title: An altered oxidant defense system in red blood cells affects their ability to release nitric oxide-stimulating ATP.
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.
authors.affiliation: Department of Chemistry, Wayne State University, 5101 Cass Ave., Detroit, MI 48202, USA.
authors.forename: Jamie
authors.initials: J
authors.lastname: Carroll
authors.forename: Madushi
authors.initials: M
authors.lastname: Raththagala
authors.forename: Wasanthi
authors.initials: W
authors.lastname: Subasinghe
authors.forename: Stacy
authors.initials: S
authors.lastname: Baguzis
authors.forename: Teresa
authors.initials: T
authors.lastname: D'amico Oblak
authors.forename: Paul
authors.initials: P
authors.lastname: Root
authors.forename: Dana
authors.initials: D
authors.lastname: Spence
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D016022:Case-Control Studies; D002417:Cattle; D048429:Cell Size; D003687:Dehydroepiandrosterone / Q000494:pharmacology; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D003958:Diamide / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004912:Erythrocytes / Q000473:pathology* / Q000502:physiology*; D005954:Glucosephosphate Dehydrogenase / Q000032:analysis / Q000037:antagonists & inhibitors; D005978:Glutathione / Q000032:analysis / Q000378:metabolism; D006801:Humans; D008297:Male; D008954:Models, Biological; D009569:Nitric Oxide / Q000032:analysis / Q000096:biosynthesis / Q000378:metabolism*; D016877:Oxidants / Q000502:physiology*; D010084:Oxidation-Reduction; D011651:Pulmonary Artery / Q000166:cytology; D011817:Rabbits; D013314:Stress, Mechanical; D013439:Sulfhydryl Reagents / Q000494:pharmacology; D013997:Time Factors
chemical_list: D004791:Enzyme Inhibitors; D016877:Oxidants; D013439:Sulfhydryl Reagents; D003958:Diamide; D009569:Nitric Oxide; D003687:Dehydroepiandrosterone; D000255:Adenosine Triphosphate; D005954:Glucosephosphate Dehydrogenase; D005978:Glutathione