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Related Experiment Videos

Superoxide and peroxynitrite in atherosclerosis

C R White1, T A Brock, L Y Chang

  • 1Department of Medicine, University of Alabama, Birmingham 35294.

Proceedings of the National Academy of Sciences of the United States of America
|February 1, 1994
PubMed
Summary
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Reactive oxygen species contribute to atherosclerosis by impairing vascular reactivity. Delivering superoxide dismutase (SOD) via liposomes improved nitric oxide function and reduced oxidative stress in cholesterol-fed rabbits.

Area of Science:

  • Biochemistry
  • Vascular Biology
  • Oxidative Stress

Background:

  • Atherosclerosis involves vascular pathology linked to reactive oxygen species.
  • Impaired vascular reactivity may stem from nitric oxide (.NO) reacting with superoxide (O2-) to form peroxynitrite (ONOO-).

Purpose of the Study:

  • To investigate the role of reactive oxygen species in atherosclerosis.
  • To test if impaired vascular reactivity is caused by .NO and O2- interaction.
  • To evaluate the therapeutic potential of superoxide dismutase (SOD) delivery.

Main Methods:

  • Femoral artery contractility studies in cholesterol-fed rabbits.
  • Utilized pH-sensitive liposomes for targeted delivery of CuZn SOD.
  • Assessed acetylcholine-induced relaxation and performed quantitative immunocytochemistry.

Related Experiment Videos

  • Measured SOD activity in vessel homogenates and lipoprotein oxidation markers.
  • Main Results:

    • Cholesterol feeding impaired acetylcholine-induced relaxation.
    • Liposomal SOD delivery significantly augmented relaxation in cholesterol-fed rabbits.
    • Enhanced SOD distribution and activity were observed in treated vessels.
    • Peroxynitrite induced oxidation of beta very low density lipoprotein.

    Conclusions:

    • The reaction between O2- and .NO contributes to atherosclerotic disease development.
    • This reaction generates peroxynitrite, a mediator of lipoprotein oxidation.
    • It also limits .NO-mediated stimulation of vascular smooth muscle guanylate cyclase.