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Is ceruloplasmin an important catalyst for S-nitrosothiol generation in hypercholesterolemia?

P Moriel1, I R Pereira, M C Bertolami

  • 1Universidade de São Paulo, Faculdade de Ciências Farmacêuticas, Av. Prof. Lineu Prestes, 580, Cidade Universitária-Butantã, 05508-900 São Paulo, Brazil.

Free Radical Biology & Medicine
|February 13, 2001
PubMed
Summary
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In hypercholesterolemia, elevated ceruloplasmin may increase S-nitrosothiols (RSNOs), which are nitric oxide (NO) reservoirs. This suggests impaired NO bioactivity is not due to low RSNOs but superoxide radical activity.

Area of Science:

  • Biochemistry
  • Cardiovascular Research
  • Oxidative Stress

Background:

  • Nitric oxide (NO) is crucial for vascular health, but its activity is impaired in hypercholesterolemia.
  • S-nitrosothiols (RSNOs) serve as NO reservoirs, releasing NO via homolytic cleavage.
  • Ceruloplasmin is implicated in catalyzing RSNO production.

Purpose of the Study:

  • To investigate the relationship between ceruloplasmin and RSNO concentrations in hypercholesterolemic (HC) patients compared to normolipidemic (N) controls.
  • To explore the implications of these findings for NO bioactivity in hypercholesterolemia.

Main Methods:

  • Plasma samples from HC patients and N controls were analyzed.
  • Concentrations of ceruloplasmin, nitrate, RSNOs, nitrated LDL, cholesteryl ester-derived hydroxy/hydroperoxides (CEOOH), and nitrite were measured.

Related Experiment Videos

  • Correlations between these markers and lipid profiles (total cholesterol, LDL cholesterol, apoB, apoE) were assessed.

    • Main Results:

    • HC patients exhibited significantly higher plasma concentrations of ceruloplasmin, nitrate, RSNOs, nitrated LDL, and CEOOH compared to N controls.
    • No significant difference in nitrite levels was observed between the groups.
    • RSNOs, nitrate, and nitrated LDL positively correlated with total cholesterol, LDL cholesterol, and apoB.
    • Ceruloplasmin levels directly correlated with apoB and apoE concentrations.

    Conclusions:

    • Ceruloplasmin may contribute to the increased RSNO levels observed in hypercholesterolemia.
    • The diminished NO bioactivity in hypercholesterolemia is unlikely due to a lack of RSNOs or impaired NO release from them.
    • Elevated nitrotyrosine levels in HC suggest superoxide radicals play a role in NO inactivation, whether endogenously generated or from RSNO decomposition.