© 1995 American Heart Association, Inc.
Articles |
Supplementation With Low Doses of Vitamin E Protects LDL From Lipid Peroxidation in Men and Women
From the Gaubius Laboratory, TNO-PG, and the Department of Cardiology, University Hospital (A. van der L.), Leiden; and TNO Nutrition and Food Research, Zeist (G. van P.), the Netherlands.
Correspondence to Dr Hans M.G. Princen, Gaubius Laboratory, TNO-PG, PO Box 430, 2300 AK Leiden, the Netherlands.
Abstract There is accumulating evidence that oxidative
modification of LDL is an important step in the process of
atherogenesis and that antioxidants may protect LDL from oxidation. We
and others have previously shown that ingestion of pharmacological
doses of the antioxidant D,L-
-tocopherol (vitamin E),
far above the recommended daily intake (ie, 12 to 15 IU/d for adults),
increases the oxidation resistance of LDL. In this study, we
ascertained the minimal supplementary dose of vitamin E necessary to
protect LDL against oxidation in vitro. Twenty healthy volunteers (10
men and 10 women, aged 21 to 31 years) ingested consecutively 25, 50,
100, 200, 400, and 800 IU/d D,L--tocopherol acetate
during six 2-week periods. No changes were observed in LDL triglyceride
content, fatty acid composition of LDL, or LDL size during the
intervention. Concentrations of -tocopherol in plasma and LDL were
both 1.2 times the baseline values after the first period (25 IU/d) and
2.6 and 2.2 times, respectively, after the last period (800 IU/d).
There was a linear increase in LDL -tocopherol levels up to an
intake of 800 IU/d (r=.79, P<.0001) and a good
correlation between -tocopherol in plasma and LDL (r=.66,
P<.0001). Simultaneously, the resistance of LDL to
oxidation was elevated dose-dependently (+28% after the last period)
and differed significantly from the baseline resistance time even after
ingestion of only 25 IU/d. Correlation between -tocopherol
content of LDL and resistance time for all data was r=.57
(P<.0001), whereas the correlation between plasma
-tocopherol and resistance time was r=.69
(P<.0001). The rate of oxidation was decreased
significantly at 400 and 800 IU/d (-13% and -17%, respectively).
Baseline resistance time was not significantly different between men
and women, but propagation rate was higher with LDL from men at
baseline and after intake of 25 and 50 IU/d. Minor differences in LDL
vitamin E levels and resistance time were found between men and women
in response to vitamin E intake. Statistical evaluation of the
relations between -tocopherol content of LDL and resistance time in
each of the 20 individual subjects showed strong and significant
correlations for 14 individuals, indicating that vitamin E was the most
important parameter that determined the oxidation resistance of LDL in
these subjects. ANOVA indicated that LDL -tocopherol content (47%)
and interindividual variation (39%) were the most prominent parameters
that contributed to the total variance in resistance time.
Key Words: LDL oxidation • atherosclerosis • lag time • vitamin E • antioxidants
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