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D B Clayson

Publications and source records attributed to D B Clayson.

At least 19 recordsLinked to original sources
PubMed1992

Calories, fat, fibers, and cellular proliferation in Swiss Webster mice.

Increased cellular proliferation has been associated with the enhanced expression of several key stages in carcinogenesis. A standard protocol was used to investigate the effect of specific dietary regimens on cellular proliferation. Young adult Swiss Webster mice were fed for 30 days with modified AIN-76A semi-purified diets designed to illustrate the effects of the levels of dietary or calorie restriction, different fibers and bulking agents, and different fats on cellular proliferation. Female mice were used for the restriction and fat studies, males for the fiber and bulking agent studies. Vaginal smears were taken from females from treatment day 15, and the mice killed 2 days following the first estrus following 30 days feeding; males were killed on the 30th day. One hour before death, mice were injected ip with 0.25 micro Ci/g 3[H]-thymidine. Slides were prepared for radioautography and histopathology. Both dietary and calorie restriction led to reduced 3[H]-thymidine labeling indices in each of the seven tissues studied, the mammary gland being the most severely affected. Different fibers and bulking agents, in specific cases, reduced labeling in the duodenum but not to a consistent statistically significant extent in the colon or colo-rectal region. In the duodenum, oat bran and oat gum were the most effective while wood cellulose (alphacel) had no effect. Investigations on the effects of different fats is continuing. High levels of lard, menhaden oil, or cod liver oil as the fat component of the AIN-76A diet, led to much higher levels of labeled cells in the mammary gland or colo-rectal region than did fat components rich in vegetable oils. The labeling indices appeared to be inversely correlated with the level of linoleic acid in the diet, a presumption that has been confirmed by investigating a series of diets containing different levels of this acid. Anti-oxidants were not used in any of these fat-modified diets. The overall results obtained in these studies clearly indicate the utility of cellular proliferation studies in investigating the effects of dietary modifications.

Animals↗
PubMed1992

Effect of varying the type of fat in a semi-purified AIN-76A diet on cellular proliferation in the mammary gland and intestinal crypts in female Swiss Webster mice.

Young virgin female Swiss Webster mice were fed AIN-76A semi-purified diets containing equal weights of different fats for approximately 30 days. Using [3H]thymidine radioautography, it was established that mice fed 100% lard or high levels of fish oils (menhaden oil or cod liver oil) developed elevated cellular proliferation in the duct cells of the mammary gland and an increased number of labeled cells/crypt in the crypts of the colo-rectum accompanied by an increase in the size of the proliferative compartment. A possible inverse correlation between the level of [3H]thymidine labeling in the mammary gland, but not in the colo-rectum, and the linoleic acid content of individual diets may help to explain the significance of these observations. The effect of adding an antioxidant mixture to these diets was to reduce the excess proliferation induced in the intestinal crypts by lard or fish oil to the level induced by soybean oil, but only partially so in the duct cells of the mammary gland.

Animals↗
PubMed1979

NCI bioassays.

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Animals↗
PubMed1979

Carcinogenic potential of hycanthone in mice and hamsters.

Hycanthone was administered to Schistosoma mansoni-infected and non-infected Syrian golden hamsters and Swiss mice by intraperitoneal and intramuscular injection of amounts up to the maximum tolerated dose. No tumors attributable to treatment were observed in hamsters. In infected mice, the overall incidence of hepatomas and hepatocellular carcinomas increased from 3.4% in untreated mice to 10.6% in those treated with hycanthone. Non-infected control mice developed 0.8% of these tumors compared to 10.2% in mice treated with hycanthone. Despite the use of high dose levels of hycanthone, statistical significance was attained only with non-infected female mice injected intraperitoneally and intramuscularly with hycanthone and then only at confidence levels of 92 and 95% respectively.

Animals↗
PubMed1979

Perinatal carcinogenesis: biologic curiosity or practical necessity?

Factors that require consideration in extending carcinogen bioassay protocols to include transplacental exposure of rodent subjects are summarized. These include metabolic complexities and biologic problems, such as the differences in fetal susceptibility to lethal, teratogenic, and carcinogenic effects of the same compound at different stages of intrauterine development, and that, with the present limited knowledge of transplacental carcinogenesis, transplacental and neonatal exposure to suspected carcinogens may lead to insoluble problems of interpretation. The view is expressed that agents to which the human fetus may be substantially exposed, including drugs and food additives, should nevertheless be tested for carcinogenicity by transplacental exposure.

Animals↗
PubMed1978

Carcinogenic effects of niridazole in rats.

Niridazole was administered in the diet to rats at levels of 0.1, 0.05 and 0.025%. The drug induced adenomas and adenocarcinomas of the kidneys and forestomach papillomas.

Adenocarcinoma↗
PubMed1977

Carcinogenic effects of niridazole on rodents infected with Schistosoma mansoni.

The carcinogenicity of 1-(5-nitro-2-thiazolyl)-2-imidazolidinone (niridazole), a widely used schistosomicide, was examined in Swiss mice and Syrian golden hamsters. Schistosoma mansoni infection was evaluated as a cofactor. High incidences of drug-related neoplasms of the forestomach, lungs, mammary glands, urinary tract, and ovaries were found in mice, and tumors of the forestomach and urinary tract were found in hamsters. Infection with schistosomes had no apparent influence on tumor incidence. The results indicated a need for reevaluation of the possible carcinogenicity of this drug in man and suggested that care should be taken during its clinical use.

Animals↗
PubMed1976

Intratracheal instillation studies with 7H-dibenzo(c,g)carbazole in the Syrian hamster.

The morphologic effects and the retention and distribution times of single and multiple intratracheal instillations in Syrian hamsters of 7H-dibenzo[c,g]carbazole (DBC) and benzo[a]pyrene (BP) were compared. A single instillation of DBC induced slight changes in the hamster respiratory tract; however, five treatments caused tracheobronchial epithelial proliferation, cell hyperplasia, and occasionally, squamous metaplasia. The particle size of both carcinogens was approximately the same. BP in saline remained longer in the lungs than did DBC in saline. The shortest retention time was recorded when DBC was administered in aqueous solution, whereas multiple doses of DBC in aqueous solution did not markedly affect retention time. DBC passed from the lungs to the intestinal tract and was mainly excreted in the feces.

Animals↗
PubMed1976

Application of the results of carcinogen bioassays to man.

Animal experiments to test for the possible carcinogenic activity of chemicals provide the best and only deeply researched method for the detection or environmental carcinogens for man. The fact that most known human carcinogens give tumors in animals encourages the belief that these tests have validity. However, there are significant differences in the numbers of the exposed populations of men and animals, in the part of the lifespan during which each is exposed, in the metabolic activation of the carcinogens, and in the longevity of men and experimental rodents. For regulatory purposes, we must assume that the results of bioassay in rodents will closely parallel tumor induction in man, although we cannot be sure of this. In some cases, such as rodent bladder tumors associated with bladder stone, or subcutaneous sarcomas arising locally to massive injection of food dyes, there may be reason to reject an association. It is only by continued research into the way in which both man and laboratory animals react to carcinogens that we may hope to refine our methodologies and obtain an accurate, well-defined net to trap potential environmental carcinogens without depriving the community of chemicals, through false associations or false positive results that may be of great value, sociiologically or economically.

Animals↗
PubMed1975

Carcinogenic effects of niridazole.

Swiss mice received chronic treatment with the schistosomacide, niridazole, at 3 dose levels. Tumors were found in several organs, including stomach, lung, manary gland, ovary and bladder. Niridazole is, without doubt, carcinogenic to mice.

Animals↗
PubMed1975

Nutrition and experimental carcinogenesis: a review.

Restriction of the total diet or the number of calories fed to rats and mice inhibits the formation of tumors in several tissues. Unless animals are fed equivalent levels of food, or attain equivalent body weights, it is difficult to assess the significance of the effect of other nutritional modifications on carcinogenesis. The effects of altering the levels of protein or fat are much less than those seen with dietary restriction. Feeding a protein-free diet is tolerated for a limited period and can alter the metabolism of carcinogens. It may thus affect the tumor incidence induced by one-shot carcinogens. Vitamins have specific effects on the activity of certain carcinogens, the fullest information being available for vitamin A, which has been shown to inhibit or enhance carcinogenesis, and vitamin C, which by reducing sodium nitrite, prevents nitrosation of secondary and tertiary amines occurring in acidic conditions of the stomach. Inorganic substances, such as iodine (thyroid) and copper (liver), may affect the tumor incidence in specific tissues. The metabolic activation of carcinogens is modified by enzyme induction and the administration of antioxidants. The relevance of these results to the induction of cancer in humans is briefly discussed.

Animals↗