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Biomedical subjects

P Pour

Publications and source records attributed to P Pour.

At least 37 records · Page 2Linked to original sources
PubMed1980

Mutagenic activities of oxidized derivatives of N-nitrosodipropylamine in the liver cell-mediated and Salmonella typhimurium assays.

The mutagenic activity of N-nitrosobis(2-oxopropyl)amine (BOP), N-nitroso(2-hydroxypropyl) (2-oxopropyl)amine (HPOP), N-nitrosobis(2-hydroxypropyl)amine (BHP), N-nitrosomethyl-2-oxopropylamine (MOP), and N-nitrosomethyl-2-hydroxypropylamine (MHP) was examined in the Ames liquid incubation assay, using hamster liver homogenate for metabolic activation, and in the hamster liver cell-mediated V79 cell assay. At similar concentrations, the cell-mediated assay showed a greater mutagenic response over background to these nitrosamines than did the bacterial assay. Also, the relative mutagenic potency in the cell-mediated assay (MOP > MHP > BOP > HPOP > BHP) correlated better than that in the Ames assay (HPOP > MHP greater than or equal to BOP = BHP = MOP) with overall carcinogenic potency in the hamster (MOP > BOP > HPOP > BHP). The liver cell-mediated assay may be an important adjunct to the battery of short-term tests for carcinogenicity prescreening.

Animals↗
PubMed1980

Carcinogenicity of N-nitrosomethyl(2-oxopropyl)amine in Syrian hamsters.

7-Methylguanine was found in hydrolysates of liver and pancreas DNA from Syrian golden hamsters given a single dose of N-[1-14C]nitrosobis(2-oxopropyl)amine (BOP). This led us to examine the carcinogenicity of a potential methylating metabolite of BOP, N-nitrosomethyl(2-oxopropyl)amine (MOP). MOP was found to be a potent pancreatic carcinogen by either single or weekly s.c. injections. A single MOP treatment (25 mg/kg body weight) induced ductular adenomas and/or adenocarcinomas in 80% of the hamsters. A higher incidence of these neoplasms was found in 93% and 87% of animals receiving, respectively, 3.5 and 1.75 mg MOP per kg body weight weekly for life. However, the lower dose (0.87 mg/kg body weight) was less effective, resulting in a 33% tumor incidence. Compared with the known potent pancreatic carcinogen BOP, MOP seemed to have a greater affinity for the pancreas since considerably lower doses were required to induce similar incidences of equivalent pancreatic tumors. Like BOP, MOP caused tumors of the liver (7 to 100% incidence), kidneys (7 to 80% incidence), and vascular system (7 to 27% incidence). However, in contrast to BOP, which was noncarcinogenic to the upper respiratory tract, MOP-treated animals developed a high incidence of nasal cavity tumors (40% after a single treatment and 27 to 100% after weekly injections). The mutagenesis studies using hamster liver cell-mediated V79 cells confirmed the stronger effect of MOP compared to BOP. The assumption that MOP might be a proximate carcinogenic metabolite of BOP could not be substantiated by our methods for determining the in vivo and in vitro metabolites of BOP.

Adenocarcinoma↗
PubMed1979

Comparative studies of neoplastic response to a single dose of nitroso compounds. 6. The effect of diethylnitrosamine in Syrian golden hamsters.

The effect of a single subcutaneous injection of different DEN doses was examined in adult Syrian hamsters observed for life. The minimal effective dose (threshold dose) for neoplastic response, reflected by induction of papillary polyps in the larynx and/or trachea, was 1.03 mg DEN/kg body weight. No tumors were found which could be related to treatment in other segments of the respiratory epithelium nor in other tissues.

Animals↗
PubMed1979

Ductular origin of pancreatic cancer and its multiplicity in man comparable to experimentally induced tumors. A preliminary study.

The histologic features of 3 randomly selected pancreatic cancer cases are compared with those found in Syrian hamsters after treatment with N-nitrosobis(2-oxopropyl)amine (BOP). The 3 human cases all exhibited hyperplastic, preneoplastic and malignant changes which were markedly multicentric, and which arose predominantly from ductules, as well as from small ducts. The findings were comparable to those in the hamster mode. Proliferation and malignant alterations of the intrainsular ductules were commonly seen in both human and experimental tumors. The data is consistent with the concept that cells of the small ducts and especially of the ductules represent a potential source of human, as well as experimental, tumors. The small number of human cases studied does not allow generalization, but the marked resemblances in all 3 randomly selected pancreatic cancer cases were remarkable.

Adenocarcinoma↗
PubMed1979

The morphologic and biologic patterns of chemically induced pancreatic adenocarcinoma in Syrian golden hamsters after homologous transplantation.

A pancreatic adenocarcinoma induced by N-nitrosobis(2-oxopropyl)amine in the Syrian golden hamster was successfully transplanted to a homologous host by subcutaneous inoculation through 10 successive passages. The rate of 'tumor take' increased progressively with each generation from 60% to 100%, and the latency period after inoculation was reduced simultaneously from 6 weeks to 1 week in the second and following passages. The tumors grew rapidly, ulcerated the overlying skin, and metastasized to the regional lymph nodes and lungs. The animals usually died with multiple lung metastases between the 5th and 20th weeks. All transplanted tumors and their metastases retained the pattern of the original, well-differentiated adenocarcinomas.

Adenocarcinoma↗
PubMed1979

Spontaneous tumors and common diseases in three types of hamsters.

Hamsters of three types designated as inbred cream (Epp/e/e), linebred white (EPP/cdcd/RB/A), and linebred albino (EPP/cdcde/e) were thoroughly examined histopathologically for spontaneous diseases. All hamsters were maintained simultaneously for life under identical standard laboratory conditions. Marked differences were found in longevity of the animals and in incidence, sites, patterns, and types of spontaneous diseases. In cream hamsters (CH), survival time was shorter than in white hamsters (WH) and albino hamsters (AH). More tumors and malignant lesions unrelated to survival were found in AH compared to CH and WH; also, the multiplicity of neoplasms were more pronounced in AH. The predominating tumor types differed in each line: Pancreatic islet cell neoplasms were most common in CH, adrenal gland tumors predominated in WH, and thyroid gland tumors in AH. Also, the relative incidence of spontaneous tumors varied among the lines. Some tumors seemed strain-specific and were not seen in other lines; malignant melanomas, for example, occurred only in CH and WH. Certain neoplasms, e.g., those of the thyroid and adrenal glands, were found more often in one sex than the other. The three hamster groups differed also in nonneoplastic diseases. Detailed histopathologic findings are presented and compared with data on the Syrian golden hamster, the ancestral line of these three groups.

Amyloidosis↗
PubMed1979

Carcinogenic effect of N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine, a postulated proximate pancreatic carcinogen in Syrian hamsters.

N-Nitroso(2-hydroxypropyl)(2-oxopropyl)amine (HPOP) proved to be a potent carcinogen in Syrian golden hamsters. The compound is an in vivo metabolite of N-nitrosobis(2-hydroxypropyl)amine, N-nitrosobis(2-oxopropyl)amine (BOP), and N-nitroso-2,6-dimethylmorpholine and a postulated proximate pancreatic carcinogen in hamsters. As with BOP, HPOP induced a higher incidence of pancreatic ductular adenocarcinomas than did N-nitrosobis(2-hydroxypropyl)amine and N-nitroso-2,6-dimethylmorpholine, and these neoplasms showed a great tendency for invasion and metastasis. Also, HPOP induced tumors of the forestomach, liver, gallbladder, kidneys, and vagina (as did BOP). However, HPOP [unlike BOP, but like N-nitrosobis(2-hydroxypropyl)amine and N-nitroso-2,6-dimethylmorpholine] led to tumor development in the nasal cavity, larynx, trachea, intestine, Harderian gland, lips, and flank organ. The possible mechanisms of HPOP carcinogenicity are discussed.

Animals↗
PubMed1979

Metabolism of three radiolabeled pancreatic carcinogenic nitrosamines in hamsters and rats.

The in vivo metabolism and disposition of three radiolabeled N-nitrosamines which are carcinogenic for the pancreas of the hamster but not the rat have been examined. N-[1-14C]Nitrosobis(2-oxopropyl)amine (BOP), N-[1-14C]nitrosobis(2-hydroxypropyl)amine (BHP), and their suggested proximate pancreatic carcinogenic metabolite N-[1-14C]nitroso-(2-hydroxypropyl)(2-oxopropyl)amine (HPOP) were metabolized and exhaled as 14CO2 to various extents somewhat proportional to their carcinogenic potency. More than 50% of the dose of BOP and HPOP was exhaled as 14CO2, whereas 26% of BHP was excreted this way, and 40% of BHP was excreted unchanged in the urine. Administered BOP was excreted to a small extent in the urine of both species as HPOP and BHP. No other nitrosamine metabolites were detected in urine. HPOP and BHP were detected in the pancreatic juice and bile of both species after administration of BOP and BHP. The results suggest that pancreatic ductular carcinogenesis in the hamster as a result of exposure to BOP is not due to secretion of carcinogenic metabolities in the pancreatic juice or reflux of bile containing nitrosamine metabolites into the ducts. Carcinogen metabolic activation appears to be by an oxidative pathway.

Animals↗
PubMed1979

Carcinogenicity of N-nitrosobis(2-hydroxypropyl)amine and N-nitrosobis(2-oxopropyl)amine in MRC rats.

Weekly sc injections of equitoxic doses of N-nitrosobis(2-hydroxypropyl)amine (BHP) and N-nitrosobis(2-oxopropyl)amine (BOP) to Wister-derived MRC rats induced tumors. The incidence, latency, multiplicity, morphologic type, and distribution of these tumors varied according to the compound given. The esophagus was the main target organ for BHP (100%), followed by the respiratory tract (87%), pharynx (80%), colon and liver (each 73%), kidneys (20%), thyroid gland (20%), and urinary bladder and urethra (each 7%). BOP was ineffective in the esophagus and pharynx but induced a higher incidence of tumors in the kidneys (27%), thyroid gland (60%), urinary bladder (33%), and urethra (73%) and fewer neoplasms in the respiratory tract (20%), colon (67%), and liver (53%). In addition, BOP caused a few, apparently primary, prostate squamous cell carcinomas. The results are compared with results of BHP treatment in Sprague-Dawley rats and with results of BHP and BOP treatment in Syrian golden hamsters.

Animals↗
PubMed1978

Induction of thyroid follicular adenomas and carcinomas by N-nitrosobis(2-oxopropyl)amine.

Subcutaneous injection of N-nitrosobis(2-oxypropyl)amine (BOP) induced thyroid follicular adenomas and carcinomas in MRC rats. The tumor yield was 50% following a single dose and 60% after weekly treatment for life. In males the tumor incidence was slightly higher and the latency period shorter, while in females, the tumors were larger. Sites of origin, size, multiplicity and morphologic patterns of tumors were analyzed in relation to dose and sex. The possible mechanisms involved in tumorigenesis are discussed.

Adenocarcinoma↗
PubMed1978

Development of biliary and hepatic neoplasms in guinea pigs treated with N-nitrosobis(2-oxopropyl)amine.

N-Nitrosobis(2-oxopropyl)amine (BOP) was administered subcutaneously to 29 male inbred strain 13 guinea pigs at weekly intervals for 4 weeks. The guinea pigs were observed until their death or termination of the experiment at the end of 55 weeks. Of 14 guinea pigs that survived more than 30 weeks, 7 animals developed cholangiocarcinomas and 2 developed hepatocellular carcinomas. Tumors of other sites were not found.

Adenoma, Bile Duct↗
PubMed1978

Pancreatic ductulitis in Syrian golden hamsters bearing homologous transplantable pancreatic adenocarcinomas.

A highly specific pancreatitis primarily affecting the intralobular and intrainsular ductules has been demonstrated in Syrian golden hamsters bearing homologous, non-syngeneic, transplantable pancreatic adenocarcinomas induced by N-nitrosobis(2-oxopropyl)amine (BOP). The ductulitis provides further evidence that induced pancreatic neoplasms originate from ductules.

Adenocarcinoma↗
PubMed1978

A new and advantageous model for colorectal cancer: its comparison with previous models for a common human disease.

Weekly subcutaneous injection of 10 mg/kg body wt. of N-nitrosobis(2-oxopropyl)amine (BOP), a pancreatic carcinogen in Syrian golden hamsters, induced colorectal cancer in MRC rats in 67% of all males and 33% of all females that survived beyond 43 and 68 weeks, respectively. Tumors were concentrated in specific segments of the large bowel and not found in the small intestine. Although the distribution of cancer in the cecum, and ascending and descending colon was similar in both sexes, rectal cancer predominated significantly in males. These data and the tumor morphology indicate the present model more closely resembles the corresponding human disease than do models in previous relevant experimental studies.

Adenocarcinoma↗
PubMed1978

Spontaneous alterations in the pancreas of the aging Syrian golden hamster.

The systematic histologic examination of the pancreas of aging Syrian golden hamsters revealed distinct alterations that affected the exocrine, endocrine, and supporting tissues. Some of these lesions showed a significant relationship to age and/or sex of the animal. Specific alterations that affected the ductules and islets represented a characteristic, probably genetically linked, process of the hamster pancreas and may have been the decisive factors for the unique carcinogenic response of this species to specific carcinogens.

Aging↗