Phenothiazines inhibit copper and endothelial cell-induced peroxidation of low density lipoprotein

Breugnot, Christine; Mazière, Cécile; Salmon, S.; Auclair, Martine; Santús, René; Morlière, Patrice; Lenaers, A.; Mazière, Jean‐Claude

doi:10.1016/0006-2952(90)90226-b

Cited by 35 publications

(10 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consistent with this, it has recently been reported that the 3‐hydroxy‐3‐methylglutaryl coenzyme A inhibitor fluvastatin can inhibit both copper and AAPH‐mediated LDL oxidation apparently as a result of drug binding to LDL phospholipids with prevention of radical diffusion into the lipoprotein core [31]. Moreover, lipophilic drugs, such as phenothiazines, calcium antagonists, beta‐blockers and tamoxifen, are known to exert inhibitory effects on LDL oxidation [4, 6, 8, 9]. Indeed, the role of the physical state of the lipid phase in the susceptibility of lipids to peroxidative processes has been pointed out [32, 33].…”

Section: Discussionmentioning

confidence: 73%

“…Some antioxidants seem to exert specific effects on LDL or other lipid system oxidation as a consequence of their lipophilicity, resulting in a less lipid propensity to undergo radical‐driven oxidant damage [4–9]. Ticlopidine, a widely used anti‐platelet agent with a proven clinical efficiency [10–12], is a thienopyridine characterized by lipophilic properties (Fig.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Antioxidant properties of ticlopidine on human low density lipoprotein oxidation

et al. 1998

View full text Add to dashboard Cite

We found that ticlopidine, at therapeutically relevant concentrations (2.5^10 W WM), but not aspirin nor salicylate, significantly counteracted copper-driven human LDL oxidation. Ticlopidine, at 5 and 10 W WM, was also antioxidant on peroxyl radical-induced LDL oxidation; yet it was ineffectual on thiol and ascorbate oxidation mediated by peroxyl radicals themselves, suggesting that drug antioxidant capacity is somehow related to the lipoprotein nature of the oxidizable substrate, but not to radical scavenging. The drug could not indeed react with the stable free radical 1,1-diphenyl-2-pycrylhydrazyl, nor had apparent metal complexing-inactivating activity. Thus, ticlopidine has antioxidant effects on LDL oxidation, which, together with its anti-platelet activity, could confer peculiar antiatherogenic properties to the drug in vivo.z 1998 Federation of European Biochemical Societies.

show abstract

Section: Discussionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Antioxidant properties of ticlopidine on human low density lipoprotein oxidation

et al. 1998

View full text Add to dashboard Cite

show abstract

“…This could be due to the fact that the molecule of probucol is more lipophilic than vitamin E and therefore can enter the lipophilic core of LDL more readily [71]. The antioxidant BHT (2,6-di-tert-butyl-4-methylphenol), structurally similar to probucol with the lipophilic tert-butyl groups, is also more efficient than vitamin E in protecting LDL from oxidation [72]. The majority of many studies have shown that treatment of hypercholesterolemic animal models with probucol leads to suppression of atherosclerosis in several species [19,66].…”

Section: Probucolmentioning

confidence: 97%

Inflammation in Atherosclerosis: New Opportunities for Drug Discovery

Meng

2005

MRMC

View full text Add to dashboard Cite

show abstract

“…This could be due to the fact that the molecule of probucol is more lipophilic than vitamin E and therefore can enter the lipophilic core of LDL more readily [75]. The antioxidant BHT (2,6-di-tert-butyl-4-methylphenol), structurally similar to probucol with the lipophilic tert-butyl groups, is also more efficient than vitamin E in protecting LDL from oxidation [76].…”

Section: Oxidative Stress and Antioxidantsmentioning

confidence: 99%

Atherosclerosis is an Inflammatory Disorder After All

Meng

2006

CTMC

View full text Add to dashboard Cite

Inflammation has been increasingly recognized as an important player in the pathophysiology of numerous human disorders. Accumulating evidence has led to the conclusion that atherosclerosis is an inflammatory disease, although it was believed to be a disorder of high cholesterol levels in the bloodstream for over a century. Cholesterol does contribute to the pathogenesis of atherosclerosis, but through inflammatory mechanisms. Statins lower cholesterol levels and hence reduce inflammation in the vasculature and prevent heart disease. Statins may also exert anti-inflammatory effects through mechanisms independent of cholesterol lowering. Adhesion molecules, cytokines, oxidative stress, etc. appear to contribute to the inflammatory state of atherosclerosis and therapeutic approaches directed toward these markers or targets have the potential to be effective in reducing inflammation and treating atherosclerosis.

show abstract

Phenothiazines inhibit copper and endothelial cell-induced peroxidation of low density lipoprotein

Cited by 35 publications

References 28 publications

Antioxidant properties of ticlopidine on human low density lipoprotein oxidation

Antioxidant properties of ticlopidine on human low density lipoprotein oxidation

Inflammation in Atherosclerosis: New Opportunities for Drug Discovery

Atherosclerosis is an Inflammatory Disorder After All

Contact Info

Product

Resources

About