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1. |
Relationships of Fusarium Mycotoxins to disorders and tumors associated with alcoholic drinks |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page 88-92
SchoentalR.,
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摘要:
AbstractThough epidemiological studies incriminate alcoholic beverages in various disorders and tumors, experimental results remain equivocal. Circumstantial evidence is presented which points to mycotoxins, especially those produced by Fusarium field‐microfungi, as the agents responsible for outbreaks of such pathological conditions as“cobalt‐beer cardiorhyopathies,”;“fetal alcohol syndrome,”; Plummer‐Vinson syndrome, and some tumors of the alimentary tract. The sporadic occurrence of mycotoxins in grain and cereals, known to correlate with wet weather, could explain inconsistencies encountered in some epidemiological and experimental studies. The effects of mycotoxins, occasionally present in fermented beverages and in various foodstuffs, may be potentiated by trace quantities of nitrosamines detected in beer and whiskey.
ISSN:0163-5581
DOI:10.1080/01635588009513663
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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2. |
Comparison of dietary histories in lung cancer cases and controls with special reference to vitamin A |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page 93-97
GregorAnna,
LeePeterN.,
RoeFrancisJ.C.,
WilsonMichaelJ.,
MeltonAilsa,
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摘要:
AbstractEstimates of current dietary vitamin A intake have been obtained from 100 lung cancer cases and 173 controls. Seventy‐eight male cases took significantly (p<0.05) less vitamin A than did 110 controls, due mainly to lower consumption of liver and of pills containing vitamin A. Twenty‐two female cases took more, but not significantly more, vitamin A than did 63 control females, a higher consumption of liver more than outweighing a lower frequency of pill taking. These differences were unrelated to the type of lung cancer diagnosed or to the diagnosis category of the controls and were not materially affected by adjustment for age, smoking or any other factor studied. No material differences between cases and controls were found in consumption of vitamin A from other sources or of pills not containing vitamin A. Trends observed based on estimates of vitamin A intake 20 years ago were similar to, but less marked than, those based on current intake. The role of vitamin A in lung cancer etiology requires further investigation.
ISSN:0163-5581
DOI:10.1080/01635588009513664
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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3. |
Weight loss and Cachexia in lung cancer |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page 98-103
CostaGiovanni,
LaneWarrenW.,
VincentRonaldG.,
SieboldJulieA.,
AragonMiriam,
BewleyPatriciaT.,
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摘要:
AbstractIncidence, timing and severity of weight loss were studied in 479 patients with lung cancer. A phase of early weight loss, associated with a∼50% reduction in survival, was identified. Food consumption was studied in normal individuals and in patients with and without weight loss. In these patients, anorexia failed to account for the weight loss. We discuss the possibility that weight loss results from interference by cancer with the metabolism of the host.
ISSN:0163-5581
DOI:10.1080/01635588009513665
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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4. |
Lipotrope deficiency in experimental carcinogenesis |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page 104-112
RogersAdrianneE.,
NewbernePaulM.,
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摘要:
AbstractDiets deficient in lipotropes (methionine, choline, and folate) and high in fat increase hepatocarcinogenesis by many chemicals, including aflatoxin B1 (AFB1) and N‐2‐fluor‐enylacetamide (AAF). The increase can be corrected in most cases by lipotrope supplementation, but the degree of correction appears to be influenced by the type of fat in the diet. A lipotrope‐deficient, high‐fat diet also increases dimethylhydrazine carcinogenesis in the colon, an effect due to the dietary fat content, not to lipotrope deficiency. In contrast, mammary carcinogenesis by dimethylbenzanthrene or AAF is decreased or unchanged in rats fed the deficient diet.Hepatic microsomal oxidase activity, cytochrome P450 and conversion of AFB 1 to a bacterial mutagen all are decreased in assays in vitro using tissues from lipotrope‐deficient rats. However, urine mutagen content is increased after AFB1 treatment, as is urine content of activated AAF. AFB1 binding to hepatic DNA in vivo is unchanged or is slightly decreased. Therefore, there is evidence that the dietary deficiency influences carcinogen activation, but the expression and direction of the effect varies. The deficiency also increases cell division in the liver and decreases hepatic s‐adenosylmethionine; carcinogenesis may be influenced by either or both of those changes.
ISSN:0163-5581
DOI:10.1080/01635588009513666
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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5. |
Dependence of the rate of metabolism of Benzo[a] Pyrene on the fatty acid composition of the liver endoplasmic reticulum and on the dietary lipids |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page 113-118
HammerCatherineT.,
WillsEricD.,
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摘要:
SummaryThe effect of dietary lipid content on the fatty acid composition of the liver endoplasmic reticulum and the effect of the fatty acid composition on the oxidative metabolism of Benzo (a) Pyrene (BP) in the liver endoplasmic reticulum were studied in rats. The rate of oxidative metabolism of BP was found to be markedly dependent on the percentage of polyunsaturated fatty acids incorporated into the membrane of the endoplasmic reticulum. Diets containing 10% lard or 10% corn oil caused the incorporation of 10.3% and 25.1% linoleicacid (C18: 2) and oxidation rates of 68.3 and 113.8 nmol 3‐hydroxybenzo (a) pyrene/30 min/g liver, respectively. Diets containing 10% herring oil caused incorporation of only 5.1 % C18: 2 but also 27.2%ω3 unsaturated fatty acids, including 8.7% eicosapentaenoic acid (C20: 5) and 17.0% doco‐sahexaenoic acid (C22: 6) and caused a high oxidation rate (145.8 nmol) 3‐hydroxybenzo (a) pyrene/30 min/g liver.Phenobarbitone (100 mg/kg) and 20‐methyl‐cholanthrene (20 mg/kg) strongly enhanced the oxidation rate of BP in groups of rats fed a herring oil diet and induction was much greater in the group fed an irradiated diet than in the group fed an untreated herring oil diet. Irradiation with 400 krad caused destruction of the major proportion of the polyunsaturated fatty acids in herring oil, incorporation of a smaller quantity ofω3 unsaturated acids into the endoplasmic reticulum, and a decrease in the rate of oxidation to 122.5 nmol 3‐hydroxybenzo (a) pyrene/30 min/g liver.The antioxidant 2,6‐di‐tert‐butyl‐4 methylphenol, BHT, (0.01 %) added to irradiated herring oil diets strongly reduced the inductive effect of phenobarbitone. This effect may therefore be caused by the presence of lipid peroxides in the irradiated diet.It is concluded that dietary C18: 2 is an important factor in the regulation of the rate of oxidative metabolism of BP in the liver endoplasmic reticulum, but C18: 2 may be effectively replaced by dietary C20: 5 and C22: 6. Oxidation of BP is regulated by changes in the fatty acid composition of the membranes of the liver endoplasmic reticulum.
ISSN:0163-5581
DOI:10.1080/01635588009513667
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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6. |
Mutagens in feces from subjects on controlled formula diets |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page 119-124
KuhnleinHarrietV.,
KuhnleinUrs,
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摘要:
AbstractFecal samples from twelve subjects who received liquid formula diet for 47 days or longer were analyzed for mutagens with the fluctuation test for weak mutagens using Salmonella typhimurium TA 100 as a tester strain. The purpose was to establish the variation of fecal mutagens among subjects on identical diets and the variation within a subject when on a constant diet. It was found that there was significant inter‐subject variability which did not disappear even after 72 days of rigorously controlled diet. There was no significant change, within a subject, of fecal mutagenicity throughout the diet period. It appears that long‐term habits (dietary or otherwise) or, perhaps, genetic traits are major factors influencing fecal mutagenicity.
ISSN:0163-5581
DOI:10.1080/01635588009513668
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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7. |
Dietary vitamin E, hepatic aryl hydrocarbon hydroxylase and the metabolic activation of procarcinogens to mutagens |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page 125-128
GairolaChandraC.,
ChowChingK.,
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摘要:
AbstractVitamin E deficiency for 12 weeks significantly reduced the hepatic aryl hydrocarbon hydroxylase (AHH) activity in rats. This resulted in a reduced ability to mutagenically activate benzo (a) pyrene (BP) and 2‐aminofluorene (2‐AF) as compared with equivalent preparations from vitamin E‐supplemented rats. PCB treatment of vitamin E‐deficient and supplemented rats increased AHH activity, and the ability of rats in both dietary groups to activate BP to mutagens. In contrast, PCB treatment caused a reduction in the mutagenic activation of aryl amines.
ISSN:0163-5581
DOI:10.1080/01635588009513669
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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8. |
Book review |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page 129-129
ShilsMauriceE.,
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摘要:
Nutritional Management of the Cancer Patient,edited by Joy J. Wollard, Raven Press, New York, 204 pages, 1979
ISSN:0163-5581
DOI:10.1080/01635588009513670
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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9. |
Editorial board |
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Nutrition and Cancer,
Volume 2,
Issue 2,
1980,
Page -
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PDF (91KB)
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ISSN:0163-5581
DOI:10.1080/01635588009513662
出版商:Taylor&Francis Group
年代:1980
数据来源: Taylor
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