It has been shown that patients with diabetes mellitus have increased oxidative stress and impaired antioxidant defense system which appears to be a contributory factor for initiation and progression of complications in diabetes.

Many in vitro and in vivo studies showed that several parameters of red blood cell function and integrity are negatively affected by increased oxidative stress. However, data referring to modifications of erythrocyte energy metabolism under these conditions are not abundant and thus it is not very clear which metabolites and hence enzymes are more sensitive to oxidative stress in diabetes.

Nucleotide and glutathione determinations are widely accepted measures of cellular energy, antioxidant status and cellular preservation. The role of purine compounds in the matter and energy metabolism is well known. ATP, ADP and AMP are in equilibrium in cells and have definite concentrations, from which it is possible to evaluate cell energy charge, phosphorylation potential (ATP/ADP) and integrity. Nucleosides and free purine bases are products of nucleotide catabolism and provide information about total regulation of purine metabolism. Glutathione has oxidized (GSSG) and reduced (GSH) forms, which reflect redox state and cell defenses against oxygen toxicity. The GSH/GSSG ratio is an index of cell redox modifications. Glutathione is currently evaluated during oxidative stress and is regarded as a major antioxidant.

The metabolism of glutathione and activities of its related enzymes as well as concentration of purine nucleotides were investigated in erythrocytes from diabetic rats.

A decrease in the levels of GSH and an increase in the levels of GSSG were observed in erythrocytes from diabetic rats. The activity of glutathione reductase (GR) was decreased in diabetics, while that of glutathione peroxidase (GPx) did no change. These data suggest that glutathione metabolism is impaired in erythrocytes from diabetics which weaken the defense mechanism against oxidative stress in these subjects.

As under these experimental conditions IMP increased up to 20-fold with respect to the control value, and because there was a massive release of inosine and hypoxanthine, we hypothesized that high IMP and low AMP levels were due to the activation of AMP-deaminase. This study indicated that AMP-deaminase is a highly sensitive enzymatic site responsible for a profound modification of erythrocytes energy metabolism during oxidative stress in diabetes.

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