Sundqvist T, Axelsson K L
Department of Medical Microbiology, Faculty of Health Sciences, University of Linköping, Sweden.
Pharmacol Toxicol. 1993 Mar;72(3):169-74. doi: 10.1111/j.1600-0773.1993.tb00311.x.
The present study was designed to assess the effect of LY83583 on H2O2/O2- production from endothelial cells and neutrophils, as determined by chemiluminiscence generation in vitro. We found that LY83583 increased H2O2/O2-production from endothelial cells, but inhibited the H2O2/O2- production from phorbol myristate acetate-stimulated neutrophils. Furthermore, LY83583 consumed NADPH under certain conditions. Since neutrophils generate superoxide anion radicals via an NADPH-oxidase, we suggest that the reduction of chemiluminiscence, seen after addition of LY83583 to phorbol myristate acetate-stimulated neutrophils, is due to increased consumption of NADPH. In endothelial cells, NADPH is required as a co-factor in the generation of nitric oxide, which may interact with superoxide anion. A consumption in NAPDH would therefore be expected to decrease the production of nitric oxide and increase H2O2/O2-generation. The consumption of NADPH in endothelial cells could also cause reduced scavenger functions of the glutathion system, resulting in a further increase in H2O2 release.
