OBJECTIVES: We have examined the effects of in-vivo supplementation with low-dose vitamin E on the susceptibility of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) to oxidative modification, and compared the oxidizability of HDL with that of LDL. METHODS: Normal humans (n = 8) ingested vitamin E (150 mg/day for 1 week, followed by 300 mg/day for 3 weeks) in divided doses with meals. The subjects did not use any medications or vitamins before being enrolled in this study. Fasting blood samples were drawn before and at the end of supplementation. LDL and HDL were separated by sequential ultracentrifugation and susceptability to copper-mediated oxidation was measured. RESULTS: After vitamin E supplementation, vitamin E content of LDL increased 1.9-fold and that of HDL increased 1.8-fold. Lag time before initiation of LDL oxidation lengthened significantly (+20%, p < 0.01), and the propagation rate of LDL decreased significantly (-10%, p < 0.05). The lag time of HDL oxidation did not change significantly, but the propagation rate of HDL oxidation decreased significantly (-24%, p < 0.001). The lag time of HDL oxidation was shorter than that of LDL. HDL contained the same or higher concentrations of vitamin E relative to lipid mass as LDL, but contained lower concentration of CoQ10 relative to lipid mass and fewer molecules of vitamin E and beta-carotene per particle than LDL. CONCLUSIONS: We conclude that in-vivo supplementation of low-dose vitamin E protects LDL against oxidative modification and decreases the propagation rate of HDL oxidation significantly. We suggest that supplementation with low-dose vitamin E would be beneficial for ameliorating atherosclerosis.
OBJECTIVES: We have examined the effects of in-vivo supplementation with low-dose vitamin E on the susceptibility of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) to oxidative modification, and compared the oxidizability of HDL with that of LDL. METHODS: Normal humans (n = 8) ingested vitamin E (150 mg/day for 1 week, followed by 300 mg/day for 3 weeks) in divided doses with meals. The subjects did not use any medications or vitamins before being enrolled in this study. Fasting blood samples were drawn before and at the end of supplementation. LDL and HDL were separated by sequential ultracentrifugation and susceptability to copper-mediated oxidation was measured. RESULTS: After vitamin E supplementation, vitamin E content of LDL increased 1.9-fold and that of HDL increased 1.8-fold. Lag time before initiation of LDL oxidation lengthened significantly (+20%, p < 0.01), and the propagation rate of LDL decreased significantly (-10%, p < 0.05). The lag time of HDL oxidation did not change significantly, but the propagation rate of HDL oxidation decreased significantly (-24%, p < 0.001). The lag time of HDL oxidation was shorter than that of LDL. HDL contained the same or higher concentrations of vitamin E relative to lipid mass as LDL, but contained lower concentration of CoQ10 relative to lipid mass and fewer molecules of vitamin E and beta-carotene per particle than LDL. CONCLUSIONS: We conclude that in-vivo supplementation of low-dose vitamin E protects LDL against oxidative modification and decreases the propagation rate of HDL oxidation significantly. We suggest that supplementation with low-dose vitamin E would be beneficial for ameliorating atherosclerosis.