vE: The two faces of ?- and ?-tocopherols: VLDL, LDL and HDL oxidation

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The *two* *faces* of ?- and ?-tocopherols: an in *vitro* and *ex* *vivo*

*investigation* into *VLDL*, *LDL* and *HDL* *oxidation*.

<http://www.ncbi.nlm.nih.gov/pubmed/21715151>

Nadeem N, Woodside JV, S, Allister R, Young IS, McEneny J.

J Nutr Biochem. 2011 Jun 27

BACKGROUND:

Vitamin E and its derivatives, namely, the tocopherols, are known

antioxidants, and numerous clinical trials have investigated their role

in preventing cardiovascular disease; however, evidence to date remains

inconclusive. Much of the in vitro research has focused on tocopherol's

effects during low-density lipoprotein (LDL) oxidation, with little

attention being paid to very LDL (VLDL) and high-density lipoprotein

(HDL). Also, it is now becoming apparent that ?-tocopherol may

potentially be more beneficial in relation to cardiovascular health.

OBJECTIVES:

Do ?- and ?-tocopherols become incorporated into VLDL, LDL and HDL and

influence their oxidation potential in an in vitro and ex vivo situation?

DESIGN:

Following (i) an in vitro investigation, where plasma was preincubated

with increasing concentrations of either ?- or ?-tocopherol and (ii) an

in vivo 4-week placebo-controlled intervention with ?- or ?-tocopherol.

Tocopherol incorporation into VLDL, LDL and HDL was measured via

high-pressure liquid chromatography, followed by an assessment of their

oxidation potential by monitoring conjugated diene formation.

RESULTS:

In vitro: Both tocopherols became incorporated into VLDL, LDL and HDL,

which protected VLDL and LDL against oxidation. However and

surprisingly, the incorporation into HDL demonstrated pro-oxidant

properties. Ex vivo: Both tocopherols were incorporated into all three

lipoproteins, protecting VLDL and LDL against oxidation; however, they

enhanced the oxidation of HDL.

CONCLUSIONS:

These results suggest that ?- and ?-tocopherols display conflicting

oxidant activities dependent on the lipoprotein being oxidized. Their

pro-oxidant activity toward HDL may go some way to explain why

supplementation studies with vitamin E have not been able to display

cardioprotective effects.