Search PubMed⌕ Search

Biomedical subjects

B S Reddy

Publications and source records attributed to B S Reddy.

At least 163 records · Page 9Linked to original sources
PubMed1987

Chemoprevention of colon carcinogenesis by dietary organoselenium, benzylselenocyanate, in F344 rats.

The effect of feeding benzylselenocyanate (BSC) and its sulfur analogue, benzylthiocyanate (BTC), 2 wk before, during, and until 1 wk after carcinogen administration (initiation phase) on intestinal carcinogenesis induced by azoxymethane (CAS:25843-45-2) was studied in male F344 rats. Weanling rats were raised on a semipurified diet (AIN-76A diet; control diet). Beginning at 5 wk of age, groups of animals consuming the control diet were fed one of the diets containing 25 ppm BSC or BTC. An additional group was continued on the control diet. At 7 wk of age, all animals in 3 groups, except the vehicle-treated controls, were administered s.c. injections of azoxymethane (15 mg/kg body weight, once weekly for 2 wk). Animals were continued on the control diet and BSC and BTC diets until 1 wk after carcinogen treatment, when those groups receiving BSC and BTC diets were fed the control diet until termination of the experiment. Tissue and blood plasma glutathione peroxidase activity was measured in vehicle-treated animals fed the control diet and BSC and BTC diets for 5 wk. The results indicate that body weights were comparable among the various dietary groups. BSC in the diet significantly inhibited the incidence (percentage of animals with tumors) and multiplicity (tumors/animal) of adenocarcinomas in the colon and multiplicity of adenocarcinomas in the small intestine compared to those fed the control diet. BTC in the diet had no effect on colon and small intestinal tumors. Selenium-dependent glutathione peroxidase activity was significantly increased in kidneys and colon and small intestinal mucosae of animals fed the BSC diet compared to animals fed the BTC and control diets.

Administration, Oral↗
PubMed1987

Dose-related inhibition of colon carcinogenesis by dietary piroxicam, a nonsteroidal antiinflammatory drug, during different stages of rat colon tumor development.

The effect of four dose levels of piroxicam administered during different stages of colon tumor development was studied in male F344 rats to obtain a data base on the efficacy of piroxicam as an inhibitor of colon carcinogenesis. Piroxicam was added at levels of 25, 50, 75, and 150 ppm to the NIH-07 open-formula diet and fed to male F344 rats starting 1, 13, and 23 wk after the carcinogen administration. At 7 wk of age, while the animals were consuming the control diet, all animals except the vehicle-treated controls were given s.c. injection of azoxymethane (CAS:25843-45-2; 29.6 mg/kg body weight, once) to induce intestinal tumors. Forty wk after AOM injection, all animals were necropsied, and tumor incidences were compared among the various dietary groups. Colon tumor incidence (percentage of animals with tumors) was inhibited in a dose-dependent manner in rats fed the diets containing 25, 50, 75, and 150 ppm piroxicam starting 1 and 13 wk after carcinogen treatment. The colon tumor incidences in animals fed the diets containing 0, 25, 50, 75, and 150 ppm of piroxicam starting at 1 wk after carcinogen treatment were 89, 61, 58, 50, and 39%, respectively. When the diets containing 0, 25, 50, 75, and 150 ppm were fed 13 wk after carcinogen treatment, the colon tumor incidences were 89, 69, 69, 44, and 33%, respectively. Colon tumor multiplicity (tumors/animal; tumors/tumor-bearing animal) was also significantly inhibited in animals fed the diets containing 25 to 150 ppm piroxicam starting 1 and 13 wk after carcinogen administration. The number of colon tumors/animal was inhibited by about 80 to 84% in animals fed the 150 ppm piroxicam diet. When the diets containing different levels of piroxicam were fed 23 wk after carcinogen treatment, the colon tumor incidence was significantly inhibited in animals fed the 75 and 150 ppm piroxicam diets. The colon tumor incidences in animals fed the diets containing 0, 25, 50, 75, and 150 ppm were 89, 78, 67, 64, and 64%, respectively. The colon tumor multiplicity (colon tumors/animal) was slightly but significantly inhibited in animals fed the diets containing 25 to 150 ppm piroxicam. The results of this study demonstrate that increasing levels of piroxicam in the diet, when fed 1 or 13 wk after carcinogen insult, inhibit colon tumor incidence in a dose-dependent manner.

Animals↗
PubMed1987

Effect of restricted caloric intake on azoxymethane-induced colon tumor incidence in male F344 rats.

The effect of 30% caloric restriction on azoxymethane (AOM)-induced colon carcinogenesis was investigated in male F344 rats. Starting at 5 weeks of age, groups of animals were fed ad libitum a high-fat (23.5%) semipurified diet. At 7 weeks of age, all animals except the vehicle-treated groups were s.c. injected with AOM (15 mg/kg body wt, once weekly for 2 weeks). Four days after the second AOM injection, groups of animals were continued on high-fat diet and fed ad libitum (ad libitum group) whereas other groups were restricted to 70% of total calories (calorie-restricted group) consumed by the ad libitum group, but received same amounts of fiber, vitamins, and minerals. Thirty-two weeks after AOM injections, all animals were necropsied. The animals in the calorie-restricted group developed significantly fewer colon tumors and had a lower colon tumor incidence than did the rats in the ad libitum group. The size of colon tumors was also reduced in the calorie-restricted group.

Animals↗
PubMed1987

Metabolic epidemiology of colon cancer: effect of dietary fiber on fecal mutagens and bile acids in healthy subjects.

Because of potential significance of fecal mutagens and secondary bile acids in the pathogenesis of colonic cancer and of inverse association between dietary fiber and colonic cancer risk, the effect of dietary wheat and rye fiber on fecal mutagenic activity and bile acid levels was studied in 15 healthy men and women who were consuming high fat/moderately low fiber diets and excreting high levels of fecal mutagens and bile acids. Each participant provided two 24-h stool specimens and a 3-day diet record while consuming their normal diet (control). All subjects were then asked to consume their normal diet plus 11 g of supplemental fiber per day in the form of whole grain bread for 4 weeks. During the last week of diet intervention, each subject provided two 24-h stool specimens and a 3-day dietary record. Fecal samples collected from both periods were analyzed for bile acids and for mutagens using Salmonella typhimurium strains TA98 and TA100 with and without microsomal activation. The concentration of fecal secondary bile acids was significantly lower during the fiber supplemental period in all subjects. Fiber supplementation also inhibited the fecal mutagenic activity in TA100 and TA98 with and without microsomal activation. Thus, the increased fiber intake in the form of whole wheat and rye bread may reduce the production and/or excretion of fecal mutagens and decrease the concentration of fecal secondary bile acids in humans.

Bile Acids and Salts↗
PubMed1987

Dietary fat and colon cancer: animal models.

During the past 15 years, human and animal model studies performed in our laboratory indicate that dietary fat plays an important role in the etiology of colon cancer. The effect of dietary fat during the stages of initiation and postinitiation of colon carcinogenesis depends on not only the amount of fat but also the type of fat and its fatty acid composition. Studies conducted in animal models have shown that high intake of dietary corn oil, beef fat, safflower oil, and lard increases colon carcinogenesis, whereas diets high in olive oil, coconut oil, and fish oil are without enhancing effect. The mechanisms by which various types of fat increase colon carcinogenesis are not fully understood; however, in most instances, the high-fat diet seems to enhance colon carcinogenesis through its elevation of agents that act as promoters of tumor development.

Animals↗
PubMed1987

Dietary fiber and colon cancer: animal model studies.

Support for a protective role for certain dietary fibers in the etiology of colon cancer has come from nutritional epidemiologic studies. Recommendations to increase consumption of fiber-containing food and decrease the intake of dietary fat should form the basis of a diet that is unlikely to do harm, and may have the potential for reducing the development of colon cancer, in humans. Studies examining the role of dietary fiber as an inhibitor of colon cancer in animal models appear to have provided some conflicting results, due mostly to differences in the nature and amount of carcinogen used to induce colon tumors, variation in the composition of the experimental diets, and relative difference in food intake by animals, to cite a few of the methodological problems. However, overall, the feeding of wheat bran appears to inhibit color tumor development to a greater degree than do other dietary sources of fiber.

Animals↗
PubMed1986

Effect of different levels of dietary corn oil and lard during the initiation phase of colon carcinogenesis in F344 rats.

The effect of various levels of polyunsaturated fat (corn oil) and saturated fat (lard) fed during the initiation stage of colon carcinogenesis was studied in male F344 rats. The animals were fed the diets containing 5, 13.6, and 23.5% corn oil or lard 2 weeks before, during, and until 1 week after sc injection of 15 mg azoxymethane [(AOM) CAS: 25843-45-2]/kg body weight, once weekly for 2 weeks (designated as initiation). One week after AOM treatment, groups of animals were transferred to their respective 5% corn oil or lard diets. Additional groups consuming 5% corn oil or lard were transferred to 23.5% corn oil or lard, respectively (post-initiation stage). All animals were fed these diets until the termination of the experiment. Fecal bile acids and colonic mucosal ornithine decarboxylase activity were measured in vehicle-treated animals fed the experimental diets for 14 weeks. Body weights and intakes of total calories, protein, nonnutritive fiber, and micronutrients were comparable among the various dietary groups. The animals fed the 23.5% corn oil diet during the postinitiation stage had a higher incidence of colon tumors than did those fed the 5% corn oil diet, whereas feeding of 23.5 and 13.6% corn oil diets during the initiation stage had no effect. In contrast, animals fed the 23.5 and 13.6% lard diet during the initiation stage and 23.5% lard diet during the postinitiation stage developed more colon adenocarcinomas than did those fed the 5% lard diet. The excretion of fecal deoxycholic acid, lithocholic acid, and 12-ketolithocholic acid and the activity of colonic mucosal ornithine decarboxylase activity were higher in animals fed the 23.5% corn oil or lard diet during the postinitiation compared to the levels in animals fed the 5% corn oil or lard diet.

1,2-Dimethylhydrazine↗
PubMed1986

Interactions of selenium deficiency, vitamin E, polyunsaturated fat, and saturated fat on azoxymethane-induced colon carcinogenesis in male F344 rats.

The effect of the interaction of selenium deficiency, excess vitamin E, and type of fat on colon carcinogenesis induced by azoxymethane (AOM) was studied in male F344 rats. The experimental diets, based on a Torula yeast diet and containing 20% stripped corn oil or 20% stripped lard, were as follows: 1) selenium deficient with adequate (50 mg/kg diet) vitamin E, 2) selenium deficient with excess (750 mg/kg diet) vitamin E, 3) selenium adequate with adequate vitamin E, and 4) selenium adequate with excess vitamin E. Starting at about 3 weeks of age, animals were fed the experimental diets, and at 7 weeks of age all animals except the vehicle-treated controls were given sc injections of AOM (15 mg/kg body wt) once weekly for 2 weeks. Animals were fed the experimental diets until termination of the experiment. Selenium deficiency significantly inhibited the incidence (percentage of animals with tumors) and multiplicity (tumors per animal) of colon adenocarcinomas and adenomas, whereas excess vitamin E had no effect on colon carcinogenesis. There was no interaction between the selenium status and vitamin E; the selenium status and type of fat; vitamin E and type of fat; and among selenium status, vitamin E, and type of fat.

1,2-Dimethylhydrazine↗
PubMed1986

Effect of dietary fish oil on azoxymethane-induced colon carcinogenesis in male F344 rats.

The effect of dietary intake of different levels of Menhaden fish oil on azoxymethane-induced carcinogenesis was examined in male F344 rats fed the semipurified diets. Starting at 5 weeks of age, groups of animals were fed the 5% corn oil (low corn oil) diet. At 7 weeks of age, all animals except the vehicle-treated controls were given s.c. injections of azoxymethane (15 mg/kg body weight/week for 2 weeks). After 4 days, groups of animals were fed the diets containing 4% Menhaden oil + 1% corn oil (low fish oil), 22.5% Menhaden oil + 1% corn oil (high fish oil), 5% corn oil, and 23.5% corn oil (high corn oil). Thirty-four weeks after azoxymethane injections, all animals were necropsied. High fish oil diet had no tumor promoting effect in the large intestine when compared to the high corn oil diet. There was no difference in large intestinal tumor incidence among the other dietary groups. The results of this study indicate that fish oils rich in highly polyunsaturated n-3 fatty acids do not enhance large bowel carcinogenesis and that the fatty acid composition of the dietary fat is one of the determining factors in large bowel carcinogenesis.

Animals↗
PubMed1985

Metabolic epidemiology of colon cancer: fecal mutagens in healthy subjects from rural Kuopio and urban Helsinki, Finland.

Fecal mutagenic activity and dietary pattern of rural and urban Finnish population groups with distinct risk for the development of colon cancer were studied in a low-risk population in rural Kuopio and an intermediate-risk population in urban Helsinki. The average daily intake of protein and fat was the same in the two groups but the frequency of consumption of whole-grain cereals and whole-grain bread, as well as the amount of fiber from the bread were higher in Kuopio as compared to Helsinki. Fecal samples collected for 2 days were incubated under anaerobic conditions at 37 degrees C for 96 h, extracted with hexane: peroxide-free diethyl ether, partially purified on a silica Sep-Pak cartridge, and assayed for mutagenic activity using the Salmonella typhimurium/mammalian microsome system. The fecal mutagenic activity was observed with the tester strains TA98 and TA100 with and without microsomal activation in both the population groups. The percentage of samples showing fecal mutagenic ratio greater than 3 with TA98 and TA100 with microsomal activation, was higher in volunteers from Helsinki than in Kuopio.

Adult↗
PubMed1985

Effect of dietary Laminaria angustata (brown seaweed) on azoxymethane-induced intestinal carcinogenesis in male F344 rats.

The effect of dietary Laminaria angustata (brown seaweed) on azoxymethane (AOM)-induced intestinal carcinogenesis was studied in male F344 rats. Five-week old rats were fed semipurified diets containing 0 and 10% seaweed. When the rats were 7 weeks old, all except the vehicle-treated groups received weekly subcutaneous injections of AOM in normal saline for two weeks (20 mg/kg body wt/week). All animals were fed the experimental diets until the termination of the experiment, which was 28 weeks after the last AOM injection. The incidence (percent of animals with tumors) and multiplicity (tumors/animal) of small intestinal tumors did not differ significantly between the control and seaweed groups. The incidence and multiplicity of colon adenomas along with the size of colon tumors were increased in rats fed the seaweed diet compared with those fed the control diet. Dietary seaweed had no major effect on the concentration of fecal bile acids; however, the concentration of fecal cholesterol and total neutral sterols was decreased in the seaweed group. These results suggest that dietary seaweed increases the risk for colon tumors.

Adenocarcinoma↗