James O'reilly

Flavonoids Protect against Oxidative Damage to LDL In Vitro: Use in Selection of a Flavonoid Rich Diet and Relevance to LDL Oxidation Resistance Ex Vivo?

The ability of a range of dietary flavonoids to inhibit low-density lipoprotein (LDL) oxidation in vitro was tested using a number of different methods to assess oxidative damage to LDL. Overall quercetin was the most effective inhibitor of oxidative damage to LDL in vitro. On this basis, a diet enriched with onions and black tea was selected for a dietary intervention study that compared the effect on the Cu2+ ion-stimulated lag-time of LDL oxidation ex vivo in healthy human subjects of a high flavonoid diet compared with a low flavonoid diet. No significant difference was found in the Cu2+ ion-stimulated lag-time of LDL oxidation ex vivo between the high flavonoid and low flavonoid dietary treatments (48 ± 1.6 min compared to 49 ± 2.1 min).

Effect of dietary quercetin on oxidative DNA damage in healthy human subjects.

The effect of dietary intake of flavonols (predominantly quercetin) on oxidative DNA damage was studied in thirty-six healthy human subjects (sixteen men, twenty women). The study was a randomised crossover study, comprising two 14 d treatments of either a low-flavonol (LF) or high-flavonol (HF) diet with a 14 d wash-out period between treatments. Subjects were asked to avoid foods containing flavonols, flavones and flavanols during the LF dietary treatment period and to consume one 150 g onion (Allium cepa) cake (containing 89.7 mg quercetin) and one 300 ml cup of black tea (containing 1.4 mg quercetin) daily during the HF dietary treatment. A 7 d food diary was kept during each dietary period and blood samples were taken after each dietary treatment. Products of oxidative damage to DNA bases were measured in DNA from leucocytes. The study had more than 95% power to detect a change of 20% in DNA damage products Plasma vitamin C and plasma quercetin concentrations were also measured. No significant differences in intake of macronutrients or assessed micronutrients, measured DNA base damage products, or plasma vitamin C were found between the HF and LF dietary treatments. The plasma quercetin concentration was significantly higher after the HF dietary treatment period (228.5 (SEM 34.7) nmol/l) than after the LF dietary treatment period (less than the limit of detection, i.e. <66.2 nmol/l). These findings do not support the hypothesis that dietary quercetin intake substantially affects oxidative DNA damage in leucocytes.