Mechanisms by which flavonol aglycones inhibit lipid oxidation better than glycosylated flavonols in comminuted muscle tissue

Abstract

The effect of glycosylation on the ability of flavonoids to inhibit lipid oxidation in comminuted muscle tissue has not been previously examined. This work examined the ability of quercetin and quercetin-β- d -glucoside to inhibit lipid oxidation in mechanically separated turkey (MST). Quercetin inhibited formation of lipid peroxides and thiobarbituric acid reactive substances (TBARS) more effectively compared to quercetin-β- d -glucoside during frozen storage ( p < 0.05). The possible mechanisms that cause glycosylation to decrease inhibition of lipid oxidation were also examined. Hydroxyl radical scavenging activity was similar when comparing quercetin and quercetin-β- d -glucoside, which indicated that the free hydroxyl group in 3 position of C ring in quercetin did not enhance its hydroxyl radical scavenging ability. Since muscle membrane lipids are susceptible to lipid oxidation, the ability of quercetin and quercetin-β- d -glucoside to incorporate into cellular membranes was studied. After adding quercetin and quercetin-β- d -glucoside to minced chicken muscle, flavonol content in the membrane fraction was determined. Around 32% of added quercetin partitioned into the membranes whereas quercetin-β- d -glucoside was not detected in the membranes. Similar trends were observed when each flavonol was added to isolated membranes. These studies suggest that glycosylation of flavonols weakens their ability to inhibit lipid oxidation in muscle tissue partly by decreasing the amount of flavonols in the membrane phase. In order to understand whether metal chelation by flavonols is a likely mechanism involved in the inhibition of lipid oxidation in MST, the role of endogenous metals in promoting lipid oxidation was examined. Addition of the metal chelators ethylenediamine tetraacetic acid (EDTA) and tetrakis(2-pyridylmethyl) ethylenediamine (TPEN) to MST did not inhibit lipid oxidation, which suggests that endogenous metals present in MST were not promoters of lipid oxidation. Hence it seems unlikely that the mechanism of inhibition by flavonols involved metal chelation in the comminuted muscle.