phytic acid / xanthine oxidase

Discussion in 'Health and medical' started by Doe, Feb 10, 2004.

  1. Doe

    Doe Guest

    Inflammation. 1993 Oct;17(5):551-61. Related Articles, Links

    Elevated levels of xanthine oxidase in serum of patients with inflammatory and autoimmune
    rheumatic diseases.

    Miesel R, Zuber M.

    Deutsches Rheumaforschungszentrum, Berlin, Germany.

    Sera of patients with various inflammatory and autoimmune rheumatic diseases were screened for the
    presence of xanthine oxidase (XOD) and compared to sera from healthy donors and patients with
    nonrheumatic diseases including AIDS, internal diseases, and different carcinomas. Up to 50-fold
    higher levels of XOD were detected in rheumatic sera (P < 0.001). In addition, serum sulfhydryls
    (SH) were determined as sensitive markers of oxidative stress. The SH status in rheumatic patients
    was diminished by 45-75% (P < 0.001) and inversely correlated to the concentration of serum XOD (R =
    0.73), suggesting a causal interrelation. The depletion of serum sulfhydryls by the oxyradical-
    producing XOD/acetaldehyde system was mimicked successfully ex vivo in human serum from healthy
    donors. Cortisone treatment of patients suffering from systemic lupus erythematosus and rheumatoid
    arthritis impressively normalized elevated XOD concentrations in rheumatic sera to those of healthy
    controls. The participation of xanthine oxidase in the depletion of serum antioxidants in rheumatic
    patients is discussed in the light of substrate availability and Km values.

    PMID: 8225562 [PubMed - indexed for MEDLINE]

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    Life Sci. 2004 Feb 13;74(13):1691-700. Related Articles, Links

    Inhibition of xanthine oxidase by phytic acid and its antioxidative action.

    Muraoka S, Miura T.

    Department of Biochemistry, Hokkaido College of Pharmacy, Katsuraoka-cho 7-1, 047-0264, Otaru, Japan

    We examined if phytic acid inhibits the enzymatic superoxide source xanthine oxidase (XO). Half
    inhibition of XO by phytic acid (IC(50)) was about 30 mM in the formation of uric acid from
    xanthine, but generation of the superoxide was greatly affected by phytic acid; the IC(50) was about
    6 mM, indicating that the superoxide generating domain of XO is more sensitive to phytic acid. The
    XO activity in intestinal homogenate was also inhibited by phytic acid. However, it was not observed
    with intestinal homogenate that superoxide generation was more sensitive to phytic acid compared
    with the formation of uric acid as observed with XO from butter milk. XO-induced superoxide-
    dependent lipid peroxidation was inhibited by phytic acid, but not by myo-inositol. Reduction of ADP-
    Fe(3+) caused by XO was inhibited by superoxide dismutase, but not phytic acid. The results suggest
    that phytic acid interferes with the formation of ADP-iron-oxygen complexes that initiate lipid
    peroxidation. Both phytic acid and myo-inositol inhibited XO-induced superoxide-dependent DNA
    damage. Mannitol inhibited the DNA strand break. Myo-inositol may act as a hydroxyl radical
    scavenger. The antioxidative action of phytic acid may be due to not only inhibiting XO, but also
    preventing formation of ADP-iron-oxygen complexes.

    PMID: 14738912 [PubMed - in process]

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