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 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin E and vitamin C are involved in the defense of the body against free radical and reactive oxygen molecule induced damage. The best characterized biological damage caused by radicals is known as lipid peroxidation. Free radical formation is known to play a major role in the development of cancer. In this study, we measured plasma levels of thiobarbituric acid reactive substances (TBARS) as a marker of lipid peroxidation, cholesterol, and vitamins E and C as antioxidants in male patients with colorectal tumors (n = 20, 54.5 +/- 8.3 years). The patients had significantly higher plasma TBARS levels than age-matched healthy subjects (p < 0.001). Plasma vitamin C levels were significantly lower in the patients compared to the healthy subjects (p < 0.001). On the other hand, plasma vitamin E levels in the patients were similar to those of healthy subjects. Plasma cholesterol levels were also found to be significantly elevated in patients with colorectal tumors (p < 0.001). Our results suggest that there is an imbalance between oxidant and antioxidant status in tumor genesis.
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PMID:Levels of plasma vitamin E, vitamin C, TBARS, and cholesterol in male patients with colorectal tumors. 1273 74

Cysteine cathepsin B and its endogenous inhibitor play an important role in tumor progression. Increase in cathepsin B expression and reduced levels of its inhibitors were associated with tumor malignancy in breast cancer. The objective of this study was to investigate the effects of a new therapy combining vitamin E and placental inhibitor on the level of endogenous protease inhibitor in sera and tumor tissues with mammary cancer. The inhibitor was used in doses of 100 and 200 micrograms per animal for 8 days. Vitamin E was added after the last treatment with inhibitor and was injected daily in doses of 10 and 20 mg per animal for one mouth. The size and survival time of treated animals as well as cathepsin B and the inhibitor activity in tumor and sera before and after treatment in comparison with the control groups were determined. The activity of cathepsin B significantly decreased both in tumor tissues and in sera (P < or = 0.0001). Cathepsin B activity in tumor tissue homogenates and in sera decreased two-fold and three-fold, respectively, after the animals were treated with vitamin E at a dose of 20 mg, and decreased five-fold and 15-fold, respectively, when treated with vitamin E plus inhibitor in comparison with untreated animals. Endogenous inhibitor activity increased six-fold and 12-fold in the sera and tissue homogenates, respectively, after the animals were treated with 200 micrograms of cysteine protease inhibitor plus 20 mg of vitamin E, in comparison with untreated animals. The total cure responses were higher in eight of 10 rats, as compared with untreated animals. The combination of placental inhibitor and vitamin E resulted in a significant reduction in breast metastasis and might provide a therapeutic basis for anti-metastasis therapy.
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PMID:Effects of combined in vivo treatment of transplantable solid mammary carcinoma in wistar rats using vitamin E and cysteine peptidase inhibitors from human placenta. 1282 15

Vitamin E is a collective term used to refer to a number of structurally and functionally different compounds. Although some vitamin E compounds are popular supplements marketed for their potential beneficial antioxidant effects for a number of chronic diseases including various forms of cancer, a recent report by the National Academy of Sciences Food and Nutrition Board concluded that too little is known at present to provide definitive answers regarding whether taking larger doses of dietary antioxidants will help prevent chronic diseases. Recent reviews of epidemiological data suggest that dietary source vitamin E may provide some protection against breast cancer, while vitamin E supplements do not. A majority of studies investigating the protective effects of certain types of vitamin E in animal models of mammary cancer prevention conclude that there is little or no effect. The study of vitamin E is complex, and the vitamin E field faces many scientific challenges.
J Mammary Gland Biol Neoplasia 2003 Jan
PMID:Vitamin E and breast cancer prevention: current status and future potential. 1458 65

Dietary docosahexaenoic acid (DHA), which integrates into tumor cell membranes, has been reported to enhance the efficacy against tumors of cytotoxic drugs that induce reactive oxygen species (ROS). Because ionizing radiation also generate ROS, we initiated a study to determine whether dietary DHA might sensitize mammary tumors to irradiation. Mammary tumors were induced by N-methylnitrosourea (NMU) in Sprague-Dawley rats. The optimal dose of radiation to examine the effect of DHA on tumor response to irradiation was determined to be 18 grays (Gy) using a 4-6 MeV electron beam (according to the depth of the target volume) delivered in a single fraction from a linear accelerator. Two groups of rats were fed a basal diet containing 7% of a mixture of peanut and rapeseed oils enriched with 8% of an oil containing either a low (palm oil) or high (DHASCO oil containing 40% DHA) DHA content. DHA group was equally subdivided into 2 groups without or with addition of vitamin E (100 IU/kg diet). Irradiation was carried out when the first tumor in each rat reached 1.5 cm2 and subsequent change in tumor size was documented over time. DHA level in adipose tissue, taken as a biomarker, was higher in the DHA supplemented group compared to the control group. Vitamin E level in liver, the best storage for this compound, was higher in the vitamin E supplemented DHA group compared to the DHA group. Tumor size decreased by 60% at 12 days after irradiation in the DHA group vs. 31% in the control group (p = 0.03) and 36% in the DHA plus vitamin E group. Therefore, dietary DHA sensitized mammary tumors to radiation. The addition of vitamin E inhibited the beneficial effect of DHA, suggesting that this effect might be mediated by oxidative damage to the peroxidizable lipids.
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PMID:Enhanced radiosensitivity of rat autochthonous mammary tumors by dietary docosahexaenoic acid. 1496 86

Epidemiological studies, preclinical investigations and clinical intervention trials support the role of selenium compounds as potent cancer chemopreventive agents; the dose and the form of selenium are critical factors in cancer prevention. Induction of apoptosis and inhibition of cell proliferation are considered important cellular events that can account for the cancer preventive effects of selenium. Toxicity should always be considered a determining factor in the selection of potential chemopreventive agents. Prior to induction of apoptosis, selenium compounds alter the expression and/or activities of a number of cell cycle regulatory proteins, signaling molecules, proteases, mitochondrial associated factors, transcriptional factors, tumor suppressor genes, polyamine and glutathione levels. Depending on the form, selenium compounds can target separate pathways but more efforts are needed to learn about disrupting different pathways converging to apoptosis. Numerous selenium compounds are known to inhibit carcinogenesis in several animal models but not all of these have been examined for their efficacy to induce apoptosis or vice versa in the corresponding target organ. Studies aimed at investigating the effects of selenium compounds on apoptosis in the target organ in vivo and in vitro are limited. On the basis of information provided in this review, we recommend that additional molecular markers should be added to those proposed in the Selenium and Vitamin E Cancer Prevention Trial (SELECT) on prostate cancer. Apart from the selenium compounds reviewed here, several novel synthetic organoselenium compounds need to be examined both in vitro and in vivo for their potential to induce apoptosis; such an investigation may provide better and mechanism-based cancer chemoprevention as well as chemotherapeutic agents.
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PMID:Apoptosis is a critical cellular event in cancer chemoprevention and chemotherapy by selenium compounds. 1496 64

Epidemiological studies have consistently associated high intakes of lycopene or vitamin E with a reduced prostate cancer risk. Both compounds were tested in the MatLyLu Dunning prostate cancer model to gain insight into the in vivo action of lycopene and vitamin E. Supplementation for 4 weeks with 200 ppm lycopene, 540 ppm vitamin E, or both led to plasma levels comparable with those in humans. Both compounds also accumulated in tumor tissue. Macroscopic evaluation of the tumors by magnetic resonance imaging showed a significant increase in necrotic area in the vitamin E and the lycopene treatment groups. Microarray analysis of tumor tissues revealed that both compounds regulated local gene expression. Vitamin E reduced androgen signaling without affecting androgen metabolism. Lycopene interfered with local testosterone activation by down-regulating 5-alpha-reductase and consequently reduced steroid target genes expression (cystatin-related protein 1 and 2, prostatic spermine binding protein, prostatic steroid binding protein C1, C2 and C3 chain, probasin). In addition, lycopene down-regulated prostatic IGF-I and IL-6 expression. Based on these findings, we suggest that lycopene and vitamin E contribute to the reduction of prostate cancer by interfering with internal autocrine or paracrine loops of sex steroid hormone and growth factor activation/synthesis and signaling in the prostate.
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PMID:Lycopene and vitamin E interfere with autocrine/paracrine loops in the Dunning prostate cancer model. 1508 15

Vitamin E in foodstuffs is a mixture of tocopherols. In mouse Mutatect tumors, a model designed to detect DNA mutations, the hypoxanthine phosphoribosyltransferase (Hprt) gene mutation frequency is associated with the number of tumor-infiltrating neutrophils and both are markedly decreased in mice fed high levels of alpha-tocopherol. Dietary alpha-tocopherol is also associated with a decrease in neutrophil-associated loss of an interleukin 8 (IL-8)-expressing transgene in this tumor model. We examined Hprt gene mutation frequency (expressed as the number of 6-thioguanine-resistant colonies per 10(5) clonable tumor cells), IL-8 transgene loss, and myeloperoxidase activity (an indirect measure of neutrophil number) in tumors from Mutatect mice fed diets supplemented with various concentrations of D-alpha-tocopherol acetate and/or D-gamma-tocopherol acetate or neither tocopherol for 4 weeks. Hprt gene mutation frequency and myeloperoxidase activity were statistically significantly lower in tumor cells from mice fed alpha-tocopherol at 50 or 100 mg/kg body weight per day than in tumor cells from mice fed 0 mg/kg body weight per day alpha-tocopherol (P<.001 for each comparison). IL-8 transgene loss occurred in 28 of 28 tumors (100%; 95% confidence interval [CI] = 86% to 100%) from mice fed alpha-tocopherol at 50 mg or less/kg body weight per day and seven of 18 tumors (39%; 95% CI = 24% to 54%) from mice fed 100 mg/kg body weight per day (P<.001, Fisher's exact test, referent groups [pooled] 0, 25, and 50 mg/kg). gamma-Tocopherol had no detectable effect on any of the three endpoints. Thus, dietary alpha-tocopherol decreases two forms of genetic instability in a dose-dependent manner in this experimental tumor model.
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PMID:Dose-dependent effects of dietary alpha- and gamma-tocopherols on genetic instability in mouse Mutatect tumors. 1515 Mar 8

The majority of cancers of the ovary are thought to originate from a surface epithelial cell perturbed by ovulation. Outgrowth of a follicle destined to ovulate brings it into apposition with the ovarian epithelium. Ovarian surface cells are consequently exposed, within a limited diffusion radius, to inflammatory agents and reactive oxidants generated during periovulatory processes. Cells that overlie the formative site of follicular rupture suffer irreparable damages and undergo apoptosis. Potentially mutagenic 8-oxoguanine modifications were detected in (surviving) cells circumjacent to postovulatory ovine and human follicles. It is conceivable that clonal expansion of a cell with unrepaired DNA, but not committed to death, could be an initiating factor in the etiology of malignancy, insofar as proliferative ovulatory wound-repair responses may propagate mutations. Since the prognosis for ovarian cancer patients with invasive disease is so poor, and early detection has proven elusive, it is imperative that prospective methods of chemo-prevention be explored. Ovulation-induced oxidative base damages to the ovarian epithelium of ewes were prevented by vitamin E. Oxoguanine adducts persisted and CA-125 (a phenotype of metaplastic transformation) was expressed in cultures of cells that were distressed by ovulation in which p53 synthesis was inhibited. Vitamin E negated this reaction. Ovarian cyclicity and fertility were not altered in vitamin-treated ewes. A prophylactic benefit of a supplemental antioxidant is suggested in "ovulating" individuals designated at risk (e.g., due to a tumor suppressor malfunction) for the development of ovarian cancer.
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PMID:Oxidative damage to DNA of ovarian surface epithelial cells affected by ovulation: carcinogenic implication and chemoprevention. 1516 74

This manuscript reviews the guidelines of the European Association of Urology (EAU) on superficial bladder tumors and adds new data which has come available since 2001. It emphasises the data which are evidenced based and clearly explained where still insufficient research is available to make clear recommendations. Intravenous urethrography (IVU) is only necessary in grade 3 tumors. A good transurethral resection (TUR), with muscle in the specimen is essential. Random biopsies are only necessary when there is positive urinary cytology or when tumor in situ (TIS) is suspected. The variability in pathology interpretation remains a problem which seems not to have been solved by the new WHO 1998 classification. A review of pathology seems indicated when aggressive therapy is planned or there is a discrepancy between the visual findings and pathology. The visual judgement of urologists in superficial bladder tumors is very good. Second resection is indicated whenever insufficient material is delivered and in any T1 G3 tumor. In the last infiltrative tumors are regularly found. The treatment largely depends on prognostic parameters. For recurrence rate multiplicity of the tumor is most important, followed by recurrence rate, volume of the tumor, grade and T category. For progression the most important tumor is the anaplasia grade and the T category. Up to 50% of T1 G3 tumors and TIS evaluate to invasive tumors. Even low risk tumors still have an important recurrence rate of at least 20%/year in the first years after diagnosis. One chemo instillation immediately after TUR is indicated in low and intermediate risk superficial bladder tumors. Intravesical chemotherapy prevents recurrence but not progression. Ideal dosage and schedule of instillation is not clearly defined. Longterm therapy is not worthwhile. Bacille Calmette-Guerin (BCG) therapy is indicated in all tumors at high risk for progression. In tumors at high risk for recurrence it is also superior to intravesical chemotherapy, but its side-effects are more pronounced. Local or systemic side-effects are not related to efficacy and side-effects do not increase over time. The ideal schedule for BCG has not yet been found. It is however clear that some kind of maintenance therapy is necessary to obtain good results. BCG failure is probably any tumor which recurs at 3 and 6 months under BCG therapy. One third dose seems as sufficient as a full dose BCG. That BCG can spare the bladder in T1g3 tumors is largely documented but the chance to save the bladder when the tumor is still present after 2 cycles of BCG is very low. Cystectomy is indicated in these BCG failures. Vitamin E, A, and Lactobacillus Casei are probably effective in the prevention of the disease. Stopping smoking is advocated. Cystoscopy is still the gold standard in follow-up. It is advocated at 3 months and thereafter according to the prognostic parameters. High grade tumors are at risk life long. Follow-up of 5 years for low risk tumors seems reasonable.
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PMID:Guidelines on diagnosis and treatment of superficial bladder cancer. 1519 31

Vitamin E is a term that describes a group of compounds with similar yet unique chemical structures and biological activities. One interesting property possessed by certain vitamin E compounds-namely, delta-tocotrienol, RRR-alpha-tocopheryl succinate [vitamin E succinate (VES), a hydrolyzable ester-linked succinic acid analogue of RRR-alpha-tocopherol], and a novel vitamin E analogue referred to as alpha-TEA (alpha-tocopherol ether linked acetic acid analogue, which is a stable nonhydrolyzable analogue of RRR-alpha-tocopherol)-is their ability to induce cancer cells but not normal cells to undergo a form of cell death called apoptosis. In contrast, the parent compound, RRR-alpha-tocopherol, also referred to as natural or authentic vitamin E and known for its antioxidant properties, does not induce cancer-cell apoptosis. Efforts to understand how select vitamin E forms can induce cancer cells to undergo apoptosis have identified several nonantioxidant biological functions, including restoration of pro-death transforming growth factor-beta and Fas signaling pathways. Recent studies with alpha-TEA show it to be a potent inducer of apoptosis in a wide variety of epithelial cancer cell types, including breast, prostate, lung, colon, ovarian, cervical, and endometrial in cell culture, and to be effective in significantly reducing tumor burden and metastasis in a syngeneic mouse mammary tumor model, as well as xenografts of human breast cancer cells. Studies also show that alpha-TEA, in combination with the cyclooxygenase-2 inhibitor celecoxib and the chemotherapeutic drug 9-nitro-camptothecin decreases breast cancer animal model tumor burden and inhibits metastasis significantly better than do single-agent treatments.
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PMID:Vitamin E and breast cancer. 1557 54


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