Role of vitamin E in preventing the oxidation of low-density lipoprotein

Esterbauer, Hermann; Dieber-Rotheneder, Martina; Striegl, G; Waeg, Georg

doi:10.1093/ajcn/53.1.314s

Cited by 591 publications

(274 citation statements)

References 17 publications

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“…Plasma was prepared by centrifugation and used immediately. For enrichment of LDL with the various vitamin E isomers [20], separate aliquots of plasma (5 ml) were supplemented with 400 gtl of DMSO (control) or stock solution of either ~-, y-and ~-TOH, incubated for 6 h at 37°C, before LDL was isolated by the 2 h ultracentrifugation method using the TL100.4 rotor [21]. Excess KBr and remaining water-soluble antioxidants were then removed from the LDL by gel filtration using a single PD-10 column (Pharmacia, Uppsala, Sweden).…”

Section: Preparation Of Native and Tocopherol-enriched Ldlmentioning

confidence: 99%

Inverse deuterium kinetic isotope effect for peroxidation in human low‐density lipoprotein (LDL): a simple test for tocopherol‐mediated peroxidation of LDL lipids

1995

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a-Tocopherol (a-TOH) can act as a pro-or antioxidant for isolated ubiquinol-10-free human low density lipoprotein (LDL). We demonstrate that a-TOH is a more potent prooxidant than other forms of vitamin E for LDL peroxidation initiated by mild fluxes of aqueous peroxyl radicals and low concentrations of Cu 2+. A simple deuterium exchange test shows that a-TOH switches from pro-to anti-oxidant at Cu2+:LDL ratios > 2.5. The results suggest that this test may be useful to distinguish 'inhibited' peroxidation of emulsion lipids propagated via the lipid peroxyl radical from that mediated via the antioxidant radical.

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Section: Preparation Of Native and Tocopherol-enriched Ldlmentioning

confidence: 99%

Inverse deuterium kinetic isotope effect for peroxidation in human low‐density lipoprotein (LDL): a simple test for tocopherol‐mediated peroxidation of LDL lipids

1995

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“…TOH is transported in plasma by lipoproteins (Traber et al, 1993). In vitamin E supplemented low density lipoprotein (LDL), oxidative resistance is signi®cantly enhanced (Esterbauer et al, 1991). The TOH content of membranes may be the most important factor in determining the susceptibility of microsomes, LDL, hepatocytes or whole organs to ROS-mediated peroxidative damage (Di Mascio et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Concentrations of tocopherols and carotenoids in maternal and cord blood plasma

et al. 1999

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Objectives: To determine the levels of tocopherols, retinol and carotenoids in maternal and umbilical cord blood plasma and to investigate the relationships between them. Design: Venous blood plasma concentrations of a, g and d-tocopherol, retinol, lutein, lycopene, zeaxanthin, bcryptoxanthin, a and b-carotene were determined by HPLC in healthy pregnant women and in pair-matched umbilical cords. Plasma levels of triglycerides and cholesterol were also measured. Subjects: Sixty-six women, between 10 and 20 weeks gestation, were recruited randomly during their ®rst antenatal appointment. From this group, 40 pair-matched umbilical cord blood samples were obtained. Results: Tocopherols, retinol, carotenoids and lipids were present in signi®cantly higher (P`0.001) concentrations in maternal plasma than in cord plasma. There was a signi®cant correlation (r 0.45, P`0.005) between maternal and cord levels of g-tocopherol, but not of a-tocopherol, retinol or carotenoids. Tocopherols and carotenoids were signi®cantly correlated with each other (P`0.05) in maternal and cord plasma. Cconclusions: Plasma levels of tocopherols, carotenoids and lipids are substantially lower at birth than in adulthood. There is a clear relationship between g-tocopherol levels in maternal and cord plasma. The importance of g-tocopherol in human nutrition should be further investigated. There are no signi®cant relationships between plasma a-tocopherol and carotenoids in pregnant mothers and cords. More research is needed to elucidate the maternal-foetal transfer of tocopherols and carotenoids, and to examine the impact of maternal antioxidant nutrient status on neonatal antioxidant capacity. It is important to determine if a low level of tocopherols and carotenoids at birth is a normal stage of human development or indicative of de®ciency.

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“…Leukocyte adhesion was significantly reduced by pretreatment of the animals with superoxide dismutase, implying a key mediator role for superoxide radicals in CS-induced leukocyte/endothelium interaction (11). Indeed, studies by Pryor and coworkers (12, 13) have shown that CS (both gas-phase and particulate matter) introduces into the organism an abundance of reactive oxygen species (ROS), including superoxide radicals.The action of superoxide radicals and other ROS can be counteracted not only by superoxide dismutase, but also by the water-soluble antioxidant vitamin C (14-16), as well as by the lipid-soluble vitamin E and probucol, both ofwhich act as chain-breaking antioxidants and interfere with the process of lipid peroxidation (17,18). Probucol and the antioxidant vitamins C and E have been demonstrated to slow the progression of atherosclerosis in laboratory animals (19,20) and to reduce cardiovascular mortality in large epidemiological surveys (21-24).…”

mentioning

confidence: 99%

“…The action of superoxide radicals and other ROS can be counteracted not only by superoxide dismutase, but also by the water-soluble antioxidant vitamin C (14-16), as well as by the lipid-soluble vitamin E and probucol, both ofwhich act as chain-breaking antioxidants and interfere with the process of lipid peroxidation (17,18). Probucol and the antioxidant vitamins C and E have been demonstrated to slow the progression of atherosclerosis in laboratory animals (19,20) and to reduce cardiovascular mortality in large epidemiological surveys (21)(22)(23)(24).…”

mentioning

confidence: 99%

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Lehr¹,

Frei²,

Arfors³

1994

Proc. Natl. Acad. Sci. U.S.A.

153

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A common feature of cigarette-smoke (CS)-associated diseases such as atherosclerosis and pulmonary emphysema is the activation, aggregation, and adhesion of leukocytes to micro-and macrovascular endothelium. A previous study, using a skinfold chamber model for intravial fluorescence microscopy in awake hamsters, has shown that exposure of hamsters to the smoke generated by one research cigarette elicits the adhesion of fluorescently labeled leukocytes to the endothelium of arterioles and small venules. By the combined use of intravital microscopy and scanning electron microscopy, we now demonstrate in the same animal model that (i) CS-induced leukocyte adhesion is not confined to the microcirculation, but that leukocytes also adhere singly and in clusters to the aortic endothelium; (ii) CS induces the formation in the bloodstream of aggregates between leukocytes and platelets; and (iii) CS-induced leukocyte adhesion to micro-and macrovascular endothelium and leukocyte-platelet aggregate formation are almost entirely prevented by dietary or intravenous pretreatment with the water-soluble antioxidant vitamin C (venules, 21.4 ± 11.0 vs. 149.6 ± 38.7 leukocytes per mm2, P < 0.01; arterioles, 8.5 ± 4.2 vs. 54.3 ± 21.6 leukocytes per mm2, P < 0.01; aortas, 0.8 ± 0.4 vs. 12.4 ± 5.6 leukocytes per mm2 P < 0.01; means ± SD of n = 7 animals, 15 min after CS exposure). No inhibitory effect was observed by pretreatment of the animals with the lipid-soluble antioxidants vitamin E or probucol. The protective effects of vitamin C on CSinduced leukocyte adhesion and aggregation were seen at vitamin C plasma levels (55.6 ± 22.2 spM, n 7) that can easily be reached in humans by dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.Cigarette smoke (CS) has been identified as an independent major risk factor for the development of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease, emphysema, atherosclerosis, and coronary artery disease (1). Although the spectrum of adverse effects of CS involves multiple tissue and organ systems, a feature common to the pathomechanism of most CS-associated diseases is the activation and adhesion of circulating leukocytes to micro-and/or macrovascular endothelium (2-4), followed by acute and/or chronic leukocyte-mediated tissue damage (5, 6). In agreement with earlier reports on the sequestration and activation of leukocytes in the pulmonary microcirculation in rabbits (7), hamsters (8, 9), and humans (10), intravital microscopy in a skinfold chamber model in hamsters revealed that the exposure of hamsters to the smoke of one cigarette elicits the rolling and adhesion of fluorescently labeled leukocytes to the endothelium of small venules and arterioles in striated muscle (11). Leukocyte adhesion was significantly reduced by pretreatment of the animals with superoxide dismutase, implying a key mediator role for superoxide radicals in CS-induced leu...

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Role of vitamin E in preventing the oxidation of low-density lipoprotein

Cited by 591 publications

References 17 publications

Inverse deuterium kinetic isotope effect for peroxidation in human low‐density lipoprotein (LDL): a simple test for tocopherol‐mediated peroxidation of LDL lipids

Inverse deuterium kinetic isotope effect for peroxidation in human low‐density lipoprotein (LDL): a simple test for tocopherol‐mediated peroxidation of LDL lipids

Concentrations of tocopherols and carotenoids in maternal and cord blood plasma

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

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