Cataract risk factors: blood level of antioxidative vitamins, reduced glutathione and malondialdehyde in cataractous patients.

T Libondi, C Costagliola, M Della Corte, F Facchiano, M Menzione, S Savastano, F Simonelli, E Rinaldi, G Auricchio
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Abstract

Since many years experimental evidences have suggested an association between nutrition and lens opacities. A dietary deficiency of antioxidants and reactive oxygen scavengers may be involved in the pathogenesis of the "idiopathic" human senile cataract, as it has been demonstrated in some experimental cataracts. We tested the levels of ascorbic acid (vit. C), alpha-tocopherol (vit. E), reduced glutathione (GSH) and malondialdehyde (MDA) in the plasma or in the red blood cells (RBC) of 42 patients who were affected by surgically significant cataract and of 40 age-matched controls. Plasma vit. C mean level was 4.46 gamma/ml in cataracts and 4.62 gamma/ml in controls, while vit. E level was 7.70 and 7.09 gamma/ml respectively. RBC GSH was found to be 342 gamma/ml in cataracts and 346 in controls, while the MDA content was 4.06 picoMol/ml and 4.08 picoMol/ml respectively. The level of each tested nutrient or metabolite was not found to be statistically different between cataractous patients and controls, nor any significant trend was found to be present when the nutrients and metabolites were correlated to each other. Our results do not support the hypothesis of a nutritional deficiency in human senile cataracts. However, a defect in the antioxidative metabolism pathways could be present either systemically or at lens level.

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白内障危险因素:白内障患者血液中抗氧化维生素、还原性谷胱甘肽和丙二醛水平。
多年来,实验证据表明营养与晶状体混浊之间存在关联。饮食中缺乏抗氧化剂和活性氧清除剂可能与“特发性”人类老年性白内障的发病机制有关,这已在一些实验性白内障中得到证实。我们测试了抗坏血酸(维生素d)的水平。C), α -生育酚(维生素C);E),血浆或红细胞(RBC)中的还原型谷胱甘肽(GSH)和丙二醛(MDA) 42例手术显著性白内障患者和40例年龄匹配对照。等离子维特。白内障患者C平均水平为4.46 γ /ml,对照组为4.62 γ /ml。E水平分别为7.70和7.09 γ /ml。白内障患者红细胞GSH为342 γ /ml,对照组为346 γ /ml, MDA含量分别为4.06 picoMol/ml和4.08 picoMol/ml。在白内障患者和对照组之间,各被测营养物或代谢物的水平没有统计学差异,当营养物和代谢物相互关联时,也没有发现任何显著的趋势。我们的结果不支持营养缺乏的假设在人类老年性白内障。然而,抗氧化代谢途径的缺陷可能存在于全身或晶状体水平。
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