DIETARY COENZYME-Q10 SUPPLEMENTATION ALTERS PLATELET SIZE AND INHIBITS HUMAN VITRONECTIN (CD51 CD61) RECEPTOR EXPRESSION/

Improved cardiovascular morbidity and mortality have been observed in several clinical studies of dietary supplementation with coenzyme Q10 (CoQ10, ubiquinone). Several mechanisms have been proposed to explain the effects of CoQ10, but a comprehensive explanation of its cardiopro tective properties is still lacking. One attractive theory links ubiqu inone with the inhibition of platelets. The effect of CoQ10 intake on platelet size and surface antigens was examined in human volunteers. S tudy participants received 100 mg of CoQ10 twice daily in addition to their usual diet for 20 days. Receptor expression was measured by flow cytometry with monoclonal murine anti-human antibodies cD9 (p24), CD4 2B (Ib), CD41b (IIb), CD61 (IIIa), CD41a (IIb/IIIa), CD49b (VLA-2), CD 62p (P selectin), CD31 (PECAM-1), and CD51/CD61 (vitronectin). An incr ease of total serum CoQ10 level (from 0.6+/-0.1 to 1.8+/-0.3 mu g/ml; p <0.001) was found at protocol termination. Fluorescence intensity wa s higher for the large platelets when compared with the whole platelet population. Significant inhibition of vitronectin-receptor expression was observed consistently throughout ubiquinone treatment. Reduction of platelet size was observed at the end of CoQ10 supplementation. Inh ibition of the platelet vitronectin receptor and a reduction of the pl atelet size are direct evidence of a link between dietary CoQ10 intake and platelets. These findings may not be fully explained by the known antioxidant and bioenergetic properties of CoQ10. Diminished vitronec tin-receptor expression and reduced platelet size resulting from CoQ10 therapy may contribute to the observed clinical benefits in patients with cardiovascular diseases.