Abstract 12436: Nox2-Mediated Arterial Dysfunction in Smokers: Effect of Dark Chocolate
Objectives: Cocoa seems to exert arterial dilation via oxidative stress inhibition but the mechanism is still unclear. We investigated whether in smokers dark chocolate elicits arterial dilation via down-regulation of NOX2, the catalytic core of NADPH oxidase.
Methods: Flow mediated dilation (FMD), oxidative stress, as assessed by urinary isoprostanes excretion, nitric oxide (NO) generation, as assessed by serum levels of nitrite/nitrate (NOx), and NOX2 activity as assessed by blood levels of soluble NOX2-dp (sNOX2-dp) and serum epicatechin were studied in 20 smokers and 20 healthy subjects (HS). Patients were randomly allocated to 40 g dark chocolate (>85% cocoa) or 40 g of milk chocolate (<35% cocoa), in a single-blind, crossover design. FMD, urinary isoprostanes excretion, NOx and sNOX2-dp were assessed at baseline and two hours after ingestion of chocolate.
Results: At baseline, smokers had lower FMD and NOx and higher sNOX2-dp compared to HS. After dark chocolate intake, urinary isoprostanes excretion and sNOX2-dp significantly decreased and FMD and NOx significantly increased in smokers but not in HS. No changes of the above variables were observed after milk chocolate intake. Multiple linear regression analysis showed that in smokers the only independent predictive variable associated with delta of FMD was delta of sNOX2-dp. Serum epicatechin increased in either group only after dark chocolate assumption reaching values higher than 0.1µM. Platelets from smokers, but not from HS, showed lower p47phox translocation to platelet membrane and higher NOx when incubated with 0.1-10 µM epicatechin.
Conclusion: This study suggests that in smokers cocoa enhances arterial dilation via lowering NOX2 activation.
- © 2011 by American Heart Association, Inc.