Abstract:
:An accelerated accumulation of advanced glycation end products (AGEs) occurs in diabetes secondary to the increased glycemic burden. In this study, we investigated the contribution of AGEs to intravascular oxidant stress by examining their action on the neutrophil burst of reactive oxygen species (ROS); this may be a significant donor to the overall vascular redox status and to vasculopathy. AGEs exerted a dose-dependent enhancement on the neutrophil respiratory burst in response to a secondary mechanical stimulus (up to 265 +/- 42%, P = 0.022) or chemical stimulation with formyl-methylleucylphenylalanine 100 nmol/l (up to 218 +/- 19%, P < 0.001), although they possessed no ability to augment the neutrophil respiratory burst alone. This phenomenon was both immediate and reversible and depended on the simultaneous presence of AGEs with the additional stimulus. It appeared to work through an upregulation of the neutrophil NADPH oxidase, the enzyme responsible for ROS generation, as seen by a diphenyleneiodonium-dependent suppression of basal and augmented ROS output. Moreover, this action of AGEs was found to be complementary to that of neutrophil priming agents, also known to upregulate neutrophil ROS production, implying the presence of distinct intracellular transduction pathways mediating the effect of these two classes of agents.
journal_name
Diabetesjournal_title
Diabetesauthors
Wong RK,Pettit AI,Davies JE,Ng LLdoi
10.2337/diabetes.51.9.2846subject
Has Abstractpub_date
2002-09-01 00:00:00pages
2846-53issue
9eissn
0012-1797issn
1939-327Xjournal_volume
51pub_type
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