Prooxidant activity of caffeic acid, dietary non‐flavonoid phenolic acid, on Cu2+‐induced low density lipoprotein oxidation
Naoki Yamanaka, Osamu Oda, Seiji Nagao
Abstract
Naoki Yamanaka, Osamu Oda, Seiji Nagao
Abstract
The effects of caffeic acid (CA) and chlorogenic acid (CHA), an ester of caffeic acid with quinic acid, were studied on isolated human Cu2+-induced low density lipoprotein (LDL) oxidation in initiation and propagation phases by measuring the formation of thiobarbituric acid reactive substances (TBARS), detecting conjugated diene and investigating the electrophoretic mobility change of LDL. Both non-flavonoids exhibited prooxidant and antioxidant activities depending on the LDL oxidation phases. CA and CHA (0.1 microM or more) enhanced LDL oxidation in the propagation phase. In agreement with previous findings, 0.5 microM CA and CHA inhibited LDL oxidation in the initiation phase. When 0.5 microM CA was added at 0 min, the duration of inhibition was about 60 min. Yet, after >9 min incubation with Cu2+, 0.5 microM CA accelerated LDL oxidation. The acceleration ratios were modified depending on the oxidation process and the concentration of added CA in the propagation phase. The maximum acceleration ratio was about 5 on addition of 2-5 microM CA, attained after 40 min incubation with Cu2+. Even in the propagation phase, an elevated concentration of CA inhibited oxidation; after 20 min incubation with Cu2+, CA at >3 microM functioned as an inhibitor. Further studies must be performed in order to clarify the counteracting deleterious prooxidant conditions of these widespread natural dietary compounds.
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The effects of caffeic acid (CA) and chlorogenic acid (CHA), an ester of caffeic acid with quinic acid, were studied on isolated human Cu2+-induced low density lipoprotein (LDL) oxidation in initiation and propagation phases by measuring the formation of thiobarbituric acid reactive substances (TBARS), detecting conjugated diene and investigating the electrophoretic mobility change of LDL. Both non-flavonoids exhibited prooxidant and antioxidant activities depending on the LDL oxidation phases. CA and CHA (0.1 microM or more) enhanced LDL oxidation in the propagation phase. In agreement with previous findings, 0.5 microM CA and CHA inhibited LDL oxidation in the initiation phase. When 0.5 microM CA was added at 0 min, the duration of inhibition was about 60 min. Yet, after >9 min incubation with Cu2+, 0.5 microM CA accelerated LDL oxidation. The acceleration ratios were modified depending on the oxidation process and the concentration of added CA in the propagation phase. The maximum acceleration ratio was about 5 on addition of 2-5 microM CA, attained after 40 min incubation with Cu2+. Even in the propagation phase, an elevated concentration of CA inhibited oxidation; after 20 min incubation with Cu2+, CA at >3 microM functioned as an inhibitor. Further studies must be performed in order to clarify the counteracting deleterious prooxidant conditions of these widespread natural dietary compounds.
Key concepts: Caffeic acid, Chemistry, TBARS, Chlorogenic acid, Antioxidant, Low-density lipoprotein, Flavonoid, Thiobarbituric acid