Plasma LDL and HDL Subspecies Are Heterogenous in Particle Content of Tocopherols and Oxygenated and Hydrocarbon Carotenoids

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Abstract
Epidemiological data indicate that dietary tocopherols and carotenoids can exert cardioprotective effects, which may be mediated by their antioxidant actions. The oxidative modification of LDL underlies the atherogenicity of these cholesterol-rich particles. The resistance of LDL to oxidation is influenced by several endogenous factors, among which the content of tocopherols and carotenoids is prominent. Of the exogenous factors, HDL inhibits oxidation of LDL via several mechanisms. In view of the paucity of data on the distribution of diverse tocopherol and carotenoid components among the apoB- and apoA-I–containing lipoproteins of human plasma, we evaluated the quantitative and qualitative features of the LDL and HDL particle subspecies in normolipidemic subjects. The bulk of tocopherols and hydrocarbon carotenoids (lycopene, α- and β-carotene) was transported in LDL (45% and 76%, respectively), in contrast to the oxygenated carotenoids (lutein/zeaxanthin, canthaxanthin, and β-cryptoxanthin), which were equally distributed between LDL and HDL. α-Tocopherol content was independently associated with lipid core size (cholesteryl ester and triglyceride) in VLDL, LDL, and HDL (P<.005); by contrast, the particle content of the oxygenated carotenoids lutein/zeaxanthin and canthaxanthin was strongly related to that of phospholipids. A significant and progressive decrease in the molar content of α- and γ-tocopherols was found with increase in density from light to dense LDL subspecies (LDL1 to LDL5); a similar trend was observed in HDL subspecies. Furthermore, particle contents of lutein/zeaxanthin, β-cryptoxanthin, β-carotene, and lycopene were markedly reduced in small, dense LDL (LDL5, d=1.050 to 1.065 g/mL). We conclude that diminished contents in such carotenoids as well as in tocopherols could underlie not only the diminished oxidative resistance of small, dense LDL but also reduced tissue targeting of antioxidants in subjects with a dense LDL phenotype.

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