Active oxygen species inhibition formation

Virus inactivation by hypericin seems to involve inhibition of various stages of virus replication depending on the integrity of the viral envelope. Photoactivation of hypericin leads to the formation of active oxygen species that likely react with viral components making them unable to assembly into complete virus particles. 

Exposure to cadmium may produce oxidative stress, which may result directly in toxicity or may occur secondary to cadmium toxicity. Results from studies using cultured cells have demonstrated cadmium-induced formation of superoxide anion radicals (Amoruso et al. 1982) and implicated superoxide anions in Cd-induced DNA single-strand scissions (Ochi et al. 1983). Cadmium inhibited superoxide dismutase in vivo, resulting in elevated superoxide levels (Shukla et al. 1987). Cadmium has been shown to increase peroxidation of lipids in isolated rat hepatocytes (Stacey et al. 1980) and in other target tissues in vivo and in vitro (Gabor et al. 1978 Wahba and Waalkes 1990) thus, increased levels of lipid peroxides following exposure to cadmium could constitute a source of active oxygen species. 

The mechanism of the antioxidant effect of vitamin E is similar to the effect of other lipophilic antioxidants. Tocopherols react with a number of free radicals including active oxygen species. One tocopherol molecule can react with two hydroperoxyl radicals. Autoxi-dation of lipids is inhibited by reaction of tocopherols (abbreviated as T-OH) with hydroperoxyl lipid radicals (R-O-O ) with the formation of hydroperoxides (R O-OH) and radicals of tocopherols (tocopheroxyl radicals, T O ). This reaction interrupts the radical chain autoxidation reaction of Hpids during the propagation phase ... 

Colquhoun and Schumacher [98] have shown that y-linolcnic acid and eicosapentaenoic acid, which inhibit Walker tumor growth in vivo, decreased proliferation and apoptotic index in these cells. Development of apoptosis was characterized by the enhancement of the formation of reactive oxygen species and products of lipid peroxidation and was accompanied by a decrease in the activities of mitochondrial complexes I, III, and IV, and the release of cytochrome c and caspase 3-like activation of DNA fragmentation. Earlier, a similar apoptotic mechanism of antitumor activity has been shown for the flavonoid quercetin [99], Kamp et al. [100] suggested that the asbestos-induced apoptosis in alveolar epithelial cells was mediated by iron-derived oxygen species, although authors did not hypothesize about the nature of these species (hydroxyl radicals, hydrogen peroxide, or iron complexes ). 

The formation of nitric oxide in microsomes results in the inhibition of microsomal reductase activity. It has been found that the inhibitory effect of nitric oxide mainly depend on the interaction with cytochrome P-450. NO reversibly reacts with P-450 isoforms to form the P-450-NO complex, but at the same time it irreversibly inactivates the cytochrome P-450 via the modification of its thiol residues [64]. Incubation of microsomes with nitric oxide causes the inhibition of 20-HETE formation from arachidonic acid [65], the generation of reactive oxygen species [66], and the release of catalytically active iron from ferritin [67],... 

Inhibition and stimulation of LOX activity occurs as a rule by a free radical mechanism. Riendeau et al. [8] showed that hydroperoxide activation of 5-LOX is product-specific and can be stimulated by 5-HPETE and hydrogen peroxide. NADPH, FAD, Fe2+ ions, and Fe3+(EDTA) complex markedly increased the formation of oxidized products while NADH and 5-HETE were inhibitory. Jones et al. [9] also demonstrated that another hydroperoxide 13(5)-hydroperoxy-9,ll( , Z)-octadecadienoic acid (13-HPOD) (formed by the oxidation of linoleic acid by soybean LOX) activated the inactive ferrous form of the enzyme. These authors suggested that 13-HPOD attached to LOX and affected its activation through the formation of a protein radical. Werz et al. [10] showed that reactive oxygen species produced by xanthine oxidase, granulocytes, or mitochondria activated 5-LOX in the Epstein Barr virus-transformed B-lymphocytes. 

Xiao XQ, Zhang HY, Tang XC, Huperzine A attenuates amyloid fl-peptide fragment 25-35-induced apoptosis in rat cortical neutons via inhibiting reactive oxygen species formation and caspase-3 activation, J Neurosci Res 67 30—36, 2002. 

From these observations it is showed that the antioxidant activities of chlorogenic acids are preserved by inhibiting the formation of reactive oxygen species or by scavenging them. As a result, chlorogenic acids may play a beneficial role in the prevention of some oxidative diseases. 

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