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Prolonged, low dose alpha-tocopherol therapy counteracts intercellular cell adhesion molecule-1 activation
Giovambattista Desideri1, Giuseppe Croce, Maria Contina Marinucci
1Department of Internal Medicine and Public Health, University of L'Aquila, Blocco 11-Via Vetoio, 67100 Coppito, Aquila, Italy. gbdesi@iol.it
Summary
Low-dose alpha-tocopherol supplementation significantly reduced soluble intercellular adhesion molecule-1 (sICAM-1) levels in healthy men. This antioxidant effect may help prevent early stages of atherosclerosis.
Area of Science:
- Cardiovascular Research
- Nutritional Science
- Vascular Biology
Background:
- Intercellular Adhesion Molecule-1 (ICAM-1) up-regulation promotes atherosclerosis development.
- Soluble ICAM-1 (sICAM-1) is a biomarker for endothelial activation.
- Understanding factors influencing sICAM-1 in healthy individuals is crucial for preventive cardiology.
Purpose of the Study:
- To investigate the effect of low-dose alpha-tocopherol on circulating sICAM-1 levels in healthy subjects.
- To determine if alpha-tocopherol supplementation can modulate endothelial activation markers.
Main Methods:
- A randomized, double-blind, placebo-controlled trial was conducted.
- 39 healthy male volunteers received either alpha-tocopherol (50 I.U./day) or placebo for 20 weeks.
- Plasma sICAM-1 and alpha-tocopherol concentrations were measured at baseline and after 20 weeks.
Main Results:
- Baseline sICAM-1 levels were inversely correlated with alpha-tocopherol concentrations.
- Alpha-tocopherol supplementation significantly decreased sICAM-1 levels (p<0.004) and increased alpha-tocopherol levels (p<0.003).
- No significant changes were observed in the placebo group; changes in sICAM-1 correlated inversely with changes in alpha-tocopherol (r=-0.597, p=0.005).
Conclusions:
- Plasma sICAM-1 concentrations are stable in healthy individuals over 20 weeks.
- Low-dose alpha-tocopherol effectively reduces circulating sICAM-1 levels in healthy men.
- Antioxidant vitamins like alpha-tocopherol may counteract endothelial changes contributing to atherogenesis.