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Vitamin E antioxidant

No unequivocal unique function for vitamin E has been defined. However, it does act as a hpid-soluble antioxidant in cell membranes, where many of its functions can be provided by synthetic antioxidants. Vitamin E is the generic descriptor for two famihes of compounds, the tocopherols and the tocotrienols (Figure 45—5). The different vitamers (compounds having similar vitamin activity) have different biologic potencies the most active is D-a-tocopherol, and it is usual to express vitamin E intake in milhgrams of D-a-tocoph-erol equivalents. Synthetic DL-a-tocopherol does not have the same biologic potency as the namrally occurring compound. [Pg.486]

Other dietary factors implicated in prostate cancer include retinol, carotenoids, lycopene, and vitamin D consumption.5,6 Retinol, or vitamin A, intake, especially in men older than age 70, is correlated with an increased risk of prostate cancer, whereas intake of its precursor, [3-carotene, has a protective or neutral effect. Lycopene, obtained primarily from tomatoes, decreases the risk of prostate cancer in small cohort studies. The antioxidant vitamin E also may decrease the risk of prostate cancer. Men who developed prostate cancer in one cohort study had lower levels of l,25(OH)2-vitamin D than matched controls, although a prospective study did not support this.2 Clearly, dietary risk factors require further evaluation, but because fat and vitamins are modifiable risk factors, dietary intervention may be promising in prostate cancer prevention. [Pg.1359]

Classic antioxidants, vitamin E, vitamin C, and others can suppress the activation of apoptosis. For example, ascorbic acid prevented cytochrome c release and caspase activation in human leukemia cells exposed to hydrogen peroxide [128], Pretreatment with A -acctylcystcinc, ascorbate, and vitamin E decreased homocysteine thiolactone-induced apoptosis in human promyelocytic leukemia HL-60 cells [129]. Resveratrol protected rat brain mitochondria from anoxia-reoxygenation damage by the inhibition of cytochrome c release and the reduction of superoxide production [130]. However, it should be mentioned that the proapoptotic effect of ascorbate, gallic acid, or epigallocatechin gallate has been shown in the same human promyelocytic leukemia cells [131]. [Pg.758]

The possible prooxidant effects of a major lipophilic antioxidant vitamin E (a-tocopherol) have already been discussed in Chapter 25. Yamashita et al. [82] showed that a-tocopherol induced extensive DNA damage including base modification and strand breakage in the... [Pg.840]

Vitamin A (retinol) is not a classic antioxidant although it is frequently related to a group of antioxidant vitamins E, C, and A. Murata and Kawanishi [83] found that retinol and its derivative retinal induced the formation of 8-HOdG in HL-60 cells. This process was supposedly mediated by hydroxyl radicals formed from hydrogen peroxide (the product of superoxide dismutation) and endogenous transition metal ions. [Pg.841]

As mentioned above, in contrast to classic antioxidant vitamins E and C, flavonoids are able to inhibit free radical formation as free radical scavengers and the chelators of transition metals. As far as chelators are concerned their inhibitory activity is a consequence of the formation of transition metal complexes incapable of catalyzing the formation of hydroxyl radicals by the Fenton reaction. In addition, as shown below, some of these complexes, for example, iron- and copper-rutin complexes, may acquire additional antioxidant activity. [Pg.858]

Chelators of iron, which are now widely applied for the treatment of patients with thalassemia and other pathologies associated with iron overload, are the intravenous chelator desferal (desferrioxamine) and oral chelator deferiprone (LI) (Figure 19.23, see also Chapter 31). Desferrioxamine (DFO) belongs to a class of natural compounds called siderophores produced by microorganisms. The antioxidant activity of DFO has been studied and compared with that of synthetic hydroxypyrid-4-nones (LI) and classic antioxidants (vitamin E). It is known that chronic iron overload in humans is associated with hepatocellular damage. Therefore, Morel et al. [370] studied the antioxidant effects of DFO, another siderophore pyoverdin, and hydroxypyrid-4-ones on lipid peroxidation in primary hepatocyte culture. These authors found that the efficacy of chelators to inhibit iron-stimulated lipid peroxidation in hepatocytes decreased in the range of DFO > hydroxypyrid-4-ones > pyoverdin. It seems that other siderophores are also less effective inhibitors of lipid peroxidation than DFO [371],... [Pg.895]

Oxidative stress Antioxidants Vitamin E National Institute on Aging (NIA)/... [Pg.228]

Most of the other medications studied to slow the course of Alzheimer s dementia presumably work as an antioxidant to protect nerve cells from damaging free radicals. Of the antioxidants, vitamin E is the safest and has the best evidence of efficacy. Thus, we recommend that all patients receive 2000 lU of vitamin E each day during... [Pg.305]

By contrast, other compounds in food may decrease cancer risk (Table 21.7). Free radical scavengers such as the antioxidants, vitamins E and C, carotenoids and fla-venoids have anti-cancer activity, while vitamins A and D and other retinoids may encourage a cell to differentiate rather than proliferate (Box 21.4). Plant oestrogens in soya prodncts may be protective since they compete with human oestrogens for the oestrogen receptors in breast and ovary bnt elicit no response. [Pg.503]

An extension of the Seven Countries Study, by Ancel Keys and colleagues, indicated the particular importance of the flavonoids. During the study, which was reported in 1980, random samples of the food eaten by the participants were taken and stored for future analysis. When this was done, it was found that the average intakes of the antioxidants vitamin E, P-carotene and vitamin C were not related to the 25-year coronary heart disease mortality rates. In contrast, the intake of flavonoids was inversely related to the mortality. [Pg.519]

Nutritional status can also influence the toxic potency of carbon tetrachloride. Animal studies have clearly demonstrated that brief fasting or consumption of diets low in antioxidants (vitamin E, selenium, methionine) can lead to increased carbon tetrachloride hepatotoxicity. The same may be true for humans, although this is not known for certain. Another aspect of nutritional status affecting carbon tetrachloride toxicity is hepatic energy status. Hepatic ATP levels might influence the ultimate outcome of toxicity (low levels may inhibit recovery mechanisms). [Pg.93]

Vitamin E (a-tocopherol) has as its active form any of several tocopherol derivatives. It functions as an antioxidant. Vitamin E deficiency is rarely seen, but can lead to red blood cell fragility that leads to hemolytic anemia. It has no known toxicity. [Pg.502]

Hall and Wolf [217] have proposed a hypothesis, concerning the pathogenesis of post-traumatic central nervous system ischaemia, which integrates an injury-induced rise in intracellular Ca2+, the increased synthesis of vasoactive prostanoids and progressive microvascular lipid peroxidation. The model used anaesthetised cats with a contusion injury to the lumbar spinal cord. Antioxidants, vitamin E and selenium, were compared with various Ca2 + antagonists, cyclo-oxygenase inhibitors, a thromboxane synthetase inhibitor and the stable prostacyclin analogue. The most impressive preservation of post-traumatic spinal cord blood flow was provided by the antioxidants. [Pg.274]

Kessopoulou, E., Powers, H.J., Sharma, K.K., Pearson, M.J., Russell, J.M., Cooke, I.D., and Barratt, C.L. 1995. A double-blind randomized placebo cross-over controlled trial using the antioxidant vitamin E to treat reactive oxygen species associated male infertility. Fertil. Steril. [Pg.156]

The use of antioxidants in human-contact applications (e.g. food-contact, medical and pharmaceutical) present a challenge in terms of their safety and level of migration into the contact media, e.g. food, body fluids. As an antioxidant, vitamin E is a suitable candidate to explore for such areas of application. [Pg.129]

The yield and composition of the volatile fraction of the pentane extracts of leaves, stems and seeds of F. vulgare Mill, have been studied by Guillen and Manzanos (1996). The yield obtained from seeds was much higher than that obtained from leaves and stems. The volatile fraction of the pentane extract of the latter two has a higher concentration of terpene hydrocarbons and a smaller concentration of oxygenated terpene hydrocarbons than that of the seeds. Sesquiterpenes and the antioxidant vitamin E have been detected in the leaves and petroselinic acid in the seeds. Saturated aliphatic hydrocarbons with 25 or more carbon atoms have been found in all the plant parts. [Pg.230]

This is a fairly heavy oil, high in the antioxidant vitamin E, making it suitable for use with other carrier oils, where it extends their keeping properties. It is useful for dry and mature skins and suitable for some types of dermatitis, and helpful for repairing sun-damaged skin. It contains a mixture of unsaturated and saturated fatty acids linoleic (54%), oleic (19%), palmitic (16%), linolenic (7%), ecisadenoic (1.5%) and stearic (1%). [Pg.218]

The oxidative modification of LDL has been implicated in atherosclerosis. This disease may be regarded as a chronic inflammatory condition, and here we discuss how oxidatively modified LDL (oLDL) may play a role not only in atherosclerosis but also in other chronic inflammatory diseases such as RA. LDL (Mr = 2.5 x 106) is one of the major plasma carriers of lipids, as well as the antioxidants vitamin E and (3-carotene. Because of its high content of unsaturated fatty acids, LDL is uniquely sensitive to lipid peroxidation [ 117]. [Pg.375]

The substantia nigra and globus pallidus are rich in iron yet cerebrospinal fluid has very little iron-binding capacity (H2). Moreover, any injury to the CNS may result in the release of iron, which by Fenton/Haber-Weiss chemistry, catalyzes free radical production. Iron has also been shown to accelerate the production of CNS lipofuscin (increased in Alzheimer s disease), while various antioxidants (vitamin E, GSH, selenium) reduce its concentration (E5). [Pg.37]

The efficacy of the spin trapping agent PBN and the antioxidant vitamin E was tested to suppress increase in NO and hpid peroxidation and prevent neurodegeneration of pyramidal neurons in the CAl hippocampal area in the model of KA-induced excitotoxicity. Vitamin E or PBN alone did not alter basal citrulline and F4-NeuroPs levels or dendritic arborization. However, vitamin E and PBN suppressed KA-induced increases in citrulline and cerebral and neuronal markers of oxidative damage, p2-IsoPs and F4-NeuroPs, respectively (Figures 42.8 and 42.9). [Pg.643]

Arvindakshan M, Ghate M, Ranjekar PK, Evans DR, Mahadik SP. Supplementation with a combination of omega-3 fatty acids and antioxidants (vitamins E and C) improves the outcome of schizophrenia. Schizophr. Res. 2003 62 195-204. [Pg.876]

Other substances that are being evaluated in Alzheimer s disease include the antioxidant vitamin E, the monoamine oxidase type B inhibitor, selegeline (see p. 425) and the plant extract gingko biloba, which is though to have antioxidant and cholinergic activity. Oestrogens and nonsteroidal anti-inflammatory agents may also have protective effects. [Pg.408]


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See also in sourсe #XX -- [ Pg.30 , Pg.524 ]




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