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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

We have previously demonstrated that diverse carotenoids inhibit chemically induced neoplastic transformation in 10T1/2 cells. To address their mechanism of action, the effects of six diverse carotenoids, with or without provitamin A activity, on gap junctional communication and lipid peroxidation have been investigated. beta-Carotene, canthaxanthin, lutein, lycopene and alpha-carotene increased gap junctional intercellular communication in a dose-dependent manner in the above order of potency, whereas m-bixin was inactive at concentrations up to 10(-5) M. alpha-Tocopherol, a potent chain-breaking antioxidant, caused a marginal enhancement of junctional communication. The enhancement of junctional communication by diverse carotenoids showed a strong statistical correlation with their previously determined ability to inhibit methylcholanthrene-induced neoplastic transformation (r = -0.75). All carotenoids tested inhibited lipid peroxidation, but with differing potencies. alpha-Tocopherol was the most active inhibitor followed by m-bixin. The capacity of carotenoids or alpha-tocopherol to inhibit lipid peroxidation was neither consistent with their ability to inhibit neoplastic transformation (r = 0.30) nor to increase junctional communication (r = 0.12). Since junctional communication appears to play an important role in cell growth control and carcinogenesis, we propose that in this system carotenoid-enhanced intercellular communication provides a mechanistic basis for the cancer chemopreventive action of carotenoids. These data also imply that carotenoids function in a manner analogous to retinoids in the 10T1/2 assay system. Interestingly this activity appears independent of their provitamin A status.
Carcinogenesis 1991 Nov
PMID:Carotenoids enhance gap junctional communication and inhibit lipid peroxidation in C3H/10T1/2 cells: relationship to their cancer chemopreventive action. 193 96

The ability of diverse carotenoid to inhibit methylcholanthrene-induced transformation of 10T1/2 cells has been investigated. When delivered using tetrahydrofuran as a novel solvent, all carotenoids were absorbed by cultured cells. When continuously administered to methylcholanthrene-treated cultures 7 days after removal of the carcinogen, canthaxanthin, beta-carotene, alpha-carotene and lycopene inhibited the production of transformed foci in a dose-dependent manner in the above order of potency. This activity was not associated with drug toxicity or antiproliferative effects. Renierapurpurin and bixin did not inhibit transformation at concentrations less than or equal to 10(-5) M. Lutein was inhibitory at 10(-5) M, but was inactive at lower concentrations. Because of differences in stability in culture medium (alpha-carotene less than beta-carotene less than canthaxanthin less than lycopene less than lutein) and structure, cellular levels of drug differed up to 8-fold after administration of identical concentrations of compounds. Carotenoids with polar groups achieved highest cellular levels, however cellular uptake did not correlate with activity. For example, lutein, the most polar and most stable, reached the highest concentration in cells yet required a concentration of 10(-5) M for activity in the transformation assay, while alpha-carotene, the least stable and least concentrated by cells, was comparably active at 3 X 10(6) M. alpha-Tocopherol, a potent lipid-phase antioxidant, was as active as lycopene in the transformation assay but at a 10-fold higher concentration did not approach the activity of beta-carotene or canthaxanthin. Because the most potent of the carotenoids tested (i.e. beta-carotene, alpha-carotene, canthaxanthin) all have the potential for conversion to retinoids (though this has never been demonstrated in mammals for canthaxanthin), it is suggested that these compounds have two components to their action; one related to their antioxidant properties, the other to their pro-vitamin A activities.
Carcinogenesis 1991 Apr
PMID:Diverse carotenoids protect against chemically induced neoplastic transformation. 201 31

1,8-Dihydroxy-3-methyl-9-anthrone (chrysarobin), a potent anthrone tumor promoter, reduced [125I] epidermal growth factor (EGF) binding to its receptor in primary epidermal cells from SENCAR mice maintained in low Ca2+ containing medium. The time course for this effect with chrysarobin was different from that of 12-O-tetradecanoylphorbol-13-acetate (TPA). Maximum inhibition of [125I]EGF binding was observed at 18 h versus 1 h respectively. Scatchard analyses revealed that the inhibition by chrysarobin was due to a decrease in the number of both high- and low-affinity classes of EGF receptors. In contrast, TPA caused a rapid inhibition of EGF binding, primarily due to a loss of high-affinity receptors. The mechanism by which chrysarobin inhibited the binding of EGF to its receptor involved neither direct activation nor membrane translocation of epidermal protein kinase C, whereas the rapid decrease in EGF binding induced by TPA was consistent with its ability to activate protein kinase C. Structure-activity relationships for EGF binding inhibition by anthrones revealed that inhibition was inversely proportional to chain length at the C10-position, which correlated closely with oxidation rate and skin tumor-promoting activity. alpha-Tocopherol was able to block partially the effect of chrysarobin but not TPA on EGF binding. These results suggest that oxidation at position C10 is at least partially responsible for the inhibition of EGF binding induced by chrysarobin. Furthermore, these studies support the hypothesis that changes in EGF receptor binding and/or function may play a role in skin tumor promotion by diverse classes of promoting agents.
Carcinogenesis 1990 Sep
PMID:Differential mechanism for the inhibition of epidermal growth factor binding to its receptor on mouse keratinocytes by anthrones and phorbol esters. 240 Oct 43

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

Investigations that have influenced the promotion of vitamin E supplementation are reviewed. The various forms of vitamin E found in foods and the composition of synthetic vitamin E in common use are described with note of a frequent error of identification made in reports of studies on vitamin E. Recent communications on the use of antioxidants to delay carcinogenesis in animals and in humans are discussed. The publicity given the reports of cancer prevention by antioxidants will probably increase self-supplementations. It is therefore necessary to understand the pharmacological limits of such supplementation with vitamin E. Daily supplementation of adults with about 200 mg of d-alpha-tocopherol equivalents per day has not been proven to be harmful, but the effects of ingestion of more than 800 mg a day have not been studied sufficiently. Special precautions should be taken in administering emulsified vitamin E preparations intravenously to premature infants.
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PMID:The promotion of vitamin E. 352 33

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


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