Antioxidant activity from extra virgin olive oil via inhibition of hydrogen peroxide-mediated NADPH-oxidase 2 activation.

Abstract

Extra virgin olive oil (EVOO) supplementation is associated with a significant reduction in cardiovascular disease but the underlying mechanism is still unclear. In platelets that were taken from healthy subjects (n = 5), agonist-induced hydrogen peroxide (H2O2) production and NADPH oxidase 2 (NOX2) activation in the presence of or without catalase, which catabolizes H2O2, were investigated. Platelet H2O2 production, NOX2 activation, EVOO vitamin E, and total polyphenols as well as EVOO's ability to scavenge H2O2 were also measured. Platelet NOX2 activation and H2O2 production were significantly inhibited in catalase-treated platelets and platelets that were incubated with five different EVOOs. The EVOO content of vitamin E was 53 to 223 mg/kg and total polyphenols 145 to 392 mg/L Gallic acid equivalent. EVOOs quenched in vitro H2O2 by 39 to 62%, which is an effect that is significantly correlated with vitamin E and total polyphenol concentrations (R = 0.688; P <0.001 and R = 0.541; P <0.001, respectively). This in vitro study provides the first evidence that EVOO downregulates platelet H2O2 and in turn NOX2 activity via H2O2 scavenging.