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Journal of Lipid Research, Vol 37, 2018-2028, Copyright © 1996 by Lipid Research, Inc.
SM Colles, KC Irwin and GM Chisolm
The relative toxicities of several lipid oxidation products formed on
oxidized LDL, their presence on oxidized LDL, and potential mechanisms of
cell injury compared to oxidized LDL were examined. Toxicities to
fibroblasts, with lipoprotein-deficient serum supplementation, were: 7
beta-hydroperoxycholesterol > 7 beta-hydroxycholesterol = 4-
hydroxynonenal > 7-ketocholesterol > 5 alpha, 6
alpha-epoxycholesterol. Lysophosphatidylcholine was only significantly
cytotoxic in the absence of lipoprotein-deficient serum. Without serum,
relative toxicities were: 7 beta-hydroperoxycholesterol >
lysophosphatidylcholine > 4- hydroxynonenal > 7
beta-hydroxycholesterol. Similar relative potencies were observed in smooth
muscle and endothelial cell cultures. 7 beta- Hydroperoxycholesterol
accumulated on oxidized LDL to greater amounts than other oxysterols and
4-hydroxynonenal, but less than lysophosphatidylcholine. Cell injury by 7
beta-hydroperoxycholesterol and oxidized LDL was inhibitable by
antioxidants but not by exogenous cholesterol or cycloheximide. In
contrast, a) toxicities by 7 beta- hydroxycholesterol, 7-ketocholesterol, 5
alpha, 6 alpha- epoxycholesterol, and 4-hydroxynonenal were not inhibited
by antioxidants; b) 7 beta-hydroxycholesterol and lysophosphatidylcholine
toxicities were inhibited by exogenous cholesterol; and c) 7 beta-
hydroxycholesterol toxicity was inhibited by cycloheximide. Injury by
lysophosphatidylcholine was reduced by vitamin E and not affected by
altering the cellular exposure to selenium; reduced selenium enhanced
toxicity by oxidized LDL and 7 beta-hydroperoxycholesterol. The high
relative toxicity of 7 beta-hydroperoxycholesterol, the level of its
accumulation on oxidized LDL, and its mechanism of action similar to
oxidized LDL suggest that it is the compound predominantly responsible for
oxidized LDL induced cytotoxicity.
ARTICLES
Roles of multiple oxidized LDL lipids in cellular injury: dominance of 7 beta-hydroperoxycholesterol
Department of Cell Biology, Cleveland Clinic Foundation, OH 44195, USA.
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