Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Azelaic acid is an aliphatic dicarboxylic acid (HOOC-(CH2)7-COOH) which has recently been shown to have some practical therapeutic applications in skin diseases of different etiologies. It possesses diverse biological activities and its mechanisms of action are still under investigation. Azelaic acid, as disodium salt (C(9)2Na), at concentrations from 0.05 mM to 1.0 mM is capable of inhibiting significantly the hydroxylation of 1-tyrosine to 1-DOPA due to hydroxylradicals (HO.) produced by Fenton reaction. Similarly C(9)2Na significantly inhibits the heterogeneous photocatalytic oxidation of toluene to cresols, and the peroxidation of arachidonic acid (C20:4,n6), due to HO. formed by dissolved oxygen in the presence of UV-irradiated semiconductor TiO2 (photo-Fenton type reaction). C(9)2Na decomposition and its by-products formation are quantifiable only at high HO. concentrations. On the contrary, C(9)2Na is not a scavenger of O2-. generated by xanthine-xanthine oxidase system. Under the same experimental conditions, mannitol behaves like C(9)2Na. These data indicate that HO. scavenging capacity of C(9)2Na in vitro, and represent a useful tool for further investigations on the mechanisms of action of azelaic acid in biological systems.
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PMID:Scavenging activity of azelaic acid on hydroxyl radicals "in vitro". 164 75

The action of ocular screening pigments of vertebrates (melanins) as well as those of invertebrates (ommochromes) on lipid peroxidation has been studied. Lipid peroxidation has been induced by one of the following systems: Fe2+ + ascorbic acid; Fe2+ + NADPH + liver microsomes; xanthine + xanthine oxidase; u.v. illumination; intense visible light, high concentration of O2. Measurements of the lipid peroxidation rate, as estimated from the accumulation of malonic dialdehyde, showed a sharp decrease of the lipid peroxidation rate in the presence of either melanosomes or ommochromes. Synthetic DOPA melanin was also found to exert a strong inhibiting effect on lipid peroxidation. A comparative study of lipid peroxidation in retinal pigment epithelium (RPE) of pigmented and albino rabbits demonstrated that the latter tissue is more sensitive to the effect of the above mentioned prooxidant systems. Apparently this finding is related to the presence of melanin-containing granules in the pigmented tissue rather than to differences in efficiency of other endogenous antioxidant systems. The activities of superoxide dismutase and glutathione peroxidase are practically equal in the RPE of pigmented and albino rabbits whereas the alpha-tocopherol content is higher in albinos. Possible mechanisms of inhibition of lipid peroxidation by melanosomes and ommochromes are discussed. It is proposed that their antioxidant function is one of the most important physiological features of melanins (vertebrate eye) and ommochromes (invertebrate eye).
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PMID:An antioxidative role of ocular screening pigments. 349 29

To investigate the involvement of oxidative tissue damage in the pathogenesis of murine cerebral malaria (CM), brain levels of protein carbonyls, 3,4-dihydroxyphenylalanine (DOPA), o-tyrosine, and dityrosine were measured during Plasmodium berghei ANKA (PbA) and P. berghei K173 (PbK) infections. During PbA infection in a CM model, brain levels of the substances were similar to those in uninfected mice. The role of phagocyte-derived reactive oxygen species in the pathogenesis of CM was examined in gp91phox gene knockout mice. The course of CM in these mice was the same as in their wild type counterparts. To examine whether superoxide production in the central nervous system could have occurred via increased xanthine oxidase activity, brain concentrations of urate were measured in CM mice and in mice infected with PbK (which does not cause CM). Brain urate concentration increased significantly in both groups of mice, suggesting that purine breakdown is not specific to CM. These results indicate that reactive oxygen species probably do not contribute to the pathogenesis of murine CM.
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PMID:Are reactive oxygen species involved in the pathogenesis of murine cerebral malaria? 984 42