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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

Summary

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.

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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.
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.