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Journal of Lipid Research, Vol 32, 449-456, Copyright © 1991 by Lipid Research, Inc.
SM Rankin, S Parthasarathy and D Steinberg
It has been suggested that the oxidative modification of low density
lipoprotein (LDL) is a key event in atherogenesis. Several mechanisms have
been proposed to explain how different types of cells modify LDL. In this
study we examine the relative contributions of superoxide anions and
cellular lipoxygenase (LO) in the modification of LDL by macrophages.
Superoxide dismutase (SOD) inhibited LDL oxidation by macrophages but only
by 25%. Under the same conditions, several LO inhibitors (eicosatetraynoic
acid (ETYA), piriprost, and A-64077) almost completely inhibited the
modification of LDL by macrophages. SOD had a greater inhibitory effect on
the modification of LDL by U937 cells and fibroblasts (32% and 64%,
respectively) but again LO inhibitors had a much greater effect (79 to 100%
inhibition). Incubation of [1-14C]linoleic acid with mouse peritoneal
macrophages resulted in its conversion to a single more polar product
coeluting with 13- and 9-HODE by reverse phase HPLC. When the cells were
preincubated with LO inhibitors, formation of this product was
significantly inhibited. It is concluded that the modification of LDL by
macrophages is mediated in large part by lipoxygenase-type activity.
ARTICLES
Evidence for a dominant role of lipoxygenase(s) in the oxidation of LDL by mouse peritoneal macrophages
Department of Medicine, University of California, San Diego, La Jolla 92093.
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