摘要:

AbstractHL‐60 human promyelocytic leukemia cells can be induced to differentiate to granulocytes by retinoic acid and dimethyl sulfoxide or monocyte‐macrophages by phorbol esters and 1,25‐dihydroxyvitamin D3. These studies show that RRR‐α‐tocopheryl succinate (TS) inhibits HL‐60 cell proliferation and induces the HL‐60 cells to differentiate toward a functionally deficient macrophage‐like cell. TS at (15μg/ml) was found to suppress HL‐60 cell proliferation by 63% and 89% at 24 and 48 hours, respectively. This suppression of proliferation, however, is not permanent and requires the presence of TS. HL‐60 cells treated for 48 hours with TS (15μg/ml) were found to be blocked in the G2/M phase of the cell cycle. HL‐60 cells blocked in the G2/M cell cycle phase by TS expressed normal levels of the transferrin receptor. TS‐treated HL‐60 cells exhibited binucleated morphological appearance; however, the cells did not exhibit chemo‐taxis, phagocytosis, or changes in the expression of the cell surf ace markers, CD11a and CD18. However, HL‐60 cells treated for 48 hours with TS (15μg/ml) could be stimulated to produce superoxide radicals and exhibited nonspecific esterase activity, two characteristics of macrophages. These results suggest a role for TS as an antitumor proliferative agent and as a modifier of human leukemia cell differentiation.

ISSN:0163-5581    

DOI:10.1080/01635589209514221

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

摘要:

AbstractThe individual and combined effects of dietary toasted soybean meal (3.13–25%) and dietary licorice root extract (0.38–3.0%) on selected liver and intestinal enzyme levels and on clinical chemistry and histopathological parameters were evaluated on male F344 rats. All parameters were measured one and three months after the 50‐day‐old rats were started on the diets. By use of newly developed high‐performance liquid chromatography‐based analytic methods, measurable levels of daidzein (2.67μg/ml) and glycyrrhetinic acid (7.87μg/ml) were detected in the sera of rats on the 25% soybean and 3% licorice diets, respectively. Histopathological evaluations of organs and tissues yielded only nonsignificant strain‐related changes. At all dosages, there were no significant soybean‐or licorice‐related anatomic lesions or hematologic changes. In the clinical biochemistry profile, soybean meal caused moderate but significant dose‐dependent decreases in serum cholesterol and increases in alkaline phosphatase, blood urea nitrogen, and phosphorus, which remained within the normal range. Liver glutathione transferase, catalase, and protein kinase C showed significant inductions (up to 50%) in response to increasing doses of soybean meal and licorice extract, with evidence for only marginal interaction between the two additives. Their effects on the intestinal mucosa were not significant. Ornithine decarboxylase levels, an indicator of promotional activity, were unchanged or repressed by the additives.The favorable effects of up to 25% toasted soybean meal and 3% licorice root extract on the levels of the four enzymes, without unfavorable changes in clinical parameters, might account in part for the chemopreventive activities of these additives. These effects would be in addition to direct inhibitory effects of known components in these additives on these or other enzymes or modulation of hormone activity that is not evaluated in this study.

ISSN:0163-5581    

DOI:10.1080/01635589209514222

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

摘要:

AbstractFrom the data obtained in a large comprehensive population‐based case‐control study of colorectal cancer (The Melbourne Colorectal Cancer Study), attributable risk was calculated for a family history of colorectal cancer in near relatives for diet (when≥5 of the 11 previously determined dietary risk factors were present) and for beer consumption (for rectal cancer only). The attributable risk was 11% in the presence of a family history of colorectal cancer and 46% in the presence of five or more dietary risk factors. The attributable risk for rectal cancer in the presence of beer consumption was 31% in males and 11% in females. These data are relevant in the consideration of primary prevention of colorectal cancer in Australia, but their general application needs to be approached with caution in view of major differences in the genetic background and the dietary practices in various regions of the world and in view of the uncertainty of what is achievable change, especially for dietary practices.

ISSN:0163-5581    

DOI:10.1080/01635589209514223

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

摘要:

AbstractA case‐control study was conducted in Melbourne, Australia of 88 consecutive males admitted for the surgical removal of a nonmelanocytic skin cancer (histologically confirmed basal cell carcinoma and squamous cell carcinoma) and of 88 male control patients admitted for small elective surgical procedures. In both cases and controls, previous diet, alcohol consumption, and smoking habit were investigated and serumβ‐carotene and vitamin A levels were measured. A statistically significant inverse relationship was found between the risk of skin cancer and a high intake offish (p = 0.05); vegetables in general (p<0.001); beans, lentils, or peas (p<0.001), carrots, silverbeet (Swiss chard), or pumpkin (p<0.001); cruciferous vegetables (cabbage, brussel sprouts, or broccoli) (p<0.001); andβ‐carotene‐and vitamin C‐containing foods (p = 0.004). Cases had a lower mean serum level ofβ‐carotene (p<0.001) and vitamin A (p = 0.02) than controls. The incidence of skin cancer in the study was inversely related to the level of serumβ‐carotene (p<0.0001). The correlation coefficient between dietaryβ‐carotene/vitamin C and serumβ‐carotene was 0.22 (p = 0.04). Smoking and alcohol consumption showed no statistically significant association with the risk of nonmelanocytic skin cancer. The results were similar for both cell types. A high intake of vegetables including cruciferous vegetables,β‐carotene‐and vitamin C‐containing foods, and fish appears to be protective for nonmelanocytic skin cancer, and this deserves further study, as does the possible etiologic relevance of the low serum levels ofβ‐carotene and vitamin A.

ISSN:0163-5581    

DOI:10.1080/01635589209514224

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

摘要:

AbstractMammary tumorigenesis is augmented when C3H/Ou mice are fed diet ad libitum but delayed when calories are restricted by 40%. Three feeding experiments were done to evaluate the effect of ethanol on mammary tumorigenesis in isocalorically fed C3H/Ou mice: 1) ad libitum feeding of semipurified solid diet, with one group receiving 12% ethanol (15 g/kg/day) in the drinking water while controls received water alone; 2) isocaloric pair feeding of semipurified solid diet, with ethanol (4 g/kg/day) administered by gavage five times per week; and 3) isocaloric pair feeding of Lieber‐DeCarli liquid diet, with one group receiving 29% of calories as ethanol (20 g/kg/day) in the diet. Despite administration of ethanol to isocalorically fed C3H/Ou mice for 65 weeks by three different methods, mammary tumor development was not enhanced. In two of the three ethanol‐consuming groups, weight gain and mean body weight were less in the ethanol‐consuming mice than in the controls, despite equal total calorie consumption. In only one ethanol‐consuming group, where mice received ethanol as a 12% solution in the drinking water, was any difference noted in the tendency to develop mammary tumors. In this case, delay in tumorigenesis was apparent in the ethanol‐consuming animals (p = 0.03). These findings do not support the hypothesis that ethanol calories augment the risk for breast tumorigenesis among breast cancer‐prone mice consuming isocaloric diets. Instead, reductions in weight gain and body weight among ethanol‐consuming mice and an apparent reduction in mammary tumorigenesis in one of three experimental groups suggest that ethanol may decrease metabolic utilization of calories and hence contribute to lowered energy availability. This in turn could decrease tumorigenesis.

ISSN:0163-5581    

DOI:10.1080/01635589209514225

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

摘要:

AbstractWe present the dietary epidemiology of bladder cancer while controlling for a number of lifestyle and environmental risk factors in a study of 351 white male cases with histologically confirmed transitional cell carcinoma of the bladder and 855 white male controls selected from Erie, Niagara, and Monroe counties of western New York from 1979 to 1985. Usual diet was estimated by comprehensive interviews with use of a detailed food frequency questionnaire. An increased risk of bladder cancer was associated with higher kilocalorie intake, but only among those under 65 years of age, with the strongest pattern associated with fat intake. Further analyses of fat, carbohydrates, and protein, with adjustment for total kilocalories, resulted in a positive association of risk with fat intake and a decreasing risk with higher protein intake. Of the vitamins, carotenoid consumption appeared to decrease risk with increased consumption for those under 65 years of age. No significant differences between cases and controls were seen for intake of calcium, retinol, thiamin, riboflavin, niacin, vitamin C, vitamin D, and vitamin E. After adjustment for kilocalories and other confounders, higher intake of dietary sodium was associated with increased risk among both age groups, and the trends were statistically significant. The importance of diet in the etiology of bladder cancer is suggested by our findings.

ISSN:0163-5581    

DOI:10.1080/01635589209514226

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

摘要:

AbstractSeven dietary patterns were identified among control subjects in the Western New York Diet Study (1975–1986) by application of principal components analysis to data from a 95‐itemfood frequency interview. The results of case‐control analyses of colon cancer risk for these patterns are presented. Cases were matched with neighborhood controls on the bases of age and sex; 205 colon case‐control male and 223 female pairs were obtained. The dietary patterns and intakes of energy, total fat, and dietary fiber were examined with logistic regression for their individual contributions to risk. In males, three of these dietary patterns were associated positively with fat and energy consumption; they elevated risk for colon cancer and accounted for more risk than did the specific nutrients. Control for energy and fat intakes allowed the protective influences of additional dietary patterns to be expressed. No patterns elevated risk in women; two patterns were protective for colon cancer. Controlling for energy and fat intake enhanced the protection afforded by one of these patterns but had no influence on that of the other. Measures of foods rather than single nutrients may be more inclusive of dietary exposures to risk as well as being related more directly to underlying health behaviors. Therefore they may be better able to account for risk in diseases with multiple causation.

ISSN:0163-5581    

DOI:10.1080/01635589209514227

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

摘要:

AbstractThe relationship between intake of various indicator foods and beverages and risk of prostatic cancer was assessed in 271 cases of prostatic cancer and 685 hospital controls recruited in two areas of northern Italy, the province of Pordenone and the greater Milan area. Increased risks were found for more frequent intake of meat [odds ratio (OR) in the highest vs. lowest consumption fertile = 1.4, 95% confidence interval (CI) 1.0–2.0], milk (OR = 1.6, 95% CI 1.1–2.4), fresh fruit (OR = 1.4, 95% CI 1.0–2.1), and vegetables (OR = 1.4, 95% CI 0.9–2.2). After allowance for the reciprocal confounding effect of various dietary habits, only frequent intake of milk seemed to be a significant independent indicator of prostatic cancer risk. There was also a clue that the unfavorable influence of frequent intake of a few food items (i.e., meat, fish, liver, ham and salami, milk and butter, and retinol) may be greater or restricted to older individuals (i.e.,≥70 yrs of age). In conclusion, the present study confirms the presence of a moderate adverse effect of high intake of foods of animal origin, chiefly milk, while it suggests that a diet rich in fresh fruit and vegetables does not convey a protection.

ISSN:0163-5581    

DOI:10.1080/01635589209514228

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

摘要:

AbstractThe effects of dietary selenium deficiency and excess on N‐nitrosomethylbenzylamine‐(NMBA) induced esophageal neoplasia in rats and forestomach tumors in mice and the effects of dietary selenium on DNA adduct formation and on the activities of DNA adduct‐repairing enzyme and oncogene expression in rat esophagus were investigated. The esophageal and forestomach tumors were induced by administration of NMBA by gavage with a total dose of 39 mg/kg body wt in rats and 12 mg/kg body wt in mice. Neither selenium dietary deficiency (Se<0.02 ppm) nor selenium excess (2.0 ppm) showed any significant effect on the incidence of tumors or number of tumors per tumor‐bearing animal. For the DNA adduct formation studies, rats were given a dose of NMBA intraperitoneally after six weeks on the different selenium‐containing diets. No significant difference in the amount of the DNA adduct O6‐methyldeoxyguanosine was found among the different selenium‐treated groups. In a parallel group of rats that did not receive NMBA, the levels of esophageal O6‐methyldeoxyguanosine DNA methyltransferase were not significantly altered by dietary selenium levels. The c‐myc oncogene expression in rat esophagus was induced by the administration of NMBA (3 mg/kg body wt) by gavage once a week for eight weeks. Dietary selenium did not show any effects on its expression. On the basis of the results of these studies, dietary selenium has no effects in the NMBA‐induced tumor model.

ISSN:0163-5581    

DOI:10.1080/01635589209514229

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor

ISSN:0163-5581    

DOI:10.1080/01635589209514220

出版商:Taylor&Francis Group    

年代:1992

数据来源: Taylor