Both HDL3 and HDL2 Exert a Powerful Anti-Oxidative and Protective Effect against Acceleration of Oxidative Modification of LDL by Ascorbic Acid

  • SAKUMA Nagahiko
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences
  • SAEKI Tomoaki
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences
  • YAJIMA Kazuhiro
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences
  • HIBINO Takeshi
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences
  • YOSHIDA Takayuki
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences
  • MIZUNO Hiromi
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences
  • MUKAI Seiji
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences
  • SAKATA Seiichiro
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences
  • KUNIMATSU Mitoshi
    Department of Biochemistry, Nagoya Women's University
  • KIMURA Genjiro
    Department of Internal Medicine and Pathophysiology, Nagoya City University Graduate School of Medical Sciences

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The objective of the present study was to establish whether high-density lipo-protein 3 (HDL3) or high-density lipoprotein 2 (HDL2) might show an anti-oxidative effect on the acceleration of the oxidative modification of low-density lipoprotein(LDL) by ascorbic acid from measurement of the agarose gel electrophoretic mobility of LDL. LDL was incu-bated without adding transitional-metal ions for 48 or 96h in phosphate-buffered saline (PBS) alone, with ascorbic acid (20μg/mL), or with both ascorbic acid (20μg/mL) and HDL3 (200μg protein/mL). The LDL autoxidation occurred in PBS alone. Although ascor-bic acid significantly suppressed oxidative modification of LDL after incubation for 48h, the opposite was true after 96h. However, since the anti-oxidative ability of HDL2 shows a weaker tendency than that of HDL3, both HDL3 and HDL2 significantly inhibited this accel-eration of oxidative modification of LDL by ascorbic acid as assessed by electrophoretic mobility. If there is an augmented oxidative modification of LDL due to ascorbic acid in vivo, HDL3 or HDL2 may thus have an important role in inhibiting this ascorbic acid-accelerated oxidation of LDL.

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