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

A case-control study examined the association between cervical intra-epithelial neoplasia (CIN) and serum and dietary alpha-carotene, beta-carotene, cryptoxanthin, lutein, and lycopene. Cases (n = 102) had biopsy confirmed CIN I, II or III. Controls matched for age, ethnic origin and clinic (n = 102) had normal Pap smears. Participants completed health history and food frequency questionnaires. Fasting venous blood samples were assayed for serum carotenoids. Multivariable conditional logistic regression analyses yielded odds ratios and 95% confidence intervals (CIs) for those in quartiles 3, 2, and 1 (lowest) compared to quartile 4 (highest) of serum lycopene of 3.5 (1.1-11.5), 4.7 (1.2-17.7) and 3.8 (1.1-12.4), respectively. Similar analyses yielded adjusted odds ratios (ORaS) and 95% CIs of 4.6 (1.1-19.7), 5.8 (1.6-21.3) and 5.4 (1.3-23.3) for dietary intake of lycopene. The findings for lycopene-rich foods (tomatoes) were consistent with this result. CIN was not associated with the lutein. Findings for alpha-carotene, beta-carotene and cryptoxanthin were ambiguous. Quartile of vitamin C intake was also inversely associated with CIN with ORaS and 95% CIs of 3.7 (0.9-14.6), 4.1 (1.0-17.2), and 6.4 (1.4-30.0) for those in quartiles 3, 2, and 1 compared to quartile 4.
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PMID:Dietary and serum carotenoids and cervical intraepithelial neoplasia. 201 56

Long-term carcinogenicity studies were carried out in male Sprague-Dawley rats maintained on vitamin A-sufficient (SLO+) and vitamin A-deficient (SLO-) diets and treated with tobacco extract (TE). Three-week-old rats received by gavage a total dose of 860 mg of TE at a daily dose of 3 mg/rat over a period of 21 months. Besides tumorigenicity, drug-metabolizing phase I and phase II enzymes in lung and liver as well as vitamin A and C levels in plasma and liver were measured at 12 and 21 months of age. The cumulative tumor incidence in TE-treated SLO- rats was significantly higher (77-100%) than that observed in TE-treated SLO+ rats (20-22%). Furthermore, SLO+ rats treated with TE showed lung and forestomach tumors, whereas TE-treated SLO- rats showed a preponderance of pituitary adenomas (87%). It was observed that TE treatment increased the activity of the hepatic and pulmonary phase I enzymes and decreased the glutathione/glutathione S-transferase detoxification system at both time points in SLO- rats. On TE treatment the vitamin A levels in the liver and plasma were significantly decreased with a concurrent increase in vitamin C levels. The data show that a vitamin A-deficient diet renders male Sprague-Dawley rats more susceptible to TE treatment than the vitamin A-sufficient diet, an effect which was associated with the augmented induction of P-450 content and activities and depletion of the glutathione/glutathione S-transferase pathway by TE.
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PMID:Carcinogenicity studies of tobacco extract in vitamin A-deficient Sprague-Dawley rats. 203 40

In this paper the progress of epidemiological research in stomach cancer during 1980-1990 is reviewed in respect to regional variation, etiology, and formation of carcinogens. The evaluation of 4 cohort and 16 case-control studies revealed a consistently inverse relationship of stomach cancer risk with raw vegetables, fruit, and wholemeal bread consumption and with vitamin C and carotene intake. Milk, cooked vegetables and vitamins A and E were not consistently found to be related to stomach cancer risk. Positive associations of increasing consumption with stomach cancer risk were occasionally found for processed or particularly prepared meat and fish, and for nitrite. Dietary nitrate intake did not appear to be related to stomach cancer risk in these studies. This latter observation is also supported by metabolic studies in high- and low-risk areas for stomach cancer. Consistently among studies, increased risk for stomach cancer was also found for later availability of refrigeration facilities in the household, non-centralized water supply (especially well water), and high salt intake. Prospective studies agreed in an increased risk for stomach cancer for cigarette smoking, but not for alcohol drinking, whereas case-control studies showed divergent results on these factors. Recent metabolic studies in high- and low-risk areas for stomach cancer or in groups with precursor lesions, with the N-nitrosoproline test as a marker for endogenous nitrosation, revealed inconsistent results. Higher nitrite concentration and increased pH in stomach juice were found to be associated with precursor conditions for stomach cancer. It is still not clear whether intake of preformed carcinogens or endogenous formation in the stomach with or without the inclusion of nitrite is the most important source of tumor-initiating or -promoting substances. Preservation or preparation of meat and fish may play an important role in this process, and vitamin C may be an inhibiting substance.
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PMID:Epidemiological research in stomach cancer: progress over the last ten years. 203 28

Male F344 rats were fed 0.2% N-[4-(5-nitro-2-furyl)-2-thiazoly]formamide for 6 weeks and then fed 3% or 5% sodium saccharin, 5% sodium ascorbate, 3.12% calcium saccharin, 1.34% sodium chloride, 5.2% calcium saccharin plus 1.34% sodium chloride, or basal diet alone for 72 weeks. Protein and DNA were extracted from 89 bladder tumors [87 transitional cell carcinomas (TCC), 1 papilloma, and 1 sarcoma] from 86 rats p21 expression was examined by Western blotting using a monoclonal antibody against p21 (NCC-RAS-004). H-ras mutations in exons 1 and 2 were examined by direct sequencing of DNA amplified by polymerase chain reaction. Sequencing results demonstrated mutations at codon 61 (CAA to CGA in 15 TCCs; CAA to CTA in 2 TCCs), at codon 12 (GGA to TGG in 1 TCC), and at codon 13 (GGC to GTC in 3 TCCs). Mutations at codon 61 were confirmed by faster mobility of the p21 band in Western blots. The level of p21 expression varied among samples, but many TCCs appeared to express more p21 than controls. The overall incidence of H-ras mutations was 24.4% (21 of 86 rats). The type of chemical used for the promoting phase had essentially no effect on H-ras mutation, suggesting that the effects observed were related to FANFT administration. The frequency of H-ras mutation in each group was negatively related to the incidence of carcinoma (r = -0.85; P less than 0.01). Two groups of tumors (with or without the mutated ras gene) were compared for tumor size (reflected by the bladder weight), histological grading, and the presence of invasion. The size of tumors with mutated ras was significantly smaller than those without mutated ras. There was no difference in the histological grading between the two groups. Although not statistically significant, histological invasion was more frequently observed in tumors with mutated ras (14.3%) than in tumors without mutation (3.1%).
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PMID:H-ras mutations in rat urinary bladder carcinomas induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide and sodium saccharin, sodium ascorbate, or related salts. 205 86

In addition to differences in needs for dietary quality and quantity, humans, as individuals and as subsets of the population, are exposed to variations in climate, stress, environmental contaminants and other confounding factors which likely impinge on susceptibility to cancer. Despite the complexity of lifestyles and dietary habits, it is impressive to review available data on the relation of nutrients to cancer. There is sufficient parallelism between controlled animal studies and human behavior that we are compelled to believe that a variety of essential nutrients can modify carcinogenesis in humans and in lower animals. The micronutrients which appear to meet criteria for classifying them as protective agents in animal models include vitamin A and some of the synthetic retinoids; beta carotene; folic acid; vitamin C; choline/methionine; zinc, and selenium. Some of the others have suggestive effects but in the view of this author, the data are often equivocal, inadequate, or conflicting. These observations clearly support the proposal that animal studies have made enormous contributions in the past 15-20 years to our understanding of carcinogenesis and that this will continue into the future. From the data now available we can state with confidence that animal studies have shown that nutrients can modify the carcinogenesis process at specific sites and through a variety of mechanisms. These include effects on the formation of carcinogens from precursors; effects on metabolism of the carcinogen; effects on one or more stages of initiation, promotion, and progression; host defense mechanisms; cellular differentiation and on growth and metastasis of the tumor. The tools of the molecular biology, just now emerging in the field of nutrition, should have an immense impact on determining more accurately where nutrients exert their effects, how this is accomplished, and to suggest appropriate prevention and intervention techniques. Using molecular biology, combined with traditional and newer methods of toxicology and pathology, we should be able within a few years to better understand carcinogenesis and with such knowledge in hand to make sound recommendations about dietary habits to the public.
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PMID:Roles of micronutrients in cancer prevention: recent evidence from the laboratory. 219 21

Ozone (O3) is the major oxidant of photochemical smog. Its biological effect is attributed to its ability to cause oxidation or peroxidation of biomolecules directly and/or via free radical reactions. A sequence of events may include lipid peroxidation and loss of functional groups of enzymes, alteration of membrane permeability, and cell injury or death. An acute exposure to O3 causes lung injury involving the ciliated cell in the airways and the type 1 epithelial cell in the alveolar region. The effects are particularly localized at the junction of terminal bronchioles and alveolar ducts, as evident from a loss of cells and accumulation of inflammatory cells. In a typical short-term exposure the lung tissue response is biphasic: an initial injury-phase characterized by cell damage and loss of enzyme activities, followed by a repair-phase associated with increased metabolic activities, which coincide with a proliferation of metabolically active cells, for example, the alveolar type 2 cells and the bronchiolar Clara cells. A chronic exposure to O3 can cause or exacerbate lung diseases, including perhaps an increased lung tumor incidence in susceptible animal models. Ozone exposure also causes extrapulmonary effects involving the blood, spleen, central nervous system, and other organs. A combination of O3 and NO2, both of which occur in photochemical smog, can produce effects which may be additive or synergistic. A synergistic lung injury occurs possibly due to a formation of more powerful radicals and chemical intermediates. Dietary antioxidants, for example, vitamin E, vitamin C, and selenium, can offer a protection against O3 effects.
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PMID:Biochemical basis of ozone toxicity. 227 33

Rats were treated for 1 week each with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), 0.2% N-bis(2-hydroxypropyl)-nitrosamine (DHPN) and 0.2% N-ethyl-N-hydroxyethylnitrosamine (EHEN) in the drinking water, and then administered diet containing 5% sodium L-ascorbate (Na-AsA), 1% butylated hydroxytoluene (BHT) or 0.05% phenobarbital (PB), or weekly intraperitoneal injections of 2 mg of pepleomycin per kg body weight until week 36. Histopathological examination revealed that all exerted significant modulation effects on tumor development in the various target organs. Na-AsA was found to inhibit liver but promote renal pelvis and bladder carcinogenesis. BHT similarly decreased liver and enhanced bladder lesion development. PB, in contrast promoted hepatocarcinogenesis. However both PB and BHT were associated with increased incidences of adenomas and adenocarcinomas of the thyroid. Thus the wide-spectrum initiation model allowed confirmation of site-specific modification potential and in addition demonstrated potentiation of kidney and bladder carcinogenesis promotion by pepleomycin.
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PMID:Modification by sodium L-ascorbate, butylated hydroxytoluene, phenobarbital and pepleomycin of lesion development in a wide-spectrum initiation rat model. 247 82

Studies were made on the possible tumor-promoting activities of various salts of food additives in the glandular stomach mucosa of F344 male rats after their administration by gastric intubation. Up to 100-fold increases in ornithine decarboxylase (ODC) activity in the pyloric mucosa of the stomach with maxima after 8 h were observed after administration of sodium acetate at doses of 3.68-13.6 mmol/kg body weight, sodium L-ascorbate at doses of 8.55-17.1 mmol/kg body weight, Na2CO3 at doses of 4.73-14.2 mmol/kg body weight, sodium L-glutamate at doses of 12.8-17.1 mmol/kg body weight, sodium sorbate at doses of 8.92-17.1 mmol/kg body weight and (NH4)2SO4 at doses of 7.56-20.1 mmol/kg body weight. Increases of up to 100-fold in ODC activity with maxima after 16 h were also observed after intubation of KCl at doses of 10.1-22.0 mmol/kg body weight, K2SO3 at doses of 2.84-8.45 mmol/kg body weight, K2S2O5 at doses of 2.25-6.75 mmol/kg body weight and CaCl2 at doses of 2.0-4.08 mmol/kg body weight. Sodium acetate at a dose of 11.0 mmol/kg body weight, KCl at a dose of 20.1 mmol/kg body weight, K2S2O5 at a dose of 5.40 mmol/kg body weight and CaCl2 at a dose of 3.4 mmol/kg body weight induced up to 10-fold increase in DNA synthesis in the pyloric mucosa of the stomach with maxima after 16-24 h. These results suggest that these salts of food additives may, like NaCl, have tumor-promoting activities in the pyloric mucosa of rat stomach.
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PMID:Various sodium salts, potassium salts, a calcium salt and an ammonium salt induced ornithine decarboxylase and stimulated DNA synthesis in rat stomach mucosa. 250 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

Over a 4-year period in a chemoprevention trial on large bowel neoplasia, 58 patients with familial adenomatous polyposis were treated with 4 g of ascorbic acid (vitamin C)/day plus 400 mg of alpha-tocopherol (vitamin E)/day alone or with a grain fiber supplement (22.5 g/day). In this randomized, double-blind, placebo-controlled study, we determined the effects of these supplements on rectal polyps in these patients. Analysis by intent to treat suggested that the high-fiber supplement had a limited effect. Analysis adjusted for patient compliance showed a stronger benefit from the high-fiber supplement during the middle 2 years of the trial. The results provide evidence for inhibition of benign large bowel neoplasia by grain fiber supplements in excess of 11 g/day in this study population. The findings are consistent with the hypothesis that dietary grain fiber and total dietary fat act as competing variables in the genesis of large bowel neoplasia.
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PMID:Effect of wheat fiber and vitamins C and E on rectal polyps in patients with familial adenomatous polyposis. 254 60


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