Investigations on the correlation of advanced glycated end products (AGE) associated fluorescence with blood glucose and oxidative stress in ethanol-administered diabetic rats.

Diabetes mellitus and alcoholism are two well-known agents causing pathological complications in the body. Both cause oxidative stress and derangements in glucose homeostasis. Advanced glycated end products (AGEs) are formed in hyperglycemia and can cause pathological changes. In this study, we investigated the relationship between AGE-associated fluorescence, in serum, tail tendon collagen, and eye lens with blood glucose and serum malondialdehyde (MDA) in alcohol administered diabetic rats. Blood glucose and glycated hemoglobin (HbA(1)C) decreased in ethanol-administered diabetic rats. Elevated AGE-associated fluorescence in serum, eye lens and tail tendon collagen were observed in alcoholic diabetic rats in spite of the reduced blood glucose levels compared to other groups. AGE-associated fluorescence correlated positively with serum MDA than with blood glucose. Up-regulation of the nuclear translocation of NFkappaB was more profound in the ethanol-administered diabetic group indicating the development of pathological complications. This indicates that the toxicity induced by diabetes has been potentiated in alcohol administered diabetic rats. Our histopathological studies also reinforce our findings. Hence serum AGE-linked fluorescence has the potential to be developed as a surrogate biomarker for oxidative stress. Copyright 2009 Elsevier GmbH. All rights reserved.