Abstract
Vitamin E (α-tocopherol) is a potent peroxyl radical scavenger. According to the oxidative theory
of atherosclerosis, it prevents oxidation of low-density lipoprotein (LDL) and thereby
lowers the risk of cardiovascular disease. It also mediates cell actions, and specifically
decreases monocyte superoxide anion-production (O2--production), which is involved in LDL oxidation. We investigated whether α-tocopherol-containing LDL decreases this production in a manner dependent on the
LDL α-tocopherol content (the α-tocopherol/apoB molar ratio) in human, phorbol ester-stimulated, adherent monocytes.
We found that O2--production was inhibited by native LDL (n-LDL) in a manner highly sensitive to the
increasing α-tocopherol content (range 4.5–8). In addition: (1) inhibition was greater when α-tocopherol was associated to acetylated LDL (ac-LDL), the maximal percentage of inhibition
being 80% as opposed to 35% for n-LDL; (2) the α-tocopherol overloading of either form of LDL did not produce further inhibition;
(3) the free form of α-tocopherol produced lower inhibition compared with the lipoprotein-associated forms;
(4) inhibition was not related to the cell content of α-tocopherol. We propose that the cell targeting of α-tocopherol is crucial to the inhibition of monocyte O2−-production, and thus that the role of normal LDL-α-tocopherol contents (range 6–8) in the prevention of atherogenic processes needs
to be reexamined.
Keywords
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Article info
Publication history
Accepted:
January 8,
1998
Received in revised form:
December 16,
1997
Received:
September 15,
1997
Identification
Copyright
© 1998 Elsevier Science Ireland Ltd. Published by Elsevier Inc. All rights reserved.