Background: A great deal of evidence has indicated that oxidatively modified LDL plays a critical role in the initiation and progression of atherosclerosis. Antioxidants that can prevent LDL oxidation may act as antiatherogens. Copper is a candidate for oxidizing LDL in atherosclerotic lesions. The binding of copper ions to LDL is usually thought to be a prerequisite for LDL oxidation by copper...

Addition of leumedin, N-[9H-(2,7-dimethylfluorenyl-9-methoxy) carbon]-L-leucine at 30-60 microM together with LDL almost completely prevented the induction of monocyte chemotactic protein mRNA, reduced monocyte chemotactic protein 1 levels by 84%, and inhibited monocyte migration into the subendothelial space of cocultures of human aortic wall cells by < or = 98%. LDL incubated with leumedin fo...

Homocysteine is an independent risk factor for cardiovascular diseases. The mechanisms by which elevated plasma concentrations of homocysteine are related to the pathogenesis of atherosclerosis are not fully understood. To examine whether homocysteine is implicated in atherogenesis through the modification of low density lipoprotein (LDL), the effect of homocysteine on the oxidation of LDL was ...

background: a great deal of evidence has indicated that oxidatively modified ldl plays a critical role in the initiation and progression of atherosclerosis. antioxidants that can prevent ldl oxidation may act as antiatherogens. copper is a candidate for oxidizing ldl in atherosclerotic lesions. the binding of copper ions to ldl is usually thought to be a prerequisite for ldl oxidation by copper...

Ascorbate at concentrations of 60-100 microM inhibits the modification of freshly prepared low-density lipoprotein (LDL) by macrophages. With 'moderately oxidized' LDL (produced by prolonged storage in a refrigerator), however, ascorbate does not inhibit LDL modification by macrophages and actually modifies the LDL itself in the absence of macrophages [Stait and Leake (1994) FEBS Lett. 341, 263...

The objective of the present study was to establish whether high-density lipoprotein 3 (HDL3) or high-density lipoprotein 2 (HDL2) might show an anti-oxidative effect on the acceleration of the oxidative modification of low-density lipoprotein (LDL) by ascorbic acid from measurement of the agarose gel electrophoretic mobility of LDL. LDL was incubated without adding transitional-metal ions for ...

Incubation of low density lipoprotein (LDL) with endothelial cells converts it to a form that is avidly degraded by macrophages via the acetyl LDL receptor. This modification has previously been shown to be accompanied by extensive breakdown of the major LDL protein (apoB-100) to smaller peptides. ApoB-100 is known to undergo partial degradation during isolation and purification which is common...

Oxidative modification of low-density lipoproteins (LDL) contributes to the pathology of atherosclerosis. Antioxidants may protect LDL against oxidative modification. Acetaminophen, a widely used analgesic and antipyretic agent, has significant antioxidant properties. However, there is little evidence to suggest that acetaminophen acts as an antioxidant for LDL oxidation in vivo. In this study,...

Oxidative modification of low-density lipoprotein (LDL) is an important feature in the initiation and progression of atherosclerosis. LDL modification by endothelial cells was studied after supplementation of the cells with oleic acid and polyunsaturated fatty acids (PUFA) of the n-6 and n-3 series. In terms of the lipid peroxidation product [thiobarbituric acid reactive substances (TBARS)] con...

Background: Oxidative modification of low-density lipoprotein (LDL) appears to be an early step in the pathogenesis of atherosclerosis. Meanwhile, myeloperoxidase (MPO)-catalyzed reaction is one of the potent pathway for LDL oxidation in vivo. The aim of this study was to evaluate in vitro antioxidant effects of vitamins C and E on LDL oxidation mediated by MPO. Methods: MPO was isolated from f...