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Author Iron chelation / Eales' disease
doe

2004-11-02, 7:12 pm

Curr Eye Res. 2004;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 K, Ramakrishnan S, Biswas J, Manoharan P.

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 - as supplied by publisher]

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