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Biomedical subjects

M Pollard

Publications and source records attributed to M Pollard.

At least 91 records · Page 5Linked to original sources
PubMed1982

Increased activity of a beta-galactosyltransferase in tissues of rats bearing prostate and mammary adenocarcinomas.

The levels of UDP-galactose: N-acetylglucosamine(beta 1-4)galactosyltransferase activity (GalT-4) were determined in the sera, in solid tumors, and in corresponding cell cultures of rats bearing two lines of prostate adenocarcinomas (PA-2 and PA-3), and in the sera of rats bearing other transplanted and autochthonous adenocarcinomas. Sera and tissues from normal (tumor-free) rats were used as controls. Prostate adenocarcinoma cell cultures had five times greater levels of enzyme activity than did tumor cell infiltrated lymph nodes from animals bearing the prostate adenocarcinomas. The levels of activity in the cells of both prostate tumor lines were equivalent, even though they metastasize through different routes. Serum levels of galactosyltransferase activity were detected in the blood, and in rats bearing a mammary adenocarcinoma with extensive necrosis of the tumor mass (tumor mass greater than 22.0 g/200 g body weight). The increase was three times the control value. The sera of L-W rats bearing prostate tumors (PA-2 and PA-3) were inactive with the GalNAc-containing acceptor, Gm2 (GalNAc beta 1-4(NeuAc alpha 2-3)Gal beta 1-4Glc-Cer) but active with either free GlcNAc (Km = 0.25 mM) or LcOse3Cer (GlcNAc beta 1-3 Gal beta 1-4Glc--Cer; GlcNAc--R).

Adenocarcinoma↗
PubMed1981

Effect of indomethacin on intestinal tumors induced in rats by the acetate derivative of dimethylnitrosamine.

Over the course of 20 weeks, Sprague-Dawley rats developed intestinal tumors in response to an intraperitoneal injection of the acetate derivative of dimethylnitrosamine. The same agent did not induce tumors in Lobund-Wistar rats. The number of tumors was significantly smaller in rats given drinking water containing indomethacin (beginning 14 days after the injections) than in control rats given drug-free water.

Animals↗
PubMed1981

Interference with in vivo growth and metastasis of prostate adenocarcinoma (PA-III) by ICRF-159.

Rat prostate adenocarcinoma III (PA III) cells metastasize spontaneously from extravascular implant sites through ipsilateral lymphatic channels to the lungs in which they develop as distinct expanding foci of tumors. ICRF-159 (30 + 60 mg/kg body weight) was administered to rats with PA-III cells at daily intervals from day 0 to 2 weeks (5 days/week). When the rats were examined after 35 and 40 days, the drug treatment caused a significant suppression of the primary tumor and of metastatic dissemination. When the treatment schedule with ICRF-159 was delayed to day 18 in rats with metastasizing PA III cells, the progress of metastasis was thereafter interrupted or retarded significantly. Rats with PA II cells which metastasize in fulminant pattern through lymphatic and blood channels to multiple target organs were administered ICRF-159 (60 mg/kg body weight) from day 0 for over 2 weeks. They did with disseminated tumors within days after cessation of treatments.

Adenocarcinoma↗
PubMed1981

Characterization of a very-low-density lipoprotein (VLDL)-associated cytotoxic factor.

A VLDL-associated cytotoxic factor was isolated from sera of pregnant rats and characterized. The inhibitory effect of this factor on the macromolecular synthesis of rat prostate adenocarcinoma cells (PA-III) was also examined. VLDL (Sf 20-400) was subfractionated by differential ultracentrifugal flotation and the Sf 100-400 fraction was associated with most of the oncolytic activity. Chemical analysis of serum VLDL at various stages of pregnancy indicated that the 4 major constituents of VLDL (protein, triglyceride, cholesterol, and phospholipid), and the cytotoxic titre, were increased significantly before parturition and restored to normal levels by 24 h post partum. The delipidation of lyophilized VLDL by n-heptane suggested that the cytotoxic component was associated with the neutral lipid core of VLDL. Kinetic studies of colony inhibition and the incorporation of radioactive thymidine and leucine into 10% TCA precipitates of PA-III cells showed that VLDL induced irreparable cellular damage during the initial 15 h of incubation. The cytotoxic activity of VLDL was not due to the association with PGF2 alpha, beta-oestradiol, progesterone, 25-hydroxycholesterol, or free fatty acids (oleic, stearic, palmitic, linoleic, linolenic and arachidonic acids), monopalmitolein, elaidyl and alpha-linolenyl alcohol. The role of this factor in host defence against neoplasia is discussed.

Adenocarcinoma↗
PubMed1980

Metastasis-enhancing effect of heparin and its relationship to a lipoprotein factor.

The effect of low-dose heparin on spontaneous metastasis formation was studied with the PA-III rat prostate adenocarcinoma cell line model system. In LW rats given heparin iv at a dose of 1,000 U/kg body weight (three times/wk), the metastatic spread of implanted PA-III cells from the footpad through ipsilateral lymphatics to the lungs was enhanced. The weights of the draining lymph nodes (popliteal, inguinal, and axillary) and the number of lung tumor colonies were significantly increased compared with those in the saline-treated control tumor-bearing rats. The growth of the primary tumor was also enhanced. Heparin alone did not induce enlarged lymph nodes in rats nor did it change the growth pattern of PA-III cells in vitro. The accelerated metastatic spread of the PA-III cells was possibly related to the destruction of the oncolytic activity of the very low-density lipoprotein by the lipoprotein lipases induced by the iv administration of heparin. However, the possibility that other mechanisms could be operative in this phenomenon has not been ruled out.

Adenocarcinoma↗
PubMed1980

Indomethacin treatment of rats with dimethylhydrazine-induced intestinal tumors.

Intestinal tumors were induced in male Sprague-Dawley rats following the administration of five weekly doses of 1,2-dimethylhydrazine (DMH) by gavage. At intervals thereafter, groups of rats were given indomethacin (IND) in the drinking water. In three trials, the incidence of rats with tumors was significantly reduced by 40% below the control rats which did not receive IND and there was no significant difference in body weights. Also, in those IND-treated rats which developed tumors, the tumors were generally smaller in numbers and sizes compared to the control rats. A group of DMH-treated rats was treated with crude IND by gavage and the differences between them and untreated control rats were not significant. It is likely that the treatment was directed at the tumors and not at the DMH which induced them.

Animals↗
PubMed1979

Patterns of spontaneous metastasis manifested by three rat prostate adenocarcinomas.

Three transplantable rat prostate adenocarcinoma cell lines were assessed for patterns of metastasis, ie, routes of dissemination and larger organ(s) selected for implantation. Two lines (I and III) were disseminated only through ipsilateral lymphatic channels to the lungs. The third cell line (II) was disseminated through lymphatic and blood channels to lungs, liver, and kidneys. The pattern of spontaneous metastasis is a characteristic of the tumor cell; but there is evidence that the rate and extent of metastasis can be modified experimentally.

Adenocarcinoma↗
PubMed1979

Ozonation of mutagenic and carcinogenic polyaromatic amines and polyaromatic hydrocarbons in water.

The Salmonella-microsome assay for mutagenesis was used to determine the effect of ozone on the mutagenesis of selected carcinogens and mutagens in water. Short periods of ozonation were shown to completely inactivate the mutagenicity of several polyaromatic amine mutagens including acriflavine, proflavine, and beta-naphthylamine. Selected polyaromatic hydrocarbons were also sensitive to ozonation. Kinetic studies revealed that the mutagenicity of benzo(a)pyrene, 3-methylcholanthrene, and 7,12-dimethylbenz(a)anthracene was destroyed after short periods of ozonation. To correlate loss of mutagenicity with loss of carcinogenicity, two polyaromatic hydrocarbons were treated with ozone, extracted from water with hexane, and tested for carcinogenicity in mice. When 7,12-dimethyl-benz(a)anthracene and 3-methyl-cholanthrene were treated with ozone, there was a substantial reduction in carcinogenicity compared to control groups treated with oxygen alone. However, a small number of tumors developed in the group of animals receiving a hexane extract of ozonated 7,12-dimethylbenz(a)anthracene. This activity may be due to breakdown products of 7,12-dimethylbenz(a)anthracene that are not mutagenic.

2-Naphthylamine↗
PubMed1979

Spontaneous liver tumors in aged germfree Wistar rats.

Liver tumors, ranging from benign nodules to carcinomas, developed spontaneously in 115 (87%) of 132 germfree Wistar rats beyond the age of 30 months. In addition, the rats developed a high incidence of benign adenomas of endocrine glands and of the breasts.

Adenoma↗
PubMed1979

Ozonation of mutagenic and carcinogenic alkylating agents, pesticides, aflatoxin B1, and benzidine in water.

The effect of ozonation on the mutagenicity of selected chemicals in water was determined. The use of the Salmonella-microsome assay for mutagensis allowed kinetic studies to be performed on the ozonation of all chemicals tested. The results indicate that the mutagenicity of certain pesticides, including captan and Dexon, was inactivated by short periods of ozonation. The mutagenicity of certain alkylating agents including bis(2-chloroethyl)amine and sodium azide was rapidly inactivated by ozonation while other alkylating agents such as beta-propiolactone, propanesultone, and N-methyl-N'-nitro-N-nitrosoguanidine were unaffected by treatment with ozone. The mutagenicity of aflatoxin B1 was rapidly inactivated by treatment with ozone. Three chemicals were shown to be converted to direct mutagens by ozone treatment. Under certain conditions, dimethylhydrazine could be converted to a mutagen that was stable for 3 weeks. A similar chemical, 2-hydroxyethylhydrazine, was converted to an unstable mutagen that was inactive after 24 hr at room temperature. When benzidine was treated with ozone, there was a transient increase in mutagenicity which was lost after longer treatment with ozone.

Aflatoxins↗
PubMed1979

Promotional effect of sodium barbiturate on intestinal tumors induced in rats by dimethylhydrazine.

Noninbred Sprague-Dawley rats were administered 1,2-dimethylhydrazine hydrochloride (DMH) by gavage or methylazoxymethanol acetate by sc inoculation. Thereafter, one group was given water to which 0.1% sodium barbiturate was added, and the other was given drug-free water. They were examined 20 weeks after onset of the experiments. A direct relationship was noted between dosage of DMH and numbers of intestinal tumors induced in the rats. The rats provided with sodium barbiturate-supplemented water developed more intestinal tumors than did those that drank drug-free water.

Animals↗
PubMed1978

In vitro effects of lipoprotein-associated cytotoxic factor on rat prostate adenocarcinoma cells.

As assayed by the colony inhibition technique, sera from rats at an advanced stage of pregnancy were cytotoxic to a number of tumorigenic and "nontransformed" cell lines. The cytotoxic effect is not species specific. Primary fetal rat kidney cells were not susceptible to this cytotoxic effect. The level of demonstrable cytotoxicity in sera rose gradually as gestation advanced; it peaked at 48 hr before parturition and disappeared thereafter. Sera from control nonpregnant rats were not cytotoxic. The cytotoxic factor(s) in sera was demonstrable only in the very low-density lipoprotein (VLDL) (hydrated density less than 1.006 g/ml) fraction. Reconstitution studies suggest that: (a) inhibitors which usually mask the cytotoxic actitivity of VLDL in whole serum, are present; and (b) pregnancy initiates enhanced VLDL synthesis, which exceeds the masking effect. The possible role of this cytotoxic VLDL in host defense against neoplasia is discussed.

Adenocarcinoma↗
PubMed1978

Induction of colon tumors in 1,2-dimethylhydrazine-resistant Lobund Wistar rats by methylazoxymethanol acetate.

Sprague-Dawley and Lobund Wistar rats, which were sensitive and resistant to induction of colon tumors by 1,2-dimethylhydrazine (DMH), respectively, were treated with methylazoxymethanol (MAM), the product of DMH metabolism by the microsomal mixed-function oxidase system. Although the colon tissue in both stocks of rats had similar NAD+-dependent dehydrogenase activities that are considered necessary to activate MAM to an ultimate carcinogen, still a sevenfold greater incidence of colon tumors was found in the Sprague-Dawley rats, and their tumors were more extensive. The results indicated that the difference in susceptibility to colon tumor induction between the rat stocks was partially related to metabolic activation of the DMH and to other, as yet undetermined, endogenous factors.

Adenocarcinoma↗