Dose-response comparison of RRR-α-tocopherol and all-racemic α- tocopherol on LDL oxidation

S. Devaraj, B. Adams-Huet, C. J. Fuller, I. Jialal

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

Much data have accrued in support of the concept that oxidation of LDL is a key early step in atherogenesis. The most consistent data with respect to micronutrient antioxidants and atherosclerosis appear to relate to α- tocopherol (AT), the predominant lipid-soluble antioxidant in LDL. There are scant data on the direct comparison of RRR-AT and all-racemic (rac)-AT on LDL oxidizability. Hence, the aim of the present study was to examine the relative effects of RRR-AT and all-rac-AT on plasma antioxidant levels and LDL oxidation in healthy persons in a dose-response study. The effect of RRR- AT and all-rac-AT at doses of 100, 200, 400, and 800 IU/d on plasma and LDL AT levels and LDL oxidation was tested in a randomized, placebo-controlled study of 79 healthy subjects. Copper-catalyzed oxidation of LDL was monitored by measuring the formation of conjugated dienes and lipid peroxides over an 8-hour time course at baseline and again after 8 weeks. Plasma AT, lipid- standardized AT, and LDL AT levels rose in a dose-dependent fashion in both the RRR-AT and all-rac-AT groups compared with baseline. There were no significant differences in plasma, lipid-standardized, and LDL AT levels between RRR-AT and all-rac-AT supplementation at any dose comparison. The lag phases of oxidation were significantly prolonged with doses ≤400 IU/d of RRR-AT and all-rac-AT, as measured by conjugated-dienes assay and at 400 IU/d of RRR-AT and 800 IU/d of both forms of AT by lipid peroxide assay. Again, there were no significant differences in the lag phase of oxidation at each dose for RRR-AT when compared with all-rac-AT. Also, there were no significant differences in LDL oxidation after in vitro enrichment of LDL with RRR-AT and all-rac-AT. Thus, supplementation with either RRR-AT or all- rac-AT resulted in similar increases in plasma and LDL AT levels at equivalent IU doses, and the degree of protection against copper-catalyzed LDL oxidation was only evident at doses ≤400 IU/d for both forms.

Original languageEnglish (US)
Pages (from-to)2273-2279
Number of pages7
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume17
Issue number10
StatePublished - 1997

Fingerprint

Tocopherols
Antioxidants
Lipid Peroxides
Lipids
Copper
Atherosclerosis
oxidized low density lipoprotein
Micronutrients
Healthy Volunteers
Placebos
low density lipoprotein inhibitor

Keywords

  • α-tocopherol
  • All-racemic α-tocopherol
  • LDL oxidation
  • RRR-α-tocopherol

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Dose-response comparison of RRR-α-tocopherol and all-racemic α- tocopherol on LDL oxidation. / Devaraj, S.; Adams-Huet, B.; Fuller, C. J.; Jialal, I.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 17, No. 10, 1997, p. 2273-2279.

Research output: Contribution to journalArticle

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abstract = "Much data have accrued in support of the concept that oxidation of LDL is a key early step in atherogenesis. The most consistent data with respect to micronutrient antioxidants and atherosclerosis appear to relate to α- tocopherol (AT), the predominant lipid-soluble antioxidant in LDL. There are scant data on the direct comparison of RRR-AT and all-racemic (rac)-AT on LDL oxidizability. Hence, the aim of the present study was to examine the relative effects of RRR-AT and all-rac-AT on plasma antioxidant levels and LDL oxidation in healthy persons in a dose-response study. The effect of RRR- AT and all-rac-AT at doses of 100, 200, 400, and 800 IU/d on plasma and LDL AT levels and LDL oxidation was tested in a randomized, placebo-controlled study of 79 healthy subjects. Copper-catalyzed oxidation of LDL was monitored by measuring the formation of conjugated dienes and lipid peroxides over an 8-hour time course at baseline and again after 8 weeks. Plasma AT, lipid- standardized AT, and LDL AT levels rose in a dose-dependent fashion in both the RRR-AT and all-rac-AT groups compared with baseline. There were no significant differences in plasma, lipid-standardized, and LDL AT levels between RRR-AT and all-rac-AT supplementation at any dose comparison. The lag phases of oxidation were significantly prolonged with doses ≤400 IU/d of RRR-AT and all-rac-AT, as measured by conjugated-dienes assay and at 400 IU/d of RRR-AT and 800 IU/d of both forms of AT by lipid peroxide assay. Again, there were no significant differences in the lag phase of oxidation at each dose for RRR-AT when compared with all-rac-AT. Also, there were no significant differences in LDL oxidation after in vitro enrichment of LDL with RRR-AT and all-rac-AT. Thus, supplementation with either RRR-AT or all- rac-AT resulted in similar increases in plasma and LDL AT levels at equivalent IU doses, and the degree of protection against copper-catalyzed LDL oxidation was only evident at doses ≤400 IU/d for both forms.",
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T1 - Dose-response comparison of RRR-α-tocopherol and all-racemic α- tocopherol on LDL oxidation

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AU - Jialal, I.

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