Toxic oxygen species

Winyard, P.G., Perrett, D., Harris, G. and Blake, D.R, (1992). The role of toxic oxygen species in inflammation with special reference to DNA damage. In Biochemistry of Inflammation (eds. J.T. Whicher and S.W. Evans) pp. 109-129. MTP Press, Lancaster. 

Balia, G., Vercelloti, G.M. and Muller-Eberhard, U. (1991). Exposure of endothelial cells to free heme potentiates damage mediated by granulocytes and toxic oxygen species. Lab. Invest. 64, 648-655. 

Moreover, in the membrane environments the tocopherols are present, which remove the toxic oxygen species (02,102, HOO and OH ). The tocopherols act here as sacrificial donors, ie scavengers, which are not restored in a subsequent reduction process but are destroyed by irreversible chemical conversion [125],... 

The altered C3 then activates the alternative complement pathway, which causes the release of chemoattractants and the assembly of the membrane attack complex of complement (Clark et al. 1990). Amidated C3 can also bind directly to phagocyte complement receptors, which causes the release of toxic oxygen species (Clark et al. 1990). It has also been suggested that NH/ depresses protein degradation in renal cells and inhibits renal cell replication, which supports the findings of renal h q)ertrophy in renal injury and indicates that NH/ may inhibit recovery from injury (Rabkin et al. 1993). 

A recent report by Parsons et a/." presented evidence for simultaneous elevation of complement fragments and measurable levels of endotoxin in plasma from patients with ARDS. Because complement activation by toxins and by other mechanisms" is thought to cause neutrophil and platelet activation" and subsequent generation of toxic oxygen species and eico-sanoids various strategies known to activate intravascular complement have been used to examine the role of eicosanoids in lung injury . To... 

Although the results of these extensive experiments are not easily interpreted, the hypotheses were made (a) that PChlide is the most important and ubiquitous photodynamic species caused to accumulate by ALA-based treatments, (b) that MV PChlide is a more effective photodynamic pigment than DV PChlide in DDV/LDV and DMV/LDV species, and (c) that both DDV/LDV and DMV/LDV species are highly susceptible to a mixture of Mg-PPIX and Mg-PPIXME (14) The results are difficult to interpret because equimolar levels of different porphyrins were not produced and the combinations of porphyrins produced by different modulators varied with species. Potential differences in tolerance to toxic oxygen species between species were not considered. Others have attempted to explain differential sensitivity to porphyrin-generating herbicides between species (15) and between herbicide-sensitive biotypes within species (16) by differences in ability to detoxify toxic oxygen species. As with other herbicides, penetration of the leaf cuticle by ALA and/or DP can also play a role in differences in efficacy of this herbicide combination (17). 

To date, only six publications (5, 13, 14> IZ-IS) exist on ALA as a herbicide. Another paper has been published on ALA as an Insecticide (2Q). Although most of these are highly substantial papers, several questions remain regarding results of these studies. The actual relative phytotoxicity of various porphyrins Is not clear. The Intracellular s1te(s) of porphyrin accumulation are also not known. Furthermore, the complex Interactions between greening type, tolerance to toxic oxygen species, and capacity to synthesize porphyrins Is poorly understood. 

UCN can be administered in therapeutic applications such as photodynamic therapy (PDT). This involves destruction of pathological cells and tissues using toxic oxygen species generated from dynamic interaction of a photosensitizing agent with light... 

A schematic representation of the possible molecular fate and effects of organic xenobiotics taken up into animals is given in Fig. 1. It shows the relationship between the biotransformation pathways involved in the detoxication and removal of xenobiotics and those involved in the generation of toxic molecular species. It identifies four potential sources of toxic molecular species derived either directly or indirectly from the presence of the organic xenobiotic, viz. the parent compound itself, reactive metabolites and free radical derivatives of the compound, and enhanced production of toxic oxygen species (oxyradicals). The scheme and the details of the reactions and enzymes involved (Table 1-3) are based largely on mammalian and other vertebrate studies. 

The other major class of herbicides involved with photosynthesis are compounds that act as divertors of electron flow at photosystem I (PSI). After the initial discovery of diquat and paraquat in the late 1950s, other related compounds have had limited use. One of these, morfamquat, has now been withdrawn. Thirty years later, there are no new chemicals or herbicide families to rival paraquat and diquat at this particular target site. We have, however, an increased understanding of the nature of the damaging radical species that are generated as a result of the action of these compounds. With these herbicides, as also with the electron transport inhibitors, toxic oxygen species have a major role. 

Finally, exogenous application of ascorbate or galactonolactone, a direct precursor of ascorbate in plants, has been reported to antagonize the activity of herbicides generating toxic oxygen species, such as paraquat and... 

Microrganisms are killed in phagocytes by an array of digestive enzymes, toxic oxygen species, and other antimicrobial agents. In addition to internalization... 

---