Reactive oxygen species radicals

Element-specific detection by ICP-MS has been widely used in the characterization of metallothioneins (MTs). The biological importance of these proteins is due to their role in homeostatic regulation of essential heavy metals like Cu and Zn. On the other hand, MT protects the cells from harmful chemicals, like nonessential and excessive essential heavy metals, reactive oxygen species, radicals, and alkylating agents. Fararello et reviewed different chromatographic approaches with ICP-MS detection for the multielemental speciation in MTs and MT-like proteins. 

This category of antioxidants can be subdivided into water soluble and lipid soluble antioxidants. Nevertheless, they all act in a similar manner when scavenging reactive oxygen species. Radicals usually react with these antioxidants as a redox system, hence, the difference in reduction potentials of the species involved is a factor in determining how efficiently the reaction proceeds. An antioxidant can either react by donating an electron or a hydrogen atom to the radical, thus producing a stable compound and an antioxidant-derived radical (non-redox reactions can also occur, such as addition). 

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... 

The protective effects of carotenoids against chronic diseases appear to be correlated to their antioxidant capacities. Indeed, oxidative stress and reactive oxygen species (ROS) formation are at the basis of oxidative processes occurring in cardiovascular incidents, cancers, and ocular diseases. Carotenoids are then able to scavenge free radicals such as singlet molecular oxygen ( O2) and peroxyl radicals particularly, and protect cellular systems from oxidation. 

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). 

Ranadive, N.S. and Menon, I.A. (1986). Role of reactive oxygen species and free radicals from melanins in photoin-duced cutaneous inflammation. Pathol. Immunopathol. Res. 5, 118-139. 

Jackson, M.J. and Edwards, RH.T. (1988). Free radicals, muscle damage and muscular dystrophy. In Reactive Oxygen Species in Chemistry, Biology and Medicine (ed. A. Quintanilha) pp. 197-210, Plenum, New York. 

Cancer is one of the diseases in which a role has been implicated (see Table 13.1) for free radicals. Comprehensive accounts of the involvement of reactive oxygen species in human diseases may be found in Halliwell and Gutteridge (1989), Aruoma (1993) and in Cheeseman and Slater (1993). 

Lipid peroxidation (see Fig. 17.2) is a chain reaction that can be attacked in many ways. The chain reaction can be inhibited by use of radical scavengers (chain termination). Initiation of the chain reaction can be blocked by either inhibiting synthesis. of reactive oxygen species (ROS) or by use of antioxidant enzymes like superoxide dismutase (SOD), complexes of SOD and catalase. Finally, agents that chelate iron can remove free iron and thus reduce Flaber-Weiss-mediated iron/oxygen injury. 

Flowers, L. Ohnishi, T. Penning, T. M. DNA strand scission by polycylic hydrocarbon o-quinone role of reactive oxygen species, Cu(II)/(I) redox cycling, and o-semiquinone anion radicals. Biochemistry 1997, 36, 8640-8648. 

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