Anti-oxidant effect of flavonoids on the susceptibility of LDL oxidation

In vitro studies have demonstrated increased atherogenicity of oxidized low-density lipoprotein (ox-LDL) compared to native LDL. Oxidative modification of LDL alters its structure allowing LDL to be taken up by scavenger receptors on macrophage, endothelial, and smooth muscle cells, leading to the f...

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2003-04, Vol.246 (1-2), p.193-196
Main Authors: Naderi, Gholam Ali, Asgary, Seddigheh, Sarraf-Zadegan, Nizal, Shirvany, Hamid
Format: Article
Language:English
Subjects:
Antioxidants
Antioxidants - pharmacology
Apigenin
Arteriosclerosis - etiology
Arteriosclerosis - metabolism
Arteriosclerosis - prevention & control
Flavonoids
Flavonoids - pharmacology
Genistein - pharmacology
Humans
In Vitro Techniques
Lipoproteins, LDL - chemistry
Lipoproteins, LDL - drug effects
Lipoproteins, LDL - metabolism
Low density lipoprotein
Oxidation
Oxidation-Reduction
Oxidizing agents
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Summary:In vitro studies have demonstrated increased atherogenicity of oxidized low-density lipoprotein (ox-LDL) compared to native LDL. Oxidative modification of LDL alters its structure allowing LDL to be taken up by scavenger receptors on macrophage, endothelial, and smooth muscle cells, leading to the formation of lipid-laden foam cells, the hallmark of early atherosclerotic lesions. The susceptibility of LDL to in vitro oxidation was assessed essentially by the technique described by Esterbauer et al. LDL oxidation were monitored by change in 234-absorbance in the presence and absence of pure flavonoids. Morin, genistein, apigenin and biochanin A, naringin and quercetin were used at different concentration. These flavonoids significantly inhibit in vitro LDL oxidation, genistein, morin and naringin have stronger inhibitory activity against LDL oxidation than biochanin A or apigenin. This study show that flavonoids prevent in vitro LDL oxidation and probably would be important to prevent atherosclerosis.
ISSN:0300-8177
1573-4919
DOI:10.1023/a:1023483223842