(±)13-HODE cholesterylester was originally extracted from atherosclerotic lesions and shown to be produced by Cu2+-catalyzed oxidation of LDL. Later studies determined that 15-LO from rabbit reticulocytes and human monocytes were able to metabolize cholesteryl linoleate, a major component of LDL, to 13-HODE cholesterylester.
9(R)-HODE cholesterylester was originally extracted from atherosclerotic lesions. It remains uncertain whether the oxidized fatty acid portion of the molecule results from enzymatic lipoxygenation or from random lipid peroxidation. 9(R)-HODE cholesterylester can be used as a standard for analysis of chiral HODE cholesterylesters.
9(S)-HODE cholesterylester was originally extracted from atherosclerotic lesions. It remains uncertain whether the oxidized fatty acid portion of the molecule results from enzymatic lipoxygenation or from random lipid peroxidation. 9(S)-HODE cholesterylester can be used as a standard for analysis of chiral HODE cholesterylesters.
13(R)-HODE cholesterylester was originally extracted from atherosclerotic lesions. It remains uncertain whether the oxidized fatty acid portion of the molecule results from enzymatic lipoxygenation or from random lipid peroxidation. 13(R)-HODE cholesterylester can be used as a standard for analysis of chiral HODE cholesterylesters.
(±)9-HODE cholesterylester was originally extracted from atherosclerotic lesions and shown to be produced by Cu2+-catalyzed oxidation of LDL. Later studies determined that 15-LO from rabbit reticulocytes and human monocytes were able to metabolize cholesteryl linoleate, a major component of LDL, to 9-HODE cholesterylester.
Cholesteryl lignocerate is a cholesterol ester that has been found in human meibum. Cholesteryl lignocerate can be hydrolyzed by cellular extracts from cultured human skin fibroblasts isolated from healthy individuals but not patients with cholesterylesterstoragedisease (CESD) or Wolman disease.