Lysophosphatidylcholine Enhances Superoxide Anions Production via Endothelial NADH/NADPH Oxidase

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  • Takeshita Saori
    First Department of Internal Medicine, Kobe University School of Medicine
  • Inoue Nobutaka
    First Department of Internal Medicine, Kobe University School of Medicine
  • Gao Dayaun
    Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University
  • Rikitake Yoshiyuki
    First Department of Internal Medicine, Kobe University School of Medicine
  • Kawashima Seinosuke
    First Department of Internal Medicine, Kobe University School of Medicine
  • Tawa Riichi
    Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University
  • Sakurai Hiromu
    Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University
  • Yokoyama Mitsuhiro
    First Department of Internal Medicine, Kobe University School of Medicine

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Abstract

Reactive oxygen species (ROS) including superoxide anions (O2-) play a key role in atherogenesis, and endothelial cells have the ability to generate ROS. To investigate the enzymatic sources of ROS and the effects of lysophosphatidylcholine (LPC), an atherogenic lipid, we measured ROS production in cultured bovine aortic endothelial cells (BAECs) by the lucigenin-enhanced chemiluminescence (CL) method and electron spin resonance (ESR). BAEC homogenates had the enzymatic activity of NADH/NADPH oxidase. BAECs cultured on microcarrier beads generated O2- under basal conditions. The inhibition of NADH/ NADPH oxidase by diphenylene iodonium (DPI) significantly attenuated O2- production, whereas no inhibitors of other oxidases suppressed it. Although LPC enhanced O2 production approximately 3.1-fold, its action was suppressed by DPI. Tyrosine kinase inhibitors significantly attenuated LPC-induced O2- production. ESR with DMPO demonstrated that LPC increased the formation of the DMPO-hydroxyl adduct in dose- and time-dependent manners. These data suggest that the basal production of O2- in endothelial cells is mainly mediated by the NADH/NADPH oxidase system and that LPC activates this oxidase to enhance O2- production through a tyrosine kinase-dependent pathway. The enhancement of ROS production by LPC is probably involved in its atherogenic property.

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