Influence of Nitric Oxide on Luminol-Enhanced Chemiluminescence Measured from Porcine-Stimulated Leukocytes
- 1 September 1997
- journal article
- research article
- Published by Wolters Kluwer Health in Journal of Cardiovascular Pharmacology
- Vol. 30 (3), 332-337
- https://doi.org/10.1097/00005344-199709000-00010
Abstract
The influence of endogenous nitric oxide (NO) and NO-releasing compounds on free radical release from porcine leukocytes was investigated by luminol-enhanced chemiluminescence (CL). The direct free radical-scavenging activity of the compounds was determined by a cell-free system using xanthine plus xanthine oxidase (X+XO). The NO donor, N-(2-hydroxyethyl)nicotinamide nitrate (nicorandil), markedly inhibited CL generated by phorbol myristate acetate (PMA)-stimulated leukocytes. In addition, nicorandil and S-nitrozo-N-acetylpenicillamine (SNAP) both decreased CL generated by X+XO. Conversely, C87 3754, a NO-releasing sydnonimine, decreased free radical release from leukocytes only when preincubated with the cells and had no effects on the X+XO system. None of the NO donors inhibited peroxynitrite-generated CL. L-, but not D-, arginine inhibited PMA-activated free radical generation without affecting X+XO-induced CL. L-Canavanine, Nω-nitro-L-arginine (L-NNA), and L-nitro-arginine methyl ester (L-NAME), inhibitors of the NO pathway, augmented PMA-induced CL. However, L-canavanine, but not L-NNA and L-NAME, produced a significant inhibition of X+XO-induced CL. It is concluded that endogenous NO may play an important role in the measurement of free radicals released from porcine leukocytes, assessed by luminol-enhanced CL, and that compounds with NO-releasing properties decrease CL, possibly by interfering with free radical generation.Keywords
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