Eale's disease / iron chelation

Discussion in 'Optometry Archives' started by ironjustice, Feb 24, 2005.

  1. ironjustice

    ironjustice Guest

    Curr Eye Res. 2004 Jun;28(6):399-407. Related Articles, Links

    Iron chelation abrogates excessive formation of hydroxyl radicals and
    lipid peroxidation products in monocytes of patients with Eales'
    disease: direct evidence using electron spin resonance spectroscopy.

    Rajesh M, Sulochana KN, Ramakrishnan S, Biswas J, Manoharan PT.

    Biochemistry Department, Vision Research Foundation, Sankara
    Nethralaya, Chennai, India.

    PURPOSE: Eales' disease (ED) is an idiopathic retinal vasculitis
    condition, which affects the retina of young adult males. Retinal
    changes include perivasculitis, non-perfusion and neovascularization.
    Disruption of blood-retinal barrier (BRB) is the common feature in
    intra-ocular inflammatory diseases. Disruption of BRB results in
    vascular hyper permeability and infiltration of circulating leukocytes
    into the retinal parenchyma. Monocyte (MC) activation results in
    oxidant thrust and subsequent tissue damage. This has been reported in
    various intra-ocular inflammatory diseases such as uveitis and Behcet's
    disease. However, there are no such reports available in ED. Hence in
    the present study we have investigated the role of MC activation and
    hydroxyl radicals (OH) production and its possible involvement in
    promoting the development of retinal vasculitis in patients with ED.
    METHODS: Twelve patients with ED and twelve healthy volunteers were
    recruited for the study. MC was separated from their peripheral blood.
    MC from patients with ED and control subjects was stimulated with
    phorbol-12-myristate-acetate (PMA) and OH generated was analyzed using
    an electron spin resonance spectrometer (ESR). Superoxide dismutase
    (SOD), thiobarbituric acid reactive substances (TBARS), and iron
    content was determined in MC to assess the oxidant thrust and
    antioxidant defense. RESULTS: OH generation was elevated in MC from
    patients with ED, which coincided with diminished SOD activity and
    elevated levels of iron and TBARS, when compared with healthy control
    subjects. OH generation was abrogated when MC from ED were co-incubated
    with PMA and iron chelators such as diethylenetriaminepentacetic acid
    (DTPA) and desferrioxamine. Iron chelation also inhibited TBARS
    accumulation restored SOD activity in MC of patients with ED.
    CONCLUSIONS: For the first time we have demonstrated the production of
    OH generation in MC of patients with ED using ESR. Further we have
    shown the beneficial effect of iron chelation in mitigating free
    radical mediated changes in cellular metabolism. Based on our findings,
    we provide further evidence for the role of oxidant thrust in promoting
    retinal tissue damage in patients with ED.

    PMID: 15512947 [PubMed - indexed for MEDLINE]

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    ironjustice, Feb 24, 2005
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