Oxidation of cholesteryl linoleate by human monocyte-macrophages in vitro

Carpenter, Keri L. H.; Ballantine, James A.; Fussell, Brynley; Enright, Jacqui H.; Mitchinson, M. J.

doi:10.1016/0021-9150(90)90167-h

Cited by 48 publications

(11 citation statements)

References 36 publications

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“…The CL/BSA emulsion has been shown to be avidly taken up by macrophages resulting in foam cell formation and ceroid accumulation (26). Mouse peritoneal macrophages and human monocyte-macrophages exposed to CL and CA/BSA rapidly accumulate lipid and oxidize the unsaturated esters (41). Antioxidants such as alpha tocopherol have been found to inhibit this macrophage-mediated lipid oxidation in vitro (42).…”

Section: Discussionmentioning

confidence: 99%

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

Devaraj¹,

Li²,

Jialal³

1996

J. Clin. Invest.

333

186

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Low levels of alpha tocopherol are related to a higher incidence of cardiovascular disease and increased intake appears to afford protection against cardiovascular disease. In addition to decreasing LDL oxidation, alpha tocopherol may exert intracellular effects on cells crucial in atherogenesis, such as monocytes. Hence, the aim of this study was to test the effect of alpha tocopherol supplementation on monocyte function relevant to atherogenesis. Monocyte function was assessed in 21 healthy subjects at baseline, after 8 wk of supplementation with d-alpha tocopherol (1,200 IU/d) and after a 6-wk washout phase. The release of reactive oxygen species (superoxide anion, hydrogen peroxide), lipid oxidation, release of the potentially atherogenic cytokine, interleukin 1 ␤ , and monocyte-endothelial adhesion were studied in the resting state and after activation of the monocytes with lipopolysaccharide at 0, 8, and 14 wk. There was a 2.5-fold increase in plasma lipid-standardized and monocyte alpha tocopherol levels in the supplemented phase. After alpha tocopherol supplementation, there were significant decreases in release of reactive oxygen species, lipid oxidation, IL-1 ␤ secretion, and monocyte-endothelial cell adhesion, both in resting and activated cells compared with baseline and washout phases. Studies with the protein kinase C inhibitor, Calphostin C, suggest that the inhibition of reactive oxygen species release and lipid oxidation is due to an inhibition of protein kinase C activity by alpha tocopherol. Thus, this study provides novel evidence for an intracellular effect of alpha tocopherol in monocytes that is antiatherogenic. ( J. Clin. Invest. 1996. 98:756-763.)

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Section: Discussionmentioning

confidence: 99%

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

Devaraj¹,

Li²,

Jialal³

1996

J. Clin. Invest.

333

186

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“…described previously [20]. The procedure comprised addition of internal standards (n-heptadecanoic acid, coprostane and 5~-cholestane), Bligh and Dyer extraction, sodium borohydride reduction, saponification and derivatisation to methyl esters and trimethysilyl esters.…”

Section: Methodsmentioning

confidence: 99%

Oxidized low‐density lipoprotein is cytotoxic to human monocyte‐macrophages: protection with lipophilic antioxidants

et al. 1995

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Human monocyte-macrophages were incubated for 24 h with low-density Hpoprotein (LDL) which had been previously oxidized for varying periods up to 24 h with copper ions, in the presence or absence of DL-ot-tocopberol or probucol. The release of radioactivity from cells preloaded with tritiated adenine was used as an assay of toxicity. Toxicity of oxidized LDL increased with duration of copper oxidation and with increasing evidence of lipid oxidation, measured by assay of thiobarbituric acid-reactive substances and by gas chromatography. Oxidation and toxicity were inhibited by DL-a-tocopherol (200/tM) and probucol (50 riM).

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“…Resident peritoneal macrophages were isolated from male Balb/c mice aged 6-8 weeks as previously described [42][43][44].…”

Section: Methodsmentioning

confidence: 99%

Glucose oxidation and low-density lipoprotein-induced macrophage ceroid accumulation: possible implications for diabetic atherosclerosis

Hunt

Bottoms

Clare

et al. 1994

Biochemical Journal

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The exposure of proteins to high concentrations of glucose in vitro is widely considered a relevant model of the functional degeneration of tissue occurring in diabetes mellitus. In particular, the enhanced atherosclerosis in diabetes is often discussed in terms of glycation of low-density lipoprotein (LDL), the non-enzymic attachment of glucose to apolipoprotein amino groups. However, glucose can undergo transition-metal-catalysed oxidation under near-physiological conditions in vitro, producing oxidants that possess a reactivity similar to the hydroxyl radical. These oxidants can fragment protein, hydroxylate benzoic acid and induce lipid peroxidation in human LDL. In this study, glycation of LDL in vitro is accompanied by such oxidative processes. However, the oxidation of LDL varies with glucose concentration in a manner which does not parallel changes in protein glycation. Glycation increases in proportion to glucose concentration, whereas in our studies maximal oxidation occurs at a glucose concentration of approx. 25 mM. The modification of LDL resulting from exposure to glucose alters macrophage ceroid accumulation, a process which occurs in the human atherosclerotic plaque. The accumulation of ceroid in macrophages is shown to be related to LDL oxidation rather than LDL glycation, per se, as it too occurs at a maximum of approx. 25 mM. Oxidative sequelae of protein glycation appear to be a major factor in LDL-macrophage interactions, at least with respect to ceroid accumulation. Our observations are discussed in the context of the observed increase in the severity of atherosclerosis in diabetes.

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Oxidation of cholesteryl linoleate by human monocyte-macrophages in vitro

Cited by 48 publications

References 36 publications

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

Oxidized low‐density lipoprotein is cytotoxic to human monocyte‐macrophages: protection with lipophilic antioxidants

Glucose oxidation and low-density lipoprotein-induced macrophage ceroid accumulation: possible implications for diabetic atherosclerosis

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