α-Tocopherol induces proatherogenic changes to HDL2 &amp; HDL3: An in vitro and ex vivo investigation

Wade, L.; Nadeem, Nida; Woodside, Jayne V.; McGinty, Ann; McMaster, Cyril; McEneny, Jane

doi:10.1016/j.atherosclerosis.2012.11.032

Cited by 11 publications

(10 citation statements)

References 30 publications

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“…It is also consistent with the interpretation of Ristow et al [7] to their disappointing results concerning the (negative) effects of vitamin E-supplementation on the health of sportsmen. Furthermore, this possibility is supported by the finding of high oxidizability of HDL in the serum of vitamin E-treated patients [60]. This may also be true for LDL and if it is not the case, we can still expect changes in LDL oxidation due to HDL oxidation, as described above.…”

Section: Antioxidants Do Not Always Inhibit Ldl Peroxidationmentioning

confidence: 72%

“…3) In another experiment, the authors tested the susceptibility of the HDL2&3 fraction to peroxidation following 6-weeks of tocopherol supplementation. The main result of this experiment was that the HDL2&3 fraction of the tocopherol-treated people were more susceptible to peroxidation than the same fraction of placebo-supplemented controls [60]. Interestingly, the increased sensitivity to peroxidation was accompanied by a decrease of the activity of both HDL2&3-PON-1 and HDL2-LCAT (lecithin-cholesterol acyltransferase), probably because in the presence of higher concentrations of Toc, lower concentrations of the latter HDL-associated protective proteins were required, as described below.…”

Section: The Effects Of Vitamin E On Hdl Peroxidationmentioning

confidence: 95%

“…The very complex effect of tocopherol on the susceptibility of lipoproteins to oxidation is demonstrated in the recent study of its effects on both in-vitro and ex-vivo peroxidation of HDL2 & HDL3. Specifically, in their recent investigation, Wade et al [60] found that the effect of added tocopherol depends on whether its peroxidation was tested before or after fractionation of the serum.…”

Section: The Effects Of Vitamin E On Hdl Peroxidationmentioning

confidence: 99%

“…5) The antioxidant interferes with the protective effect of HDL against LDL peroxidation [60], as discussed above.…”

Section: Antioxidants Do Not Always Inhibit Ldl Peroxidationmentioning

confidence: 99%

“…D. Lichtenberg, I. Pinchuk / Advances in Bioscience and Biotechnology 4 (2013)[48][49][50][51][52][53][54][55][56][57][58][59][60][61] …”

mentioning

confidence: 99%

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Atherogenesis, the oxidative LDL modification hypothesis revisited

Lichtenberg¹,

Pinchuk²

2013

ABB

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The commonly-accepted "oxidized LDL hypothesis of atherogenesis" is based on a large number of indirect evidence that shows that oxidatively-modified LDL plays a role in atherogenesis. Yet, the exact role is not clear. Some researchers think that oxidatively modified biomolecules initiate atherogenesis; others believe that they "only" promote this multifactorial process. Regardless of the exact mechanism responsible for the effect of peroxidation on atherogenesis, the "oxidative theory of AS" is apparently inconsistent with the results of meta-analysis, in which (the "expected") significant correlation between CVD and oxidative stress (OS) was found only when the OS was evaluated on the basis of the plasma concentrations of malondialdehyde (MDA), often based on the concentration of thiobarbituric acid reactive substances (TBARS). Notably, even this association is questionable due to 1) poor reliability of the laboratory assay of MDA and 2) possible publication bias. Hence, it appears that the commonly accepted paradigm regarding the role of oxidative damage in the pathogenesis of CVD has been overestimated. Furthermore, the hypothesis is apparently inconsistent with the disappointing results of most of the clinical trials that were designed to reduce OS by means of supplementation of antioxidants, mostly vitamin E. These apparent inconsistencies do not contradict the oxidative modification hypothesis of AS. The source of the apparent contradictions is probably the oversimplified considerations on which the predictions have been based. Many reasonable arguments can be raised to explain the apparent contradictions, which means that our current knowledge is insufficient to test the relationship of oxidative stress to cardiovascular disease.[85] Tynkkynen, T., Mursu, J., Nurmi, T., Tuppurainen, K., Laatikainen, R. and Soininen, P. (2012) NMR protocol for determination of oxidation susceptibility of serum lipids and application of the protocol to a chocolate study. Metabolomics,8,[386][387][388][389][390][391][392][393][394][395][396][397][398]

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Section: Antioxidants Do Not Always Inhibit Ldl Peroxidationmentioning

confidence: 72%

Section: The Effects Of Vitamin E On Hdl Peroxidationmentioning

confidence: 95%

Section: The Effects Of Vitamin E On Hdl Peroxidationmentioning

confidence: 99%

“…5) The antioxidant interferes with the protective effect of HDL against LDL peroxidation [60], as discussed above.…”

Section: Antioxidants Do Not Always Inhibit Ldl Peroxidationmentioning

confidence: 99%

“…D. Lichtenberg, I. Pinchuk / Advances in Bioscience and Biotechnology 4 (2013)[48][49][50][51][52][53][54][55][56][57][58][59][60][61] …”

mentioning

confidence: 99%

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Atherogenesis, the oxidative LDL modification hypothesis revisited

Lichtenberg¹,

Pinchuk²

2013

ABB

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Tocopherols in the Prevention and Treatment of Atherosclerosis and Related Cardiovascular Disease

Mathur

Ding

Saldeen

et al. 2015

Clinical Cardiology

111

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Oxidants/antioxidants play an important role in cellular homeostasis. The human body has endogenous molecules that work as antioxidants, such as glutathione, superoxide dismutase, peroxidases, and catalase. Exogenous substances in the diet, such as β‐carotene, ascorbate, and vitamin E, are vital antioxidants. Of these, vitamin E is likely the most important antioxidant in the human diet, and many studies have been performed to elucidate its role in health and disease. Vitamin E is a family of several compounds, of which α‐tocopherol is the most widely known analog. α‐Tocopherol exhibits antioxidative property in vitro and inhibits oxidation of low‐density lipoprotein cholesterol. In addition, α‐tocopherol shows anti‐inflammatory activity and modulates expression of proteins involved in the uptake, transport, and degradation of atherogenic lipids. Though α‐tocopherol exhibits important antioxidant, anti‐inflammatory, and antiatherogenic features in vitro, α‐tocopherol supplements have failed to consistently reduce atherosclerosis‐related events in human trials. The conflicting results have led to reconsideration of the importance previously given to α‐tocopherol and led to interest in other members of vitamin E family, especially γ‐tocopherol, which exerts a much more potent antioxidant, anti‐inflammatory, and cardioprotective effect than α‐tocopherol. This reconsideration has been backed by solid laboratory and clinical research. We suggest that the absence of γ‐tocopherol in traditional preparations may be one reason for the lack of consistent salutary effects of vitamin E preparations in clinical trials. This review summarizes our current understanding of tocopherols as antioxidant molecules and emerging evidence of an important role of γ‐tocopherol in the pathophysiology of atherosclerosis‐related cardiovascular disease.

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A New Method for Determination of α-Tocopherol in Tropical Fruits by Ultra Performance Convergence Chromatography with Diode Array Detector

Gong

Wang

et al. 2014

Food Anal. Methods

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α-Tocopherol induces proatherogenic changes to HDL2 & HDL3: An in vitro and ex vivo investigation

Cited by 11 publications

References 30 publications

Atherogenesis, the oxidative LDL modification hypothesis revisited

Atherogenesis, the oxidative LDL modification hypothesis revisited

Tocopherols in the Prevention and Treatment of Atherosclerosis and Related Cardiovascular Disease

A New Method for Determination of α-Tocopherol in Tropical Fruits by Ultra Performance Convergence Chromatography with Diode Array Detector

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