LDL oxidation by arterial wall macrophages depends on the oxidative status in the lipoprotein and in the cells: role of prooxidants vs antioxidants.

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Hi All,

 

Here again we see clear support of oxidized LDL causing plaque formation and

that both mono & poly fatty acids carried

in LDL elevate oxidation risk.

 

" The LDL oxidative state is elevated by increased ratio of poly/mono unsaturated

fatty acid "

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=9\

823020 & dopt=Abstract

Mol Cell Biochem 1998 Nov;188(1-2):149-59 Related Articles, Books, LinkOut

LDL oxidation by arterial wall macrophages depends on the oxidative status in

the lipoprotein and in the cells: role of

prooxidants vs. antioxidants.

Aviram M, Fuhrman B.

Lipid Research Laboratory, Technion Faculty of Medicine, Rappaport Family

Institute for Research in the Medical

Sciences, Haifa, Israel.

 

Oxidized LDL is highly atherogenic as it stimulates macrophage cholesterol

accumulation and foam cell formation, it is

cytotoxic to cells of the arterial wall and it stimulates inflammatory and

thrombotic processes.

 

LDL oxidation can lead to its subsequent aggregation, which further increases

cellular cholesterol accumulation.

 

All major cells in the arterial wall including endothelial cells, smooth muscle

cells and monocyte derived macrophages

can oxidize LDL.

 

Macrophage-mediated oxidation of LDL is probably a hallmark in early

atherosclerosis, and it depends on the oxidative

state of the LDL and that of the macrophages.

 

The LDL oxidative state is elevated by increased ratio of poly/mono unsaturated

fatty acids, and it is reduced by

elevation of LDL-associated antioxidants such as vitamin E, beta-carotene,

lycopene, and polyphenolic flavonoids.

 

The macrophage oxidative state depends on the balance between cellular

NADPH-oxidase and the glutathione system.

 

LDL-associated polyphenolic flavonoids which inhibit its oxidation, can also

reduce macrophage oxidative state, and

subsequently the cell-mediated oxidation of LDL.

 

Oxidation of the macrophage lipids, which occurs under oxidative stress, can

lead to cell-mediated oxidation of LDL even

in the absence of transition metal ions, and may be operable in vivo.

 

Finally, elimination of Ox-LDL from extracellular spaces, after it was formed

under excessive oxidative stress, can

possibly be achieved by the hydrolytic action of HDL-associated paraoxonase on

lipoprotein's lipid peroxides.

 

The present review article summarizes the above issues with an emphasis on our

own data.

 

PMID: 9823020 [PubMed - indexed for MEDLINE]

 

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Good Health & Long Life,

Greg Watson, http://optimalhealth.cia.com.au gowatson

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