Abstract
A novel microflow technique is used to demonstrate that a weakened oxidant defense system found in diabetic erythrocytes leads to decreased levels of deformation-induced release of adenosine triphosphate (ATP) from erythrocytes. Addition of an oxidant to rabbit erythrocytes resulted in a 63% decrease in deformation-induced ATP release before eventually recovering to a value that was statistically equivalent to the initial value. Inhibition of glucose-6-phosphate dehydrogenase prevents recovery from the oxidant attack. Finally, results indicated that the ATP release from the erythrocytes of type II diabetics (91 nM +/- 10 nM) was less than half of that measured from the erythrocytes of healthy controls (190 +/- 10 nM). These data suggest that the antioxidant status of erythrocytes is a critical determinant in the ability of these cells to release ATP, a known nitric oxide stimulus.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / metabolism*
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Adenosine Triphosphate / pharmacology
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Animals
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Case-Control Studies
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Cattle
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Cell Size
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Dehydroepiandrosterone / pharmacology
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Diabetes Mellitus, Type 2 / physiopathology
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Diamide / pharmacology
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Dose-Response Relationship, Drug
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Endothelium, Vascular / metabolism
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Enzyme Inhibitors / pharmacology
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Erythrocytes / pathology*
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Erythrocytes / physiology*
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Glucosephosphate Dehydrogenase / analysis
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Glucosephosphate Dehydrogenase / antagonists & inhibitors
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Glutathione / analysis
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Glutathione / metabolism
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Humans
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Male
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Models, Biological
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Nitric Oxide / analysis
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Nitric Oxide / biosynthesis
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Nitric Oxide / metabolism*
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Oxidants / physiology*
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Oxidation-Reduction
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Pulmonary Artery / cytology
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Rabbits
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Stress, Mechanical
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Sulfhydryl Reagents / pharmacology
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Time Factors
Substances
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Enzyme Inhibitors
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Oxidants
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Sulfhydryl Reagents
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Diamide
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Nitric Oxide
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Dehydroepiandrosterone
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Adenosine Triphosphate
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Glucosephosphate Dehydrogenase
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Glutathione