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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antioxidant and/or free radical scavenger vitamins (A, E) as beta carotene are unequally distributed among intertropical peoples from Africa. In Ivory coast for example the values observed are clearly enhanced in the regions where Palm oil is usually eaten than in savanna regions. Primary liver cancer (PLC) is more frequently observed in savanna regions. Furthermore it has been recently suggested that retinoic acid which is derived from vitamin A and beta carotene could interact with the genes which are involved in the primary liver carcinogenesis. In PLC patients as in subjects suffering from sickle cell anaemia, malaria, kwashiorkor or marasmus, and AIDS, the plasma levels of vitamin A, Vitamin E and beta carotene are decreased. Though disturbances in the digestion of fats that may be observed in some pathologies (mainly in Kwashiorkor) affect the discussion of the results, haemolysis and/or acute phase reaction with increased respiratory burst are always observed. That explain, at least in part, the lowering of lipophilic-antioxidant-vitamin plasma levels. As a consequence crude palm oil addition or vitamin A and E therapy would enhance the natural defences against the deleterious effects of the oxidative stress induced by these affections. It is worth checking about.
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PMID:[Antioxidant and/or free radical scavenger vitamins in tropical medicine]. 130 94

Thirty-seven adult male and female golden hamsters (Mesocricetus auratus) were divided into four experimental groups. In Group A, the animals served as untreated controls, having the left buccal pouches painted with mineral oil. In Group B, the animals received 10 mg vitamin E (alpha tocopherol) in peanut oil by the oral route, with a fine pipette, twice weekly. In Group C animals, the left buccal pouch was painted three times weekly with DMBA (0.5% solution of 7,12 dimethylbenz(a)anthracene in heavy mineral oil). Group D animals received both vitamin E and DMBA in the amounts indicated for Groups B and C, with the vitamin E being administered on days alternate to the DMBA painting, also in the manner described for the above groups. All animals were killed after eight weeks of treatment. Epithelial whole mounts were prepared from the left buccal pouches. These specimens were then stained for ATPase to demonstrate the presence of Langerhans cells (LCs). A notably decreased density of LCs was observed after treatment with DMBA. Vitamin E administration in addition to DMBA treatment resulted in a less dramatic decrease in LC density. Since vitamin E has been shown to retard experimental oral carcinogenesis, vitamin E may retard carcinogenesis by maintaining the number of Langerhans cells.
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PMID:Alpha tocopherol alters the distribution of Langerhans cells in DMBA-treated hamster cheek pouch epithelium. 257 13

The influences of vitamin C and vitamin E on cancer reported in the literature are reviewed. Several correlational studies and case-control studies suggest that the consumption of vitamin C-containing foods is associated with lower risk for certain cancers, particularly gastric and esophageal cancer. No definite links between dietary vitamin E and human cancer have been demonstrated. Animal and in vitro studies have shown that vitamins C and E can effectively inhibit the formation of carcinogenic nitrosamines. However, animal studies examining the effects of these two vitamins on other chemically-induced cancers are not conclusive. Vitamin C supplementation has been reported to inhibit skin, nerve, lung and kidney carcinogenesis. Vitamin E has been shown to inhibit skin, liver, oral, ear duct, and forestomach carcinogenesis; and to enhance, to have no effect on, or to inhibit mammary gland or colon carcinogenesis, depending upon the method of administration, the level of dietary selenium or fat, and the species and strain of animals used. Both vitamin C and vitamin E can inhibit mutagenesis and carcinogenesis in vitro. Each of the vitamins has been shown to inhibit tumor cell growth and carcinogen-induced DNA damage. The mechanism of action of the two vitamins against carcinogens is not clearly understood. Several suggested mechanisms of action include modification of the metabolism of polycyclic hydrocarbons, reduction of mutagenic activity and reaction with genotoxic free radicals. It is concluded that the potential usefulness of vitamin C and vitamin E in the prevention and treatment of cancer should not be ignored because under certain experimental conditions these two vitamins exert inhibitory effects on chemical carcinogenesis. More carefully standardized and controlled experiments are required to adequately evaluate this potential.
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PMID:Vitamin C, vitamin E and cancer (review). 305 51

Oxidative damage to membranes initiates lipid peroxidation chain reactions and stimulation of the arachidonic acid cascade. The products of these reactions may mediate the genetic toxicity of oxygen radicals. Arachidonic acid alone induced sister chromatid exchange (SCE) formation and significantly augmented the genetic damage observed with an oxygen radical-generating system. The number of SCEs was reduced significantly in oxygen radical-treated Chinese hamster ovary cells incubated with inhibitors of the cyclo-oxygenase and lipoxygenase pathways. Vitamin E, when combined with inhibitors of arachidonic acid metabolism, protected target cells completely from oxygen radical-induced genotoxicity. These data support the hypothesis that lipid peroxidation intermediates may be involved in the genesis of radical-generated genetic lesions.
Carcinogenesis 1987 Nov
PMID:Effects of inhibitors of arachidonic acid metabolism and vitamin E on oxygen radical-induced sister chromatid exchanges. 311 4

The effects of vitamins A, C, and E and of selenium on carcinogenesis are briefly summarized and updated. These vitamins and minerals were selected because they have been studied extensively in recent years with a variety of carcinogenesis models. The consumption of vitamin A and its precursors (carotenoids) has been negatively correlated with cancer at a number of sites, particularly the lung. Animal investigations on vitamin A involvement in carcinogenesis have generally been of three types: those assessing the effect of vitamin A deficiency, the effect of excess vitamin A, or the effect of supplementation with synthetic analogs of vitamin A. Vitamin A deficiency had no effect on salivary gland carcinogenesis, enhanced urinary bladder, lung, and liver carcinogenesis, and inhibited colon carcinogenesis. Excess of various forms of vitamin A enhanced or inhibited skin tumorigenesis, inhibited mammary carcinogenesis in rats (but not in mice), and carcinogenesis of the forestomach, liver, and urinary bladder (with one model, but not with another), or enhanced or did not influence lung carcinogenesis. Vitamin A analogs have enhanced or inhibited skin tumorigenesis, inhibited salivary gland, mammary, and urinary bladder carcinogenesis, enhanced tracheal and liver carcinogenesis, and either enhanced or inhibited pancreas carcinogenesis, depending upon the model employed. Although retinoids have been shown to inhibit carcinogenesis at many sites, numerous negative studies have been reported and some reports have indicated enhanced carcinogenesis. The most convincing evidence for the involvement of vitamin C in cancer prevention is the ability of ascorbic acid to prevent formation of nitrosamine and of other N-nitroso compounds. In addition vitamin C supplementation was shown to inhibit skin, nose, tracheal, lung, and kidney carcinogenesis, to either not influence or enhance skin, mammary gland, and colon carcinogenesis, and to enhance urinary bladder carcinogenesis, when given as sodium ascorbate, but not when given as ascorbic acid. Like vitamin C, vitamin E can inhibit nitrosation. Vitamin E was shown to inhibit skin, cheek pouch, and forestomach carcinogenesis, to enhance or inhibit colon carcinogenesis, and to have no effect on or to inhibit mammary gland carcinogenesis, depending upon the method of vitamin E administration or the level of dietary selenium or dietary fat. Selenium effects on carcinogenesis have been recently reviewed and the present discussion only updates this area by indicating that enhancement of carcinogenesis by dietary selenium supplements has been observed in the liver, pancreas, and skin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Update on the effects of vitamins A, C, and E and selenium on carcinogenesis. 354 Sep 70

The effects of cabbage and vitamin E on colon carcinogenesis were investigated in Swiss mice treated with 1,2-dimethylhydrazine. Throughout the experiment the mice were fed a laboratory chow diet (46 mg vitamin E per kg) or chow containing 13 g cabbage per 100 g or 180 mg vitamin E per kg. Starting after 31 days of diet treatment the mice received 7 weekly s.c. injections of DMH. They were sacrificed 17 weeks after the first dose of DMH. While diet did not significantly alter colon tumor response, some trends were observed. Female mice given cabbage had a higher incidence (percent of mice with a tumor) and multiplicity (tumors per tumor bearing mouse) of colon tumors. Males were little affected by cabbage apart from a lower incidence of adenocarcinomas. Compared with mice fed the control diet those given vitamin E had a higher colon tumor incidence. This effect, which was stronger in females, was due to an increased incidence of adenomas. Vitamin E had little apparent affect on tumor multiplicity apart from a reduction in adenocarcinomas in females and adenomas in males. The data do not support the view that cabbage and vitamin E are protective against colon cancer.
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PMID:Cabbage and vitamin E: their effect on colon tumor formation in mice. 356 89

In the Basel study (BS) (1960-73) on cardiovascular and peripheral arterial diseases, a mortality follow-up was completed for the period 1965-80. Of the 4,224 men at risk for these diseases, 531 died. The causes of death were established from the death certificates and classified into 8 groups. For each case 2 age- and sex-matched controls were selected and compared with the corresponding cases with regard to the various variables obtained at the three examinations (1960, 1965, 1971). This report dealth with cancer mortality, plasma lipids, plasma vitamins, alcohol and cigarette consumption, and intake of milk and citrus fruits. The results were all obtained at the second follow-up examination (BS III, 1971-73). Cancer of the lung, stomach, large bowel, and all other sites were treated separately. The average follow-up from BS III until death varied from 3.7 years (other sites) to 4.9 years (cancer of the lung). Of 129 cancer deaths, the highest incidence was found for cancer of the lung (38) followed by stomach (19) and large bowel, (15) and the remainder (57) was for other sites. Plasma lipids did not differ significantly among cases and controls. However, the lowest values were observed in colorectal cancer and gastric carcinoma (mean cholesterol, 213 mg/dl). beta-Carotene was significantly lower in cancer cases of the lung than in controls (14.8 micrograms/dl vs. 23.7; P less than .05). It was also low in gastric cancer cases (13.0 micrograms/dl). Vitamin A was below average only in cases with gastric cancer (difference due to the small number not significant). Vitamin C was consistently lower in cancer cases than in controls. The lowest value was found for cancer of the stomach and corresponded to a below-average consumption of citrus fruits. Vitamin E was low in cancer of the colon. Plasma lipids correlated strongly with vitamin E (tau = 0.5) and to a lesser extent with vitamin A (tau = 0.25). beta-Carotene correlated poorly with beta-lipoproteins (low-density and very low-density lipoproteins) but significantly with total cholesterol. Smoking was inversely related, as was alcohol consumption, to the beta-carotene level. From these results, the conclusion was that vitamins influence carcinogenesis in humans.
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PMID:Cancer, vitamins, and plasma lipids: prospective Basel study. 659 56

Lead chromate induces chromosomal damage as a result of extracellular dissolution producing solubilized chromium and lead and we show here that the dissolution process is greatly accelerated by the presence of cells. We have sought to determine which of these ions is involved in lead chromate-induced clastogenicity. Cell-mediated extracellular dissolution of particulate lead chromate resulted in the accumulation of both solubilized chromium and solubilized lead, reaching concentrations in the extracellular medium of 15 and 1.9 microM respectively and reaching concentrations inside the cell of 2700 and 97 microM respectively. Both the extracellular and intracellular accumulation of chromium was time dependent and both the solubilized lead and chromium increased proportionately from a lower dose to a higher dose. Exposing cells to water soluble sodium chromate under conditions which produced similar time-dependent intracellular concentrations of chromium also produced a similar amount and spectrum of chromosome damage as lead chromate. In contrast, exposure to lead glutamate resulted in intracellular lead levels 438-times higher than those produced by lead chromate, but produced no chromosome damage. A higher dose of lead glutamate was weakly clastogenic, but it induced a different spectrum of chromosomal aberrations than lead chromate. Pretreatment of cells with vitamin E had no effect on the uptake of chromium, but reduced both sodium chromate- and lead chromate-induced clastogenesis by 54-93%. Vitamin E pretreatment did not affect lead glutamate-induced clastogenesis. The results of this study indicate that although lead(II) is weakly clastogenic at high doses, hexavalent chromium is the proximate clastogen in lead chromate-induced clastogenesis. Additionally, this is the first report that pretreatment of cells with vitamin E can block clastogenesis induced by particulate chromates.
Carcinogenesis 1994 Oct
PMID:Cell-enhanced dissolution of carcinogenic lead chromate particles: the role of individual dissolution products in clastogenesis. 795 62

The dorsal skins of 6-8 week old female SENCAR mice were initiated with a single application of 10 nmol of 7,12-dimethylbenz[a]anthracene (DMBA) and subsequently promoted twice/week with topical applications of vitamin E (dl-alpha-tocopherol, 80 mumol/treatment). Vitamin E from two separate commercial suppliers was tested. For comparison, a group of similar mice, also initiated with DMBA, was promoted twice/week with the known tumor promoter 12-O-tetradecanoylphorbol-13- acetate (TPA, 2 micrograms/treatment). Papillomas appeared 39 and 50 days respectively after promotion began with vitamin E from the two different sources, as compared with 32 days in the group receiving TPA promoted. Hundred per cent of TPA-promoted animals and 92-96% of the vitamin E-promoted mice developed tumors. A maximum of 15 papillomas/animal appeared in the TPA-promoted mice. The two vitamin E preparations were somewhat less effective than TPA and showed different relative potencies, producing about seven and 12 papillomas per animal respectively. Unlike TPA, vitamin E showed very little ability to produce an inflammatory response in skin. To test whether initiated cells that did not appear as papillomas after vitamin E promotion were still viable, and had proceeded past stage I of promotion (conversion), the group that developed 12 papillomas/animal from vitamin E promotion was further promoted with mezerein, a stage II promoter. In this group, the papilloma frequency then increased to approximately 17/animal. The animals were followed over the course of their lifespan and monitored for skin carcinomas. In the TPA-promoted group 64% of the mice developed carcinomas, while the two vitamin E-promoted groups showed 48 and 60% incidence respectively. These results indicate that topically applied vitamin E acts as a complete tumor promoter in DMBA-initiated mouse skin, with an efficiency approaching that of TPA. Since vitamin E is a powerful antioxidant, they also suggest that reduction of cellular oxidant levels may trigger the tumor promotional process, and it may therefore be prudent to avoid repetitive or prolonged topical exposure of human skin to antioxidants like vitamin E.
Carcinogenesis 1993 Apr
PMID:Vitamin E is a complete tumor promoter in mouse skin. 847 30

To a great extent carcinogenesis depends on the environment. Some vitamins contribute to the "exogenous" protection against aggressors (i.e., on a molecular scale, active forms of oxygen and free radicals). Epidemiology provides numerous data in favour of this protection, but these date are sometimes ambiguous or contradictory. Current, active experimental studies will probably lead to firm conclusions within the next few years. As regards vitamin A, considerable advances have been made in fundamental research (we now know its molecular mechanism of action, notably on genes) and in applied research (differentiation of leukaemic cells). In various aspects vitamin D resembles vitamin A and also acts on the haematopoietic tissue. Vitamin E is difficult to study, but its protective effect on cell membranes and structures cannot be questioned. Vitamin C emerges from a period of controversy and is increasingly studied at present: it might be a useful adjuvant for the treatment of cancers.
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PMID:[Vitamins and cancers]. 850 31


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