Reactive oxygen metabolites ROMs

In addition to the well-characterized role of iron in catalysing redox interactions, other metallic contaminants, for example, nickel, may also contribute. In vivo toxicity studies have demonstrated the capacity of nickel particulate compounds to induce tumours following intraperitoneal injection (Pott etal., 1987). Such activity is proportional to their phagocytic uptake, and to the associated respiratory burst and generation of PMN-derived reactive oxygen metabolites (ROMs), a proposed pathogenic mechanism (Evans et al., 1992a). 

Fig. 1. Schematic diagram showing the different mechanisms of action proposed for the antiulcer action of flavonoids. 1. Blockade of add secretion by decreasing histamine production or inhibiting the proton pump. 2. Bactericidal effect on H. pylori. 3. Antioxidative activity by scavenging free radicals and preventing ROM formation. 4. Potentiation of the mucosal protective factors. PAF platelet activating factor ROM reactive oxygen metabolites H2 histamine receptor 2 M muscarinic receptor G gastrin receptor.

Fig. 2. Schematic diagram delineating some of the multiple stages of mutagenesis and the interference by flavonoids. 1. Flavonoids induce apoptosis and enhance mutagen detoxification and extrusion from the cell. 2. Flavonoids interfere with the metabolic activation of mutagens and protect DNA by means of their antioxidative action. GST glutathione-S-transferase ROM reactive oxygen metabolites.

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