Oxidation of plasma low-density lipoproteins from coronary patients with various forms of hypercholesterolemia.

Abstract

The duration of lag-phase of copper-induced free-radical oxidation of atherogenic LDL isolated from the plasma of coronary patients without hypercholesterolemia virtually does not differ from that of normal human LDL. On the other hand, lag-phase of plasma LDL oxidation was minimal in coronary patients with primary hypercholesterolemia without familial history and especially in patients with familial hypercholesterolemia. This can be attributed to sharply decreased content of natural lipid antioxidants in LDL of patients with familial hypercholesterolemia. However, therapy with natural antioxidant vitamin E did not modulate oxidizability of these LDL. By contrast, therapy with beta-hydroxy-beta-methylglutaryl-coenzyme A reductase inhibitor suppressing biosynthesis of ubiphenol Q induced sharp accumulation of lipoperoxides in LDL in vivo. These data suggest that reduced form of ubiquinone Q is the main antioxidant protecting LDL from free-radical oxidation.

• Authors: V Z Lankin, G G Konovalova, A K Tikhaze, I B Nezhdanova, A M Olfer'ev, V V Kukharchuk
• Journal: Bulletin of experimental biology and medicine (Bull Exp Biol Med) Vol. 136 Issue 1 Pg. 42-5 (Jul 2003) ISSN: 0007-4888 [Print] United States
• PMID: 14534607 (Publication Type: Journal Article)

Chemical References

• Antioxidants
• Free Radicals
• Hydroxymethylglutaryl-CoA Reductase Inhibitors
• Lipid Peroxides
• Lipoproteins, LDL
• Ubiquinone
• Cholesterol
• Oxygen

Topics

• Adult
• Antioxidants (pharmacology)
• Cholesterol (metabolism)
• Female
• Free Radicals
• Heart Diseases (blood)
• Humans
• Hydroxymethylglutaryl-CoA Reductase Inhibitors (pharmacology)
• Hypercholesterolemia (pathology)
• Kinetics
• Lipid Peroxides (metabolism)
• Lipoproteins, LDL (blood)
• Male
• Middle Aged
• Models, Chemical
• Oxygen (metabolism)
• Time Factors
• Ubiquinone (analogs & derivatives, antagonists & inhibitors, biosynthesis)