Mechanisms of Ascorbyl Radical Formation in Human Platelet-Rich Plasma. (17th February 2014)

• Record Type: Journal Article
• Authors: Shyu, Kou-Gi; Chang, Chao-Chien; Yeh, Yu-Chieh; Sheu, Joen-Rong; Chou, Duen-Suey
• Other Names: Thomas Philip Aloysius Academic Editor.
• Is Part Of: BioMed research international. Volume 2014(2014)
• Publication Date: 2014-02-17
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2014/614506
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : Recently, many clinical reports have suggested that the ascorbyl free radical (Asc ∙ ) can be treated as a noninvasive, reliable, real-time marker of oxidative stress, but its generation mechanisms in human blood have rarely been discussed. In this study, we used upstream substances, enzyme inhibitors, and free radical scavengers to delineate the mechanisms of Asc ∙ formation in human platelet-rich plasma (PRP). Our results show that the doublet signal was detected in PRP samples by using electron spin resonance, and the hyperfine splitting of the doublet signal was a H = 1.88 gauss and g -factor = 2.00627, which was determined to be the Asc ∙ . We observed that the inhibitors of NADPH oxidase (NOX), cyclooxygenase (COX), lipoxygenase (LOX), cytochrome P450 (CYP450), mitochondria complex III, and nitric oxide synthase (NOS), but not xanthine oxidase, diminished the intensity of the Asc ∙ signal dose dependently. All enzyme inhibitors showed no obvious antioxidant activity during a Fenton reaction assay. In summary, the obtained data suggest that Asc ∙ formation is associated with NOX, COX, LOX, CYP450, eNOS, and mitochondria in human PRP.