Journal of Lipid Research, Vol 32, 775-781, Copyright © 1991 by Lipid Research, Inc.
Role of lipid peroxidation in the inhibition of mononuclear cell proliferation by normal lipoproteins
BL Kasiske and WF Keane
Department of Medicine, University of Minnesota College of Medicine, Hennepin County Medical Center, Minneapolis 55415.
Stimulated peripheral blood mononuclear cells (PBMC) can oxidize normal
lipoproteins, and sufficiently oxidized lipoproteins are cytotoxic.
However, the role of lipid peroxidation in the inhibition of mitogen-
stimulated PBMC proliferation by physiologic concentrations of normal
lipoproteins is unclear. In the present investigation, normal low density
lipoprotein (LDL) and very low density lipoprotein (VLDL) suppressed
[3H]thymidine incorporation and gamma interferon production in concanavalin
A-stimulated PBMC without causing cell death. This suppression was
accompanied by parallel increases in lipid peroxidation products measured
as thiobarbituric acid reactive substances (TBARS). In contrast, high
density lipoprotein (HDL) failed to inhibit PBMC and TBARS remains low.
Differences between the PBMC suppression from LDL, VLDL, and HDL were best
accounted for by normalizing the lipoprotein concentrations by their total
lipid content. Moreover, the antioxidants superoxide dismutase and
butylated hydroxytoluene each substantially ameliorated the inhibition of
PBMC caused by LDL, and reduced the levels of lipid peroxidation products
that were generated. Altogether, these results suggest that reactive oxygen
species generated by stimulated PMBC may cause oxidative alterations of
normal lipoproteins that may, in turn, account for much of the previously
reported inhibition of PBMC by normal lipoproteins.
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