle is central to the initiation and regulation of apoptosis. In addition, mitochondria are critically involved in the modulation of intracellular calcium concentration and the mitochondrial respiratory chain is the major source of damaging reactive oxygen species. Mitochondria also play a crucial role in numerous catabolic and anabolic cellular pathways. 

As indicated in Fig. 16.2, in addition to energy transfer, chemical reactions of excited UCs ( UC, 3UC ) may lead to the formation of other reactive oxygen species (ROS) that may react with organic pollutants. Such ROS include DOM-derived oxyl- and peroxyl radicals (RO , ROO ), superoxide radical anions (02 ) that may be further reduced to H202, and hydroxyl radicals (HO ). In the case of HO , however, DOM is a net sink rather than a source. Finally, some of the 3UC may react directly with certain more easily oxidizable pollutants (see below). 

Boveris A, Cadenas E (1997) Cellular sources and steady-state levels of reactive oxygen species. In BiadaszClerch L, Massaro DJ (eds) Oxygen, gene expression, and cellular function. Dekker, New York, pp 1-25... 

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