| tom hennessy 2004-11-02, 7:08 am |
| 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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