Reactions of the α‐tocopheroxyl radical in micellar solutions studied by nanosecond laser flash photolysis

Bisby, Roger H.; Parker, Anthony W.

doi:10.1016/0014-5793(91)81260-f

Cited by 63 publications

(57 citation statements)

References 19 publications

(3 reference statements)

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“…Together, these studies show that ascorbate is highly effective in preventing oxidation reactions induced by most 1e-oxidants and that it also strongly protects, but does not completely prevent, oxidative damage induced by 2e-oxidants, particularly ONOO Ϫ . The ability of ascorbate to reduce ␣-TO⅐ to ␣-TOH, recognized first by Packer et al (688), is now well established as a mechanism that spares vitamin E from oxidation in micelles (62,1059) and isolated biological membranes (462,606). Ascorbate completely inhibits LDL lipid oxidation initiated by aqueous and lipophilic peroxyl radicals (78,79,802), horseradish peroxidase (1058), and lipoxygenase (965) in vitro.…”

Section: Role Of Oxidative Modifications In Atherosclerosismentioning

confidence: 99%

Role of Oxidative Modifications in Atherosclerosis

Stocker¹,

Keaney²

2004

Physiological Reviews

2,244

1,756

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This review focuses on the role of oxidative processes in atherosclerosis and its resultant cardiovascular events. There is now a consensus that atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall. The oxidative modification hypothesis of atherosclerosis predicts that low-density lipoprotein (LDL) oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis. In support of this hypothesis, oxidized LDL can support foam cell formation in vitro, the lipid in human lesions is substantially oxidized, there is evidence for the presence of oxidized LDL in vivo, oxidized LDL has a number of potentially proatherogenic activities, and several structurally unrelated antioxidants inhibit atherosclerosis in animals. An emerging consensus also underscores the importance in vascular disease of oxidative events in addition to LDL oxidation. These include the production of reactive oxygen and nitrogen species by vascular cells, as well as oxidative modifications contributing to important clinical manifestations of coronary artery disease such as endothelial dysfunction and plaque disruption. Despite these abundant data however, fundamental problems remain with implicating oxidative modification as a (requisite) pathophysiologically important cause for atherosclerosis. These include the poor performance of antioxidant strategies in limiting either atherosclerosis or cardiovascular events from atherosclerosis, and observations in animals that suggest dissociation between atherosclerosis and lipoprotein oxidation. Indeed, it remains to be established that oxidative events are a cause rather than an injurious response to atherogenesis. In this context, inflammation needs to be considered as a primary process of atherosclerosis, and oxidative stress as a secondary event. To address this issue, we have proposed an “oxidative response to inflammation” model as a means of reconciling the response-to-injury and oxidative modification hypotheses of atherosclerosis.

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Section: Role Of Oxidative Modifications In Atherosclerosismentioning

confidence: 99%

Role of Oxidative Modifications in Atherosclerosis

Stocker¹,

Keaney²

2004

Physiological Reviews

2,244

1,756

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“…It is possible that, in this study, the α-tocopherol stock had not yet been used at the moment the analysis in the liver was made, or the body had had enough time to replace the used vitamin by decreasing vitamin excretion or increasing α-tocoferoxil radical regeneration to α-tocopherol through the action of different agents, such as ascorbic acid [25,33,34,35,36]. …”

Section: Discussionmentioning

confidence: 99%

Vitamin E Alters Inflammatory Gene Expression in Alcoholic Chronic Pancreatitis

Monteiro¹,

Silva²,

Ambrosio³

et al. 2012

Lifestyle Genomics

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Objective: To evaluate the effect of vitamin E supplementation on pancreatic gene expression of inflammatory markers in rats with alcoholic chronic pancreatitis. Methods: Wistar rats were divided into 3 groups: control (1), alcoholic chronic pancreatitis without (2) and with (3) vitamin E supplementation. Pancreatitis was induced by a liquid diet containing ethanol, cyclosporin A and cerulein. α-tocopherol content in plasma and liver and pancreas histopathology were analyzed. Gene expression of inflammatory biomarkers was analyzed by the quantitative real-time PCR technique. Results: The animals that received vitamin E supplementation had higher α-tocopherol amounts in plasma and liver. The pancreas in Group 1 showed normal histology, whereas in Groups 2 and 3, mild to moderate tissue destruction foci and mononuclear cell infiltration were detected. Real-time PCR analysis showed an increased expression of all genes in Groups 2 and 3 compared to Group 1. Vitamin E supplementation decreased the transcript number of 5 genes (α-SMA, COX-2, IL-6, MIP-3α and TNF-α) and increased the transcript number of 1 gene (Pap). Conclusion: Vitamin E supplementation had anti-inflammatory and beneficial effects on the pancreatic gene expression of some inflammatory biomarkers in rats with alcoholic chronic pancreatitis, confirming its participation in the inflammatory response mechanisms in the pancreas.

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“…Known physiological coantioxidants include ascorbate (15,21), CoQ 10 H 2 (16,22), and bilirubin (23). In contrast, urate (15,24), reduced glutathione (25), and ␤-carotene (26) are incapable of efficiently reducing the ␣-TO ⅐ and are not generally potent inhibitors of LDL lipid peroxidation.…”

Section: Oxidative Modification Of Low Density Lipoprotein (Ldl)mentioning

confidence: 99%

“…EPR Spectroscopic Studies-Micellar dispersions of ␣-TOH (500 M, final concentration) were prepared in cetyltrimethyl ammonium chloride or sodium dodecyl sulfate micelles as described (25). The generation and observation of ␣-TO ⅐ in such micellar dispersions and LDL (see below) by EPR spectroscopy was carried out using a spectrometer (ESP 300; Bruker) with an X-band cavity as described (36).…”

Section: ϫ6mentioning

confidence: 99%

3-Hydroxyanthranilic Acid Is an Efficient, Cell-derived Co-antioxidant for α-Tocopherol, Inhibiting Human Low Density Lipoprotein and Plasma Lipid Peroxidation

Thomas

Witting

Stocker

1996

Journal of Biological Chemistry

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␣-Tocopherol (␣-TOH) can promote lipid peroxidation in human low density lipoprotein (LDL) unless co-antioxidants are present that eliminate the chain-carrying ␣-tocopheroxyl radical (␣-TO ⅐ ) (Bowry, V. W., Mohr, D., Cleary, J., and Stocker, R. (1995) J. Biol. Chem. 270, 5756 -5763). Interferon-␥ inhibits human monocyte/ macrophage-facilitated LDL lipid peroxidation via induction of cellular tryptophan degradation and production and release of 3-hydroxyanthranilic acid (3HAA) (Christen, S., Thomas, S. R., Garner, B., and Stocker, R. (1994) J. Clin. Invest. 93, 2149 -2158). We now report on the mechanism of antioxidant action of 3HAA. 3HAA directly reduced ␣-TO ⅐ in UV-exposed micellar dispersions of ␣-TOH or in LDL incubated with soybean 15-lipoxygenase (SLO), as assessed by electron paramagnetic resonance spectroscopy. 3HAA did not inhibit SLO enzyme activity. Anthranilic acid, which lacks the phenoxyl group, was incapable of reducing ␣-TO ⅐ . 3HAA dose-dependently inhibited the peroxidation of surface phospholipids and core cholesteryl esters in LDL exposed to SLO, peroxyl radicals (ROO ⅐ ), or Cu 2؉ ; oxidants that convert ␣-TOH to ␣-TO ⅐ . In all cases, sparing of LDL's ␣-TOH, but not ubiquinol-10 (CoQ 10 H 2 ), was observed until the majority of 3HAA was consumed. Addition of 3HAA or ascorbate prevented further consumption of ␣-TOH and accumulation of lipid hydroperoxides when added to aqueous or lipophilic ROO ⅐ -oxidizing LDL after complete and partial consumption of CoQ 10 H 2 and ␣-TOH, respectively. In contrast, addition of urate, an efficient ROO ⅐ scavenger incapable of scavenging ␣-TO ⅐ , did not efficiently inhibit ongoing lipid peroxidation. Oxidation of 3HAA-supplemented human plasma by aqueous ROO ⅐ resulted in the successive consumption of ascorbate, CoQ 10 H 2 , 3HAA, bilirubin, ␣-TOH, and urate. Lipid peroxidation was prevented as long as ascorbate, CoQ 10 H 2 , and 3HAA were present, but subsequently proceeded as a free-radical chain reaction concomitant with ␣-TOH, bilirubin, and urate consumption. Addition of 3HAA to aqueous ROO ⅐ -oxidizing plasma, after complete consumption of ascorbate and CoQ 10 H 2 , strongly inhibited ongoing lipid peroxidation and consumption of ␣-TOH, bilirubin, and urate immediately and as efficiently as did ascorbate. These findings demonstrate that 3HAA is a highly efficient co-antioxidant for plasma lipid peroxidation by virtue of its ability to interact with ␣-TO ⅐ in lipoproteins. Since interferon-␥ is the principal inducer of tryptophan degradation and release of 3HAA by monocytes/macrophages, this may represent a localized extracellular antioxidant defense against LDL oxidation in inflammation.

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Reactions of the α‐tocopheroxyl radical in micellar solutions studied by nanosecond laser flash photolysis

Cited by 63 publications

References 19 publications

Role of Oxidative Modifications in Atherosclerosis

Role of Oxidative Modifications in Atherosclerosis

Vitamin E Alters Inflammatory Gene Expression in Alcoholic Chronic Pancreatitis

3-Hydroxyanthranilic Acid Is an Efficient, Cell-derived Co-antioxidant for α-Tocopherol, Inhibiting Human Low Density Lipoprotein and Plasma Lipid Peroxidation

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