Disease relevance of Cholesteryl linoleate

• The only change in plasma lipids that appears to be relevant to the toxicity and its reversal by safflower oil is an increase in cholesteryl linoleate and a corresponding decrease in the cholesteryl ester of the dietary monoacylglycerol [1].
• The reduction of cholesteryl linoleate in lipoproteins: an index of clinical severity in beta-thalassemia/Hb E [2].
• An inverse relationship between the cholesteryl linoleate/cholesteryl oleate ratio (CL/CO) and the degree of clinical severity suggested that the CL/CO ratio is an index of damaged lipoproteins and could be used as a pathologic marker of underlying iron overload [2].

High impact information on Cholesteryl linoleate

• These results indicate that G2A is activated by oxidized free fatty acids produced by oxidation and subsequent hydrolysis of phosphatidylcholine or cholesteryl linoleate [3].
• Even when the LDL particle was loaded with free linoleic acid, cholesteryl linoleate constituted the major LOX substrate [4].
• To elucidate the details of how HDL-core composition can affect the molecular structure of different kinds of HDL particles, the conformation and stability of apoA-I have been investigated in homogeneous recombinant HDL particles (LpA-I) containing palmitoyloleoyl phosphatidylcholine (POPC), triolein (TG), and/or cholesteryl linoleate (CE) [5].
• The liberated [3H]cholesterol thereby becomes available for reesterification by LCAT as indicated by its appearance as newly synthesized cholesteryl linoleate [6].
• The action of adrenocorticotropin (ACTH) on the specific (receptor-mediated) uptake of cholesteryl linoleate . low density lipoprotein complexes was examined in Y-1 mouse adrenal tumor cells [7].

Biological context of Cholesteryl linoleate

• Regioisomeric distribution of cholesteryl linoleate hydroperoxides and hydroxides in plasma from healthy humans provides evidence for free radical-mediated lipid peroxidation in vivo [8].
• 9-Oxononanoyl cholesterol proved to be the major cholesterol core-aldehyde formed during t-BuOOH/FeSO4 oxidation of cholesteryl linoleate and Cu2+-induced LDL oxidation, findings confirmed by atmospheric pressure chemical ionization-mass spectrometry [9].
• The influence of R(-) apomorphine, S(+) apomorphine and dopamine on the oxidation kinetics of two polyunsaturated fatty acids (PUFA) (cholesteryl linoleate (CL) and Trilinolein (TL)) was investigated [10].

Anatomical context of Cholesteryl linoleate

• To determine whether deficient processing of cholesteryl esters in oxidized (ox) low density lipoprotein (LDL) contributes to ceroid formation, we studied the hydrolysis of internalized [3H] cholesteryl linoleate (CL) in oxLDL by mouse peritoneal macrophages (MPM) [11].
• Macrophages that cultured with cholesteryl linoleate also contained many oil red O-stainable particles [12].
• These results suggest that decomposition products of extensively oxidized cholesteryl linoleate that are also present in atherosclerotic lesions, are not adequately degraded by mouse peritoneal macrophage lysosomes and could interact with proteins to form ceroid [11].
• In the present work, we synthesized, characterized, and detected a nitrated derivative of cholesteryl linoleate (Ch18:2) in human blood plasma and lipoproteins using a high-pressure liquid chromatography coupled to electrospray ionization tandem mass spectrometry method [13].
• The amount of cholest-5-en-3 beta,7 beta-diol (CD) was significantly higher in cultures of human monocytes incubated with cholesteryl linoleate-bovine serum albumin (CL/BSA) artificial lipoproteins than in no-cell control incubations of CL/BSA [14].

Associations of Cholesteryl linoleate with other chemical compounds

• Antioxidants such as the flavonoids glabridin or quercetin, when present during LDL oxidation in the presence of PON, reduced the amount of lipoprotein-associated lipid peroxides and preserved PON activities, including its ability to hydrolyze Ox-LDL cholesteryl linoleate hydroperoxides [15].
• We conclude that intracellular accumulation of cholesteryl linoleate hydroperoxide and cholesteryl linoleate hydroxide can follow charge modification or aggregation of mildly oxidized LDL, and that LDL-derived oxidation products may inhibit hydrolysis of LDL-derived CE in foam cell macrophages [16].
• Absolute concentrations of aortic C, hydroperoxides and hydroxides of CE (CE-O(O)H) and alpha-TOH increased gradually while aortic CE increased more markedly with changes to cholesteryl linoleate being most pronounced [17].
• Mouse peritoneal macrophages were therefore incubated in the presence of cholesteryl linoleate/bovine serum albumin emulsion with and without the addition of dl-alpha tocopherol [18].
• The major components were the C4-C10 oxoalkanoyl esters of cholesterol and 7-ketocholesterol, and accounted for 1-2% of the cholesteryl linoleate and arachidonate consumed [19].

Gene context of Cholesteryl linoleate

• In contrast, treatment of monocytes with oxidized low-density protein (oxLDL) containing oxidized lipids, such as cholesteryl linoleate 13-hydroxide. but not with LDL, increased CCR2 protein and mRNA expression [20].
• The cholesteryl esters accumulating in lipoproteins of WHHL rabbits are rich in cholesteryl linoleate and appear to be produced almost exclusively by lecithin-cholesterol acyltransferase [21].
• Based on time-course of the formation of conjugated dienes, cholesteryl linoleate hydroxides and hydroperoxides as well as the antioxidant consumption, two oxidation types were distinguished [22].
• The inverse association between the plasma cholesteryl linoleate-to-oleate ratio, a marker for the dietary polyunsaturated-to-saturated fatty acid ratio, and triglycerides was also stronger in E2 carriers (-0.33 versus -0.17 in E3/3 and -0.24 in E4 carriers) [23].
• The radioactive substances derived from cholesteryl linoleate appeared more polar than the parent compound when analyzed by reverse-phase liquid chromatography, but were not identical with free cholesterol [24].

Analytical, diagnostic and therapeutic context of Cholesteryl linoleate

• By fast atom bombardment mass spectrometry and infrared spectroscopy, we identified the inactivating lipids as the 9- and 13-hydroperoxy derivatives of cholesteryl linoleate, cholesteryl hydroperoxyoctadecadienoate [25].
• Perfusion resulted in the rapid removal of Ch18:2-O(O)H from HDL with a half-life (t1/2)of 11.4 min., faster than that of unoxidized cholesteryl linoleate, and dependent of the presence of the liver [26].
• With this method, cholesteryl-linoleate only could be incorporated into LDL in a stable manner as shown by dialysis and autoradiography results [27].
• Six healthy males were given intravenous infusions of autologous high-density (d, 1.063-1.21; n = 2), low-density (d, 1.019-1.063; n = 2) or intermediate-density (d, 1.006-1.019; n = 2) lipoproteins that had been labelled in vitro with radioactive cholesteryl linoleate (n = 5) or cholesteryl oleate (n = 1) [28].
• Human low density lipoproteins (LDL) in combination with cholesterol or cholesteryl linoleate as precursors for progesterone synthesis of human placenta in organ culture [29].

References