Resveratrol and cancer: chemoprevention, apoptosis, and chemo-immunosensitizing activities.
Curr Med Chem Anticancer Agents. 2003 Mar;3(2):77-93.
Cal C1, Garban H, Jazirehi A, Yeh C, Mizutani Y, Bonavida B.
The polyphenolic compound Resveratrol is a naturally occurring phytochemical and can be found in many plant species, including grapes, peanuts and various herbs. Several studies have established that Resveratrol can exert anti-oxidant and anti-inflammatory activities. It also has activity in the regulation of multiple cellular events associated with carcinogenesis. This review describes the general properties of Resveratrol including its relationship to estrogen, its effect on lipid metabolism, its cardiovascular effects, and its role on gene expression. Resveratrol has also been examined in several model systems for its potential effect against cancer. Its anti-cancer effects include its role as a chemopreventive agent, its ability to inhibit cell proliferation, its direct effect in cytotoxicity by induction of apoptosis and on its potential therapeutic effect in pre-clinical studies. In addition, Resveratrol has been shown to exert sensitization effects on cancer cells that will result in a synergistic cytotoxic activity when Resveratrol is used in combination with cytotoxic drugs in drug-resistant tumor cells. Clearly, the studies with Resveratrol provide support for the use of Resveratrol in human cancer chemoprevention and combination with chemotherapeutic drugs or cytotoxic factors in the treatment of drug refractory tumor cells.
Vitamine A et bêta-carotène
Le bêta-carotène est un précurseur hydrosoluble de la vitamine A , et est un antioxydant en soi , alors que la vitamine A n’a pas de d’activité antioxydante.
On en trouve dans
Maïs, courge et carottes , jaune d’oeuf , fruits et légumes pigmentés ( couleur jaune)
Donne ses électrons facilement lorsque nécessaire
Aide à régénérer la viatamine E
Peut les recevoir à nouveau pour devenir réactifs, ce qui leur donne la capacité de se recycler à l’infini.
Protège l’oxygène et le fer de l’oxydation
Protège du stress oxydatif
Aide à la protection des artères contre les dommages oxydatifs
Hydrosoluble et peut être éliminé rapidement , environ 24-48 h de rétention avant excrétion
ALIMENTS RICHES EN VITAMINE E
Portions vitamine E
huile de germe de blé 15 ml (1 cà table) 21 mg
Amandes non blanchies, rôties à sec ou dans l’huile ou déshydratées 60 ml 9-18 mg
Graines de tournesol rôties à sec 60 ml 8 mg
Noisettes , avelines non blanches, rôties à sec 60 ml 5-8 mg
Huile de tournesol 15 ml 7 mg
Huile de carthame 15 ml 7 mg
Céréales à déjeuner , 100 % son (type All bran) 30 g 3.5 mg
Boisson de soya enrichie 250 ml 3 mg
Huile de maïs ou de canola 15 ml 3 mg
Arachides rôties dans l’huile 60 ml 2-3 mg
Huile de soya 15 ml 3 mg
Pâte de tomate en conserve 60 ml 3 mg
Graines de lin 60 ml 2 mg
Son de maïs ou de blé brut 30 g 2 mg
Vitamin E regulates mitochondrial hydrogen peroxide generation.
Department of Nutrition and Food Science, University of Kentucky, Lexington 40506-0054, USA. email@example.com
Chow CK, Ibrahim W, Wei Z, Chan AC
The mitochondrial electron transport system consumes more than 85% of all oxygen used by the cells, and up to 5% of the oxygen consumed by mitochondria is converted to superoxide, hydrogen peroxide, and other reactive oxygen species (ROS) under normal physiologic conditions. Disruption of mitochondrial ultrastructure is one of the earliest pathologic events during vitamin E depletion. The present studies were undertaken to test whether a direct link exists between vitamin E and the production of hydrogen peroxide in the mitochondria. In the first experiment, mice were fed a vitamin E-deficient or-sufficient diet for 15 weeks, after which the mitochondria from liver and skeletal muscle were isolated to determine the rates of hydrogen peroxide production. Deprivation of vitamin E resulted in an approximately 5-fold increase of mitochondrial hydrogen peroxide production in skeletal muscle and a 1-fold increase in liver when compared with the vitamin E-supplemented group. To determine whether vitamin E can dose-dependently influence the production of hydrogen peroxide, four groups of male and female rats were fed diets containing 0, 20, 200, or 2000 lU/kg vitamin E for 90 d. Results showed that dietary vitamin E dose-dependently attenuated hydrogen peroxide production in mitochondria isolated from liver and skeletal muscle of male and female rats. Female rats, however, were more profoundly affected by dietary vitamin E than male rats in the suppression of mitochondrialhydrogen peroxide production in both organs studied. These results showed that vitamin E can directly regulate hydrogen peroxide production in mitochondria and suggest that the overproduction of mitochondrial ROS is the first event leading to the tissue damage observed in vitamin E-deficiencysyndromes. Data further suggested that by regulating mitochondrial production of ROS, vitamin E modulates the expression and activation of signal transduction pathways and other redox-sensitive biologic modifiers, and thereby delays or prevents degenerative tissue changes.
Absorbé dans l’intestin grêle
Première défense contre les effets des radicaux libres dans l’organisme
Protection des membranes cellulaires
stocké dans le foie et les adipocytes
Protège les composants cellulaires et leur membrane
Protection des membranes cellulaires
RDA homme 15 mg/j
RDA femme 15 mg/j
Les tissus cellulaires exposés aux quantités les plus importantes des radicaux libres semblent contenir a plus grande quantité de vitamine E
Chemopreventive mechanisms of selenium
□ The element selenium (Se) was recognized only 40 years ago as being essential in the nutrition of animals and humans.It is recognized as being an essential component of a number of enzymes in which it is present as the amino acid selenocysteine (SeCys). Selenium compounds have also been found to inhibit tumorigenesis in a variety of animal models and recent studies indicate that supplemental Se in human diets may reduce cancer risk. Anti-tumorigenic activities have been associated with Se intakes that are more than sufficient to correct nutritionally deficient status; that is, Se appears to be anti-tumorigenic at intakes that are substantially greater than those associated with maximal expression of the known SeCys-containing enzymes. Therefore, while some cancer protection may involve one or more Se-enzymes, it is probable that anti-tumorigenic functions of Se are discharged by certain Se-metabolites produced in significant amounts at relatively high Se intakes.
□ Thus, Se supplementation of individuals with relatively low or frankly deficient natural intakes of the element can be expected to support enhanced antioxidant protection due to increased expression of the Se-dependent glutathione peroxidases and thioredoxin reductase. Higher levels of Se-supplementation can be expected to affect other functions related to tumorigenesis: carcinogen metabolism, immune function, cell cycle regulation and apoptosis. Thus, according to this 2-stage model of the roles of Se in cancer prevention, even individuals with nutritionally adequate Se intakes may benefit from Sesupplementation.
Dietary selenium repletion may reduce cancer incidence in people at high risk who live in areas with low soil selenium.
Studies examining the relationship between dietary selenium intake and risk of various cancers have shown that low selenium intake is associated with higher cancer rates. A recent well-controlled intervention trial studied whether selenium supplementation can prevent cancer in subjects who have a history of skin cancer and live in areas of the United States with low soil selenium levels. Selenium supplementation did not reduce skin cancer rates, but the incidence of total, lung, colorectal, and prostate cancers was significantly reduced by the intervention. Although these data need confirmation, they suggest that adequate selenium intake is essential for cancer prevention.
Serum antioxidants and skin cancer risk: an 8-year community-based follow-up study.
Antioxidant nutrients can help prevent skin damage caused by ultraviolet radiation from sunlight, but it is not clear whether serum concentrations of such nutrients influence skin cancer risk.
We carried out a prospective study of the associations between serum concentrations of antioxidant nutrients and incidence (person-based and tumor-based) of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) of the skin among a random subsample of 485 adults from an Australian community. Participants were divided into thirds, ranked according to their serum concentrations of carotenoids, alpha-tocopherol, and selenium measured in 1996 and were monitored for incident, histologically confirmed BCC and SCC tumors until 2004.
Although there were no associations between baseline serum carotenoids or alpha-tocopherol concentrations and incidence of BCC or SCC, baseline serum selenium concentrations showed strong inverse associations with both BCC and SCC tumor incidence. Compared with participants with lowest selenium concentrations at baseline (0.4-1.0 micromol/L), those with the highest serum selenium concentrations (1.3-2.8 micromol/L) had a decreased incidence of BCC tumors (multivariate relative risk, 0.43; 95% confidence interval, 0.21-0.86; P(trend) = 0.02) and SCC tumors (multivariate relative risk, 0.36; 95% confidence interval, 0.15-0.82; P(trend) = 0.02).
Relatively high serum selenium concentrations are associated with an approximately 60% decrease in subsequent tumor incidence of both BCC and SCC, whereas serum concentrations of carotenoids or alpha-tocopherol are not associated with later skin cancer incidence. A possible U-shaped association between serum selenium concentrations and SCC of the skin needs confirmation.
Plasma selenium level before diagnosis and the risk of prostate cancer development.
J Urol. 2001 Dec;166(6):2034-8
Epidemiological studies and a randomized intervention trial suggest that the risk of prostate cancer may be reduced by selenium intake. We investigated whether plasma selenium level before diagnosis correlated with the risk of later developing prostate cancer.
MATERIALS AND METHODS:
A case control study was performed on men from the Baltimore Longitudinal Study of Aging registry, including 52 with known prostate cancer and 96 age matched controls with no detectable prostatic disease. Plasma selenium was measured at an average time plus or minus standard deviation of 3.83 +/- 1.85 years before the diagnosis of prostate cancer by graphite furnace atomic absorption spectrophotometry. Adjusted odds ratio and 95% confidence interval were computed with logistic regression.
After correcting for years before diagnosis, body mass index, and smoking and alcohol use history, higher selenium was associated with a lower risk of prostate cancer. Compared with the lowest quartile of selenium (range 8.2 to 10.7 microg./dl.), the odds ratios of the second (10.8 to 11.8), third (11.9 to 13.2) and fourth (13.3 to 18.2) quartiles were 0.15 (95% confidence interval 0.05 to 0.50), 0.21 (0.07 to 0.68) and 0.24 (0.08 to 0.77, respectively, p =0.01). Furthermore, plasma selenium decreased significantly with patient age (p <0.001).
Low plasma selenium is associated with a 4 to 5-fold increased risk of prostate cancer. These results support the hypothesis that supplemental selenium may reduce the risk of prostate cancer. Because plasma selenium decreases with patient age, supplementation may be particularly beneficial to older men.
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