Plasmalogens as a marker of elevated systemic oxidative stress in Parkinson's disease.

Experimental evidence indicates a significant role of oxidative stress in the pathogenesis of idiopathic Parkinson’s disease (PD). However, some studies report no decrease in common antioxidants in blood plasma as a marker of oxidative stress (1). The aim of this study was to estimate plasmalogen levels in blood plasma samples of patients with PD, a group of 1-alkenyl-2-acyl-sn-glycero-3-phospholipids considered to be a sensitive surrogate marker of oxidative stress. The precise role played by plasmalogen phospholipids of lipoproteins and cell membranes is not well understood. Considerable attention has been focused on the role of plasmalogens as a source of lipid mediators, based on the activity of calcium-independent phospholipase A2 which was shown to catalyze the hydrolysis of arachidonic acid located at the sn2 position of plasmalogens (2). However, plasmalogen status appears to have no influence on stimulated arachidonic acid release in plasmalogendeficient macrophages (3). In addition, plasmalogens can act directly as endogenous antioxidants in defending cell membranes and lipoproteins from reactive radical species. This is accomplished primarily by means of the radical scavenging activity of their vinyl ether bond at the sn1 position (2, 4–6). The present study describes plasmalogen-derived hexadecanal dimethyl acetal (16:0 DMA) concentrations in blood plasma total phospholipid samples from patients with PD, and from age-matched control sub-