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

Clinical and experimental evidence indicates a possible role for vitamin A deficiency in the pathogenesis of bronchogenic carcinoma. We, therefore, measured serum vitamin A levels in 67 newly diagnosed non-resectable lung cancer patients. In 43 of these patients daily vitamin A intake was also determined. Serum vitamin A levels were within the normal range of the general population of 66 of the 67 patients. Eighteen of 43 patients had daily vitamin A intakes less than 5000 IU/day while 25 patients had daily intake above this level. The serum vitamin A level did not correlate with histologic subtype, extent of disease or presence or absence of hepatic metastases. While these data suggest that vitamin A deficiency was not implicated in pulmonary carcinogenesis, more definitive conclusions await prospective evaluation of high risk individuals followed serially for many years.
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PMID:Vitamin A serum and dietary vitamin A intake in lung cancer patients. 62 13

Male, weanling rats, divided into two groups were maintained for 45 days on a corn-based diet containing 5 mg vitamin A palmitate per kg diet (Group 1, normal animals) and without the vitamin (Group 2, dificient animals). Fifteen hours after the last feeding, the animals were decapitated and liver microsomes and colon mucosal epithelial homogenates were prepared and used to investigate the relative activities of the mixed function oxidase (MFO) and epoxide hydrase (EH) enzyme systems. The sequential metabolism of aflatoxin B1 (AFB1) and its epoxide AFBepox) product, respectively, were also estimated by measuring apparent maximal velocities (Vmax) and Michaelis constants (Km) for ethylmorphine (EM) N-demethylase and styrene oxide hydratase. The Vmax data indicated that MFO activity in the liver and colon was not rate-limiting in the two groups of animals but the reverse were observed with calculated reaction rates at concentrations above (0,03 mM) for EM N-demethylase only. In both organs, styrene oxide hydratase depict calculated reaction rates which are not rate-limiting for all the concentration range (0,001 to 3,00 mM). If these reaction rates are applied to AFB1 metabolism, it may be concluded that MFO and not epoxide hydrase (EH) activity is a critical agent under vitamin A deficiency in AFB1 toxicity and/or carcinogenesis. Measurements of AFT1 metabolism both in terms of substrate disappearance and product formation do not confirm this observation except for the production of AFR0 and compounds of unknown structure at the origin which may embody the critical factor(s) that promotes colon carcinogenesis under vitamin A deficiency.
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PMID:Effect of vitamin A deficiency on hepatic microsomal and colon mucosal mixed function oxidase. IV--Influence on aflatoxin B1 metabolism, ethylmorphine and epoxide hydrase activity. 74 84

The mechanism by which vitamin A prevents or delays in chemical carcinogenesis remains unclear. In the present study, we assess the suggestive role of vitamin A in the initiation phase of carcinogenesis. We have conducted a dose-effect relationship between vitamin A dietary intake and aflatoxin B1 (AFB1) genotoxicity measured both in vitro and in vivo. Thus AFB1-induced mutagenesis in Salmonella typhimurium TA98 was investigated and compared to AFB1-induced single-strand breaks (SSBs) in DNA of rat hepatocytes. Rats were fed ad libitum with diet containing 0, 5, 50 or 500 IU of retinyl palmitate for 8 weeks. The AFB1-treated rats were injected i.p. with 1 mg/kg body weight. In the Ames test conditions TA98 back-reversion was negatively correlated with the log of vitamin A concentration in liver S9 fractions from experimental groups. However, the activities of metabolizing enzymes which specifically activate or deactivate AFB1 were found to be significantly decreased in vitamin A-deficient animals and weakly modified in vitamin A-supplemented animals. For in vivo experiments, the DNA elution rate of both AFB1-treated and untreated rats was increased in vitamin A deficiency condition (+79% and +17% respectively) and was reduced with the higher vitamin A dietary level (-44% and -53% respectively). DNA damage measured in vivo showed a significant positive correlation with mutagenic activity measured in the Ames test. These results confirm that the vitamin A status of animals can influence AFB1 genotoxic activity in vitro and indicate that this phenomenon also occurs in vivo. Thus a similar mechanism may be considered for the protective action of vitamin A both in vitro and in vivo. However, this mechanism is unlikely to involve modulation of the microsomal enzyme system responsible for AFB1 metabolism. Therefore a protective mechanism at the cytosolic or nuclear levels may be suggested.
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PMID:Effect of vitamin A dietary intake on in vitro and in vivo activation of aflatoxin B1. 138 11

The present investigation shows the effect of combined dietary deprivation of fat and vitamin A on N-nitrosodiethylamine (NDEA) induced lung carcinogenesis in male Swiss NMRI mice. Lung tumors were induced by three intragastric administrations of NDEA (80, 80, 40, mg/kg body wt.) in normal saline with a gap of 4 weeks between each administration. The tumor incidence and tumor burden in control animals were found to be 39.1 and 3.9%, respectively. Fat deficiency decreased the tumor incidence to 30.4% and tumor burden to 3.7%. On the other hand, vitamin A deficiency increased them to 95.6 and 6.8%, respectively. Fat deprivation in the diet of animals fed with vitamin A deficient diet decreased the tumor burden and tumor incidence to 59.0 and 4.0%, respectively which were still more than in the control animals. This study suggests a protective role for low intake of fat in vitamin A deficiency.
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PMID:Effect of combined deficiency of fat and vitamin A on N-nitrosodiethylamine-induced lung carcinogenesis in mice. 154 Sep 32

Vitamin A deficiency caused a significant increase (P less than 0.05) in benzo[a]pyrene (BP)-induced lung tumor incidence and tumor burden in male Wistar rats. Inhalation of cigarette smoke during initiation and post-initiation phases of carcinogenesis resulted in higher tumor burden as compared to the same observed in the animals exposed to cigarette smoke during the post-initiation phase only. Stimulation in tumor burden by cigarette smoke was increased further by vitamin A deficiency.
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PMID:Effect of cigarette smoke inhalation on benzo[a]pyrene-induced lung carcinogenesis in vitamin A deficiency in the rat. 226 18

The modulating influence of vitamin A deficiency on carcinogenesis induced by two potent carcinogens, diethylnitrosamine (DEN) and acetoxymethyl methylnitrosamine (AMMN), was studied in BALB/c mice. DEN was administered intragastrically every 30 days at a total dose of 200 mg/kg body weight, split into four doses. AMMN was applied continuously every 14 days on the tongue, at a dose of 2 mg/kg body weight. AMMN and DEN treated animals fed the vitamin A deficient diet had a significantly higher tumor incidence that mice fed the normal diet (p less than 0.05). Studies on the levels of vitamins A, C, B2 and folic acid in the liver and plasma of mice treated with the two carcinogens revealed that both the carcinogens increased vitamin C in both tissues, decreased folic acid and had no effect on vitamin A, while hepatic vitamin B2 was lowered by treatment with AMMN by not by DEN.
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PMID:Diethylnitrosamine and acetoxymethyl methylnitrosamine-induced carcinogenesis in mice and vitamin A deficiency. 251 57

This paper provides an overview of our knowledge on the involvement in cancer of vitamins A, C and E and of calcium, selenium and zinc. This work is a background for studies on dietary magnesium's effects on cancer. Consumption of vitamin A and its dietary precursors has been associated with reduced cancer at several sites in human and animal studies. Carcinogenesis studies using several models of cancer have been conducted on the influence of vitamin A deficiency, vitamin A excess and supplementation of vitamin A analogues. Vitamins C and E are effective in the prevention of N-nitroso compound (nitrosamine) formation. Vitamin C is effective in aqueous and vitamin E is effective in non-aqueous media. Both of these vitamins also have inhibited carcinogenesis by preformed carcinogens at several sites, but enhancement has been observed at some sites when excess vitamin treatment was studied. The potential role of calcium in the prevention of colon cancer is being pursed. Few experimental studies have been conducted but data support an effect of calcium on colonic epithelial proliferation. Epidemiological and especially experimental results suggest an inhibition of cancer by dietary selenium. In animal studies, selenium supplementation has been particularly effective in inhibiting colon and mammary carcinogenesis, but enhanced carcinogenesis was observed in some studies on skin, liver and pancreas cancer. Data suggest that zinc deficiency may be a factor in esophageal cancer; however, studies on tumor growth have demonstrated retarded tumor growth in zinc-deficient animals.
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PMID:Effects of the intake of selected vitamins and minerals on cancer prevention. 266 27

Evidence pertaining to the role of dietary factors in carcinogenesis comes from both epidemiological studies and laboratory experiments. In 1982, the Committee on Diet, Nutrition, and Cancer of the National Research Council conducted a comprehensive evaluation of this evidence. That assessment as well as recent epidemiological and laboratory investigations suggest that a high fat diet is associated with increased susceptibility to cancer of different sites, particularly the breast and colon, and to a lesser extent, the prostate. Current data permit no definitive conclusions about other dietary macroconstituents including cholesterol, total caloric intake, protein, carbohydrates and total dietary fiber. Specific components of fiber, however, may have a protective effect against colon cancer. In epidemiological studies, frequent consumption of certain fruits and vegetables, especially citrus fruits and carotene-rich and cruciferous vegetables, is associated with a lower incidence of cancers at various sites. The specific components responsible for these effects are not clearly identified, although the epidemiological evidence appears to be most consistent for a protective effect of carotene on lung cancer and less so for vitamins A and C and various cancer sites. The laboratory evidence is most consistent for vitamin A deficiency and enhanced tumorigenesis, and for the ability of various nonnutritive components in cruciferous vegetables to block in-vivo carcinogenesis. The data for minerals and carcinogenesis are extremely limited, although preliminary evidence from both epidemiological and laboratory studies suggests that selenium may protect against overall cancer risk. Frequent consumption of cured, pickled, or smoked foods, possibly because they may contain nitrosamines or polycyclic aromatic hydrocarbons, appears to increase the risk of esophageal or stomach cancer, however, the specific causative agents in these foods are not clearly identified. Excessive alcohol consumption among smokers appears to be associated with an elevated risk of cancers of the oral cavity, esophagus, larynx, and respiratory tract. The mechanisms of action of dietary factors on carcinogenesis are poorly understood. The NRC committee, and more recently, the National Cancer Institute and the American Cancer Society have proposed interim dietary guidelines to lower the risk of cancer. These guidelines are consistent with general dietary recommendations proposed by U.S. government agencies for maintenance of good health.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet, nutrition, and cancer. 301 Mar 79

Ornithine decarboxylase (ODC, EC 4.1.1.17) activity was measured, without exogenous stimulation, in the liver, oesophagus and lung of Wistar rats which were vitamin A deficient or supplemented with retinol or retinoic acid. The enzyme basal activity in such deficiency conditions was higher, when compared with controls, in the oesophagus and especially in the lungs. Retinoic acid normalized enzyme activity only at high doses (300 micrograms/day). In the liver, initial retinol deficiency did not sensitively modify ODC activity, and retinoic acid then stimulated the enzyme abnormally. This phenomenon could not be observed at later stages of vitamin deficiency (but there again without cytological abnormalities or thymidine incorporation disturbances): liver ODC response then became comparable to that of other tissues. These results highlight the particular basal hyperactivity of pulmonary ODC during the initial stages of vitamin A deficiency, indicative of an enhanced tendency to cell proliferation. A special stimulating effect of retinoic acid on ODC, contemporary with early deficiency, was observed in the liver; this effect was not observed at a later stage in normally fed rats.
Carcinogenesis 1988 Dec
PMID:Ornithine decarboxylase basal activity in liver, oesophagus and lung of vitamin A deficient rats, and the effect of retinoic acid. 319 61

Liver plasma membranes (LPM) were prepared from vitamin A-deficient and -sufficient rats as well as from animals treated with retinoic acid, with or without ethanol. Although the fluorescence polarization value of LPM prepared from retinoic acid-fed animals was significantly lower than that of controls (0.201 +/- 0.008 vs. 0.254 +/- 0.005, P less than 0.001), no effect was seen with a vitamin A-deficient diet (0.259 +/- 0.005). No change in the fluorescence polarization was observed in erythrocyte ghost membranes with either vitamin A deficiency or chronic ethanol consumption. The sialic acid concentration of the membranes was significantly higher in LPM and erythrocyte ghosts obtained from vitamin A-deficient animals (37.6 +/- 1.1 vs. 29.6 +/- 0.7 nmol/mg protein for LPM, P less than 0.01, and 77.7 +/- 0.6 vs. 62.0 +/- 1.7 for erythrocyte ghosts, P less than 0.001); the LPM of retinoic acid-treated animals had the lowest values (26.9 +/- 1.6 nmol/mg protein). This sialic acid concentration of LPM was positively correlated with the fluorescence polarization (r = 0.775, P less than 0.001). Chronic ethanol feeding resulted in lower hepatic and LPM vitamin A and greater LPM fluidity with higher cholesterol esters in all diet groups (P less than 0.001). Because increased sialic acid concentration has been incriminated in the pathogenesis of tumor development, it may provide a mechanism whereby lowered hepatic vitamin A promotes carcinogenesis and retinoic acid feeding opposes this process.
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PMID:Differential effects of retinoids and chronic ethanol consumption on membranes in rats. 341 17


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