Title of article :
Abnormalities of Retinal Metabolism in Diabetes or Experimental Galactosemia. IV. Antioxidant Defense System
Author/Authors :
Renu A. Kowluru، نويسنده , , Timothy S. Kern، نويسنده , , Ronald L. Engerman، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1997
Pages :
6
From page :
587
To page :
592
Abstract :
Activities of enzymes that protect the retina from reactive oxygen species were investigated in experimentally diabetic rats and experimentally galactosemic rats, two animal models known to develop vascular lesions consistent with diabetic retinopathy. Diabetes or experimental galactosemia of 2 months duration significantly decreased the activities of glutathione reductase and glutathione peroxidase in the retina while having no effect on the glutathione synthesizing enzymes glutathione synthetase and γ-glutamyl cysteine synthetase. Activities of two other important antioxidant defense enzymes—superoxide dismutase (SOD) and catalase—also were decreased (by more than 25%) in retinas of diabetic rats and galactosemic rats. Administration of supplemental antioxidants, vitamins C and E, for the 2 months prevented the diabetes-induced impairment of antioxidant defense system in the retina. In experimentally galactosemic rats, the supplemental antioxidants were not as effective: SOD activity was normalized, but the enzymes of the glutathione redox cycle were only partly restored, and the subnormal catalase activity was unaffected. Diabetes or experimental galactosemia results in significant impairment of the antioxidant defense system in the retina, and exogenous antioxidant supplementation can help alleviate the subnormal activities of antioxidant defense enzymes. Copyright © 1997 Elsevier Science Inc.
Keywords :
free radicals , antioxidant , glutathione , Hyperglycemia , oxidative stress , catalase , Diabetes , Retina , superoxide dismutase
Journal title :
Free Radical Biology and Medicine
Serial Year :
1997
Journal title :
Free Radical Biology and Medicine
Record number :
517517
Link To Document :
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