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  • Title: Antioxidant supplementation improves platelet membrane fluidity in idiopathic retinal periphlebitis (Eales' disease).
    Author: Saxena S, Srivastava P, Khanna VK.
    Journal: J Ocul Pharmacol Ther; 2010 Dec; 26(6):623-6. PubMed ID: 20973744.
    Abstract:
    PURPOSE: Oxidative damage to cellular membranes plays an important role in the pathobiology of tissue injury. Retinal photoreceptors and platelets are an easy target of oxidants because of high proportion of polyunsaturated fatty acids. A tertiary-care center-based prospective study was undertaken to study the effect of antioxidant supplementation over membrane fluidity in platelets in idiopathic retinal periphlebitis (Eales' disease) for the first time. METHODS: Assay of thiobarbituric acid reactive substances (TBARS) levels was done following a standard protocol and membrane fluidity in platelets was estimated using a fluorescent probe, 1,6-diphenyl-1,3,5-hexatrience, in 15 cases and 12 healthy controls. Prednisolone (1 mg/kg) in a weekly tapering dose for 6 weeks and a commercially available antioxidant preparation [lutein 3.2 mg (containing zeaxanthin 256 mcg), L-glutathione 5 mg, vitamin E 15 IU, vitamin C 150 mg, zinc 40 mg, copper 2 mg, selenium 40 mcg, and manganese 5 mg] was administered once a day for 3 months to all the cases. Pre- and postantioxidant supplementation platelet TBARS and membrane fluidity levels were assessed in all the cases. RESULTS: Significant increase was observed in TBARS levels in the cases when compared with controls (P = 0.01). Platelet fluorescence polarization was significantly higher in cases, indicating decreased membrane fluidity, when compared with controls (P = 0.005). Antioxidant supplementation led to marked decrease in TBARS levels (P = 0.01) and improved levels of platelet membrane fluidity (P = 0.001). CONCLUSION: Antioxidant supplementation leads to significant decrease in oxidative stress and a significant improvement in platelet membrane fluidity, thereby helping to prevent retinal photoreceptor dysfunction.
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