Toxicity of oxidised low density lipoprotein towards mouse peritoneal macrophages in vitro

Reid, V.C.; Mitchinson, M. J.

doi:10.1016/0021-9150(93)90219-k

Cited by 95 publications

(47 citation statements)

References 22 publications

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“…ox-LDL is cytotoxic to cultured cells (9,36) and ␣-tocopherol is known to inhibit this cytotoxic effect of ox-LDL (36). One must consider that our results may primarily reflect a protective role of ␣-tocopherol against cytotoxicity from ox-LDL.…”

Section: Discussionmentioning

confidence: 78%

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Vascular incorporation of alpha-tocopherol prevents endothelial dysfunction due to oxidized LDL by inhibiting protein kinase C stimulation.

Keaney¹,

Guo²,

Cunningham³

et al. 1996

J. Clin. Invest.

199

114

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Excess vascular oxidative stress has been linked to impaired endothelium-dependent arterial relaxation in hypercholesterolemia. ␣ -Tocopherol (AT) preserves endothelial function in hypercholesterolemia although the mechanism(s) for this protective effect is (are) not known. We examined the tissue-specific effects of AT on oxidized LDL (ox-LDL)-mediated endothelial dysfunction in male New Zealand White rabbits. Animals consumed chow deficient in ( Ͻ 10 IU/kg) or supplemented with (1,000 IU/kg) AT for 28 d. Exposure of thoracic aortae from AT-deficient animals to ox-LDL (0-500 g/ml) for 4 h produced dose-dependent inhibition of acetylcholine-mediated relaxation ( P Ͻ 0.05) while vessels derived from animals consuming AT were resistant to ox-LDL-mediated endothelial dysfunction. Animals consuming AT demonstrated a 100-fold increase in vascular AT content and this was strongly correlated with vessel resistance to endothelial dysfunction from ox-LDL ( R ϭ 0.67; P ϭ 0.0014). These results were not explained by an effect of AT on ox-LDL-mediated cytotoxicity by LDH assay or scanning electron microscopy. Vascular incorporation of AT did produce resistance to endothelial dysfunction from protein kinase C stimulation, an event that has been implicated in the vascular response to ox-LDL. Human aortic endothelial cells loaded with AT also demonstrated resistance to protein kinase C stimulation by both phorbol ester and ox-LDL. Thus, these data indicate that enrichment of vascular tissue with AT protects the vascular endothelium from ox-LDL-mediated dysfunction, at least in part, through the inhibition of protein kinase C stimulation. These findings suggest one potential mechanism for the observed beneficial effect of AT in preventing the clinical expression of coronary artery disease that is distinct from the antioxidant protection of LDL. ( J. Clin. Invest. 1996. 98: 386-394)

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Section: Discussionmentioning

confidence: 78%

“…Oxidized LDL is cytotoxic to cells in culture and ␣-tocopherol is known to inhibit this cytotoxicity (36). Therefore, we sought to determine if the known effects of ␣-tocopherol on ox-LDLmediated cytotoxicity were responsible for the results reported here.…”

Section: Resultsmentioning

confidence: 98%

Vascular incorporation of alpha-tocopherol prevents endothelial dysfunction due to oxidized LDL by inhibiting protein kinase C stimulation.

Keaney¹,

Guo²,

Cunningham³

et al. 1996

J. Clin. Invest.

199

114

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“…The isolated compounds were evaluated for their inhibitory activity against copper-induced LDL oxidation by four methods: thiobarbituric acid reactive substances (TBARS) assay, 15) measurement of the formation of conjugated dienes, 16) relative electrophoretic mobility (REM), 17) and fragmentation of apoB-100.…”

mentioning

confidence: 99%

Low Density Lipoprotein (LDL)-Antioxidant Flavonoids from Roots of Sophora flavescens

Jeong

Ryu

Kim

et al. 2008

Biological & Pharmaceutical Bulletin

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Oxidation of low density lipoprotein (LDL) is strongly implicated as a key process in the onset of atherosclerosis. In this study, nine alkylated (C 10 -C 5 ) flavonoids from Sophora flavescens were examined for their inhibitory effects on copper-induced LDL oxidation. Of the flavonoids tested, sophoraflavanone G (1), kurarinone (2), kurarinol (3), norkurarinol (4), and kuraridin (9) inhibited the generation of thiobarbituric acid reactive substances (TBARS) with IC 50 s of 7.9, 14.5, 22.0, 26.9, and 17.5 m mM, respectively. The most potent inhibitor, compound 1, also demonstrated significant activities in complementary in vitro investigations, such as lag time (130 min at 5 m mM), relative electrophoretic mobility (REM) of ox-LDL (80% inhibition at 20 m mM), and fragmentation of apoB-100 (inhibition of 71% at 20 m mM). Analysis of the structures of these compounds reveals that a resorcinol moiety in the B-ring is strongly correlated with protection of LDL-oxidation.

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“…Quinn and co-workers have shown that oxidised LDL induces chemotaxis in human monocytes, with lysophosphatidyl choline being one of its active components [3,4]. Further, oxidised LDL has been shown to be toxic for a variety of cell types including smooth muscle cells, fibroblasts [5] and more recently mouse peritoneal macrophages [6,7], the macrophage-like cell line P388D1 [8] and human monocyte-macrophages [9]. However, oxidised LDL is a complex mixture of various components including lipid hydroperoxides, oxysterols and aldehydes [10].…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic and chemotactic potencies of several aldehydic components of oxidised low density lipoprotein for human monocyte‐macrophages

et al. 1996

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Toxicity of oxidised low density lipoprotein towards mouse peritoneal macrophages in vitro

Cited by 95 publications

References 22 publications

Vascular incorporation of alpha-tocopherol prevents endothelial dysfunction due to oxidized LDL by inhibiting protein kinase C stimulation.

Vascular incorporation of alpha-tocopherol prevents endothelial dysfunction due to oxidized LDL by inhibiting protein kinase C stimulation.

Low Density Lipoprotein (LDL)-Antioxidant Flavonoids from Roots of Sophora flavescens

Cytotoxic and chemotactic potencies of several aldehydic components of oxidised low density lipoprotein for human monocyte‐macrophages

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