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

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.