J. Nutr. 133:3047-3051, October 2003 1,2 Robert J. Hillstrom, Angela K. Yacapin-Ammons* and Sean M. Lynch3 Department of Biochemistry, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, IL 60515 and * Department of Biology, North Central College, Naperville, IL 60540
3To whom correspondence should be addressed. E-mail: firstname.lastname@example.org.
HDL are susceptible to oxidation, which affects their cardioprotective properties. Although several studies have reported inhibition of HDL oxidation by vitamin E, none has determined the potential protective effect of vitamin C, another important blood antioxidant. We investigated whether vitamin C protects HDL from oxidation by incubating HDL (0.2 g of protein/L) at 37°C with cupric (Cu2+) ions (10 µmol/L) in the absence (control) or presence of vitamin C (20–200 µmol/L).
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In the absence of vitamin C, lipid oxidation in HDL began immediately and proceeded rapidly. Cholesteryl linoleate declined to a minimum, whereas lipid oxidation products (lipid dienes and TBARS) increased to near-maximal levels within 1 h. Vitamin C (50–200 µmol/L) retarded initiation of lipid oxidation for at least 4 h under the same conditions. The ability of vitamin C to preserve the cardioprotective antioxidant function of HDL was also assessed. HDL (0.5 g of protein/L) preincubated with Cu2+ (10 µmol/L) for 2 h in the absence of vitamin C lost antioxidant activity (45.4 ± 6.2% inhibition of LDL oxidation compared with 93.2 ± 3.6% for native HDL, P < 0.05).
The addition of vitamin C (50–200 µmol/L) during preincubation of HDL with Cu2+, however, resulted in no significant loss of HDL antioxidant activity (77.3 ± 0.3 to 89.8 ± 5.4% inhibition of LDL oxidation, P > 0.05 compared with native HDL). Our results demonstrate that vitamin C inhibits lipid oxidation in HDL and preserves the antioxidant activity associated with this lipoprotein fraction.
© 2003 The American Society for Nutritional Sciences