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1. |
Effects of wheat, rice, corn, and soybean bran on 1,2‐dimethylhydrazine‐induced large bowel tumorigenesis in F344 rats |
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Nutrition and Cancer,
Volume 5,
Issue 1,
1983,
Page 1-9
BarnesDavidS.,
ClappNealK.,
ScottDavidA.,
OberstDonnaL.,
BerrySusanG.,
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摘要:
AbstractThis study was designed to determine the relative effects of four dietary brans on large bowel tumorigenesis in rats treated with 1,2‐dimethylhydrazine (DMH). Four‐week‐old F344 rats were fed a 20% bran (either wheat, rice, corn, or soybean) semisynthetic diet or a no‐fiber‐added control diet for life. All rats except for one control diet for life. All rats except for one control group were injected with DMH (2SC doses;∼150 mg/kg body weight) at 8 and 10 weeks of age. Two additional groups were fed the control diet and then at 4 and 18 weeks, respectively, after the second DMH dose, were fed the wheat bran diet. All surviving rats were killed 9 months following the first DMH dose. Survival was increased in all groups receiving bran diets. Large bowel tumor incidences in the DMH group were as follows: control, 95%; wheat, 75%; rice, 86%; corn, 100%; soybean, 84%; wheat after 4 weeks, 62% (lower than control group, p<0.05); wheat after 18 weeks, 84%. All but one of the DMH groups had approximately two tumors/tumor‐positive rat; the corn group had four. The effect of bran on large bowel carcinogenesis appears to depend both on the source of bran and when it is fed in relation to tumor initiation.
ISSN:0163-5581
DOI:10.1080/01635588309513772
出版商:Taylor&Francis Group
年代:1983
数据来源: Taylor
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2. |
High‐dose pyridoxal supplemented culture medium inhibits the growth of a human malignant melanoma cell line |
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Nutrition and Cancer,
Volume 5,
Issue 1,
1983,
Page 10-15
DiSorboDennisM.,
NathansonLarry,
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摘要:
AbstractThein vitrogrowth characteristics of a human malignant melanoma cell line cultured in 0.5 mM pyridoxal supplemented medium were studied. Experimentation revealed that the high‐dose pyridoxal supplemented medium severely inhibited the growth of melanoma cells over a 72‐hour growth period. Additional experimentation showed that cells cultured for 6 hours in the pyridoxal supplemented medium took up 25% less and incorporated 20% less [3H]uridine than control cultures. [3H]Glucose uptake was reduced by 23% at this time point. [3H] Thymidine uptake was inhibited by 12%, but no inhibition was detected in [3H]thymidine incorporation. When the vitamin B6 antagonist 4‐deoxypyridoxine (which competes with pyridoxal for pyridoxal kinase) was added to the pyridoxal supplemented medium, the inhibition in [3H]uridine incorporation was reduced from 19% to 6%. However, 4‐deoxypyridoxine did not reverse the inhibition of [3H]uridine uptake. These results indicate that pyridoxal and its metabolite, pyridoxal 5'‐phosphate, may be involved in the growth regulation of a human malignant melanoma cell line.
ISSN:0163-5581
DOI:10.1080/01635588309513773
出版商:Taylor&Francis Group
年代:1983
数据来源: Taylor
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3. |
Modification of dimethylhydrazine‐induced carcinogenesis in rats by dietary cholesterol |
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Nutrition and Cancer,
Volume 5,
Issue 1,
1983,
Page 16-25
KlurfeldDavidM.,
AglowElsa,
TepperShirleyA.,
KritchevskyDavid,
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摘要:
AbstractDiets capable of affecting serum cholesterol levels were examined for effects on tumorigenesis in male Fischer 344 rats given 1,2‐dimethylhydrazine dihydrochloride (DMH). Four regimens were used: Group A was maintained on a semipurified diet; Group B was maintained on the same diet with cholesterol and bile salts added; Group C was fed the cholesterol and bile salt diet and then switched to the semipurified diet; and Group D was fed the cholesterol and bile salt diet and then placed on a semipurified diet containing bile salts. Six months after DMH administration, Groups B and D exhibited similar tumor incidence (77% and 83 %, respectively) and yield (2.3 and 2.4 tumors/tumor‐bearing rat). These yields were significantly greater than those seen in Group A (70% incidence and 1.4 tumors/tumor‐bearing rat) or Group C (52% incidence and 1.7 tumors/tumor‐bearing rat). Tumors in Groups B and D were larger in size and closer to the rectum than those seen in the other groups. In each of Groups A, C, and D, approximately 26% of the tumors were malignant; in Group B, 42% were malignant. Colonic epithelial cell kinetics in rats from Groups C and D not given DMH were determined using autoradiographic study of [3H]thymidine incorporation. Group D showed enhanced cell proliferation and expansion of the crypt cell population. These results suggest that dietary bile salts increase cell turnover and frequency of tumors, and that the addition of cholesterol to a cocarcinogenic diet can be associated with a significantly higher percentage of invasive tumors.
ISSN:0163-5581
DOI:10.1080/01635588309513774
出版商:Taylor&Francis Group
年代:1983
数据来源: Taylor
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4. |
Genotoxicity of brown‐colored polymerization products formed in smoke flavors |
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Nutrition and Cancer,
Volume 5,
Issue 1,
1983,
Page 26-33
PoolBeatriceL.,
RennerHeinzW.,
BakesWerner,
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摘要:
AbstractSmoke aroma essences, which are prepared from smokehouse smoke by condensation and purification, are used for flavoring raw food products. The essences spontaneously decompose and produce brown‐colored polymerization products, which may react with protein and be liberated within the acidic environment of the human stomach. The potential of these products to cause DNA damage was studied in two microbio/ and twoin vivoassay systems. The polymerization products induced his* reversion inSalmonella typhimuriumTA 100 after metabolic activation by liver enzymes. There was no significant activity in a differential killing assay with repair‐deficient strains ofEscherichia coliWP2.In vivotests demonstrated significant increases in the rate of sister chromât id exchanges in bone marrow cells of Chinese hamsters, but no increase in micronuclei was detectable. Thus, genotoxic components may be present in the brown‐colored fractions of smoke aroma essences, but further study is needed.
ISSN:0163-5581
DOI:10.1080/01635588309513775
出版商:Taylor&Francis Group
年代:1983
数据来源: Taylor
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5. |
Metabolie epidemiology of colon cancer: Dietary pattern and fecal sterol concentrations of three populations |
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Nutrition and Cancer,
Volume 5,
Issue 1,
1983,
Page 34-40
ReddyBandaruS.,
EkelundGoran,
BoheMans,
EngleAlthea,
DomellofLennart,
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摘要:
AbstractThe nutrient intake, fecal neutral sterol concentration, and bile acid concentration of populations with a varied risk for colon cancer development were investigated. High‐risk populations in the metropolitan New York area and Malmo, Sweden, were compared with an intermediate‐risk population in Umea, Sweden. The mean daily intake of protein and fat was comparable in all groups, but the total daily fiber intake was higher in Umea, as was the total daily stool output. There was no difference in the total fiber intake and stool output between Malmo and metropolitan New York. The fecal secondary bile acid concentration was lower in Umea than in the other two areas; no difference was observed between Malmo and metropolitan New York.These results suggest that high fiber intake may be considered protective against colon cancer even in a population with a high fat intake. A high dietary fiber intake may limit colon cancer risk by increasing stool bulk, and thus diluting and/or binding tumor promoters.
ISSN:0163-5581
DOI:10.1080/01635588309513776
出版商:Taylor&Francis Group
年代:1983
数据来源: Taylor
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6. |
Vitamin A and aflatoxin: Effect on liver and colon cancer |
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Nutrition and Cancer,
Volume 5,
Issue 1,
1983,
Page 41-50
SuphakarnVoranuntS.,
NewbernePaulM.,
GoldmanMark,
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摘要:
AbstractA vitamin A (retinyl acetate)‐deficient diet enhanced liver cancer in rats exposed to aflatoxin B1 (AFB1) and also caused a 29% incidence of colon cancer. The following factors were considered in attempts to define conditions under which vitamin‐A‐deprived rats were more susceptible to colon cancer induced by AFB1: liver morphology, enterohepatic recirculation, level of reduced glutathione (GSH) in liver, and differing capacities for conjugation of aflatoxin to GSH. Enzyme concentrations in liver, in intestinal and colon mucosa, and in intestinal and colon contents suggested that AFB1 may have different metabolites and that there may be differing susceptibilities of colon mucosa to carcinogenesis. Binding studies supported this hypothesis. Previous studies have shown that colon epithelium from vitamin‐A‐deficient rats binds more AFB1 than colon epithelium from normal, vitamin‐A‐supplemented animals. In the present study, vitamin A supplementation to the vitamin‐A‐deficient rats before oral administration of3H‐AFB1 significantly decreased the binding capacity at 12 and 15 hours after dosing with the carcinogen. These results suggest that the effect of vitamin A on the metabolism of the carcinogen, particularly on binding of AFB1 to cellular macromolecules, may be the mechanism by which vitamin A modifies aflatoxin's carcinogenic potential, influenced in part through enzymatic mechanisms.
ISSN:0163-5581
DOI:10.1080/01635588309513777
出版商:Taylor&Francis Group
年代:1983
数据来源: Taylor
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7. |
Should we worry about animal growth promoters? |
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Nutrition and Cancer,
Volume 5,
Issue 1,
1983,
Page 51-54
HorwitzCrystal,
RozenPaul,
GilatTuvia,
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摘要:
AbstractEstrogens and compounds with estrogenic activity have been used for many years as animal growth promoters and to synchronize estrus in cows. The resorcylic acid lac tones (RALS), which include zearalenone, are being used increasingly for these purposes. These estrogenic mycotoxins, now produced commercially, have teratogenic, mutagenic, and carcinogenic properties. There is some evidence that their residues could remain in certain organs at the time the animal products come to market, and this may be of medical significance.
ISSN:0163-5581
DOI:10.1080/01635588309513778
出版商:Taylor&Francis Group
年代:1983
数据来源: Taylor
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8. |
Editorial board |
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Nutrition and Cancer,
Volume 5,
Issue 1,
1983,
Page -
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ISSN:0163-5581
DOI:10.1080/01635588309513771
出版商:Taylor&Francis Group
年代:1983
数据来源: Taylor
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