Biomedical subjects
Publications and source records attributed to G B Pliss.
Experimental data connected with prophylaxis of vesical cancer are reviewed. The following prophylactic measures are discussed: influence on metabolism of carcinogens and inactivation of metabolites; forced clearance of carcinogenic metabolites; carcinogenesis promoters arrest. Specific inhibition of beta-glucuronidase in urine and forced diuresis appeared to be extremely effective.
Long-term treatment of rats and mice with riboxyn failed to reveal the carcinogenic effect of the drug. Chronic experiments showed the drug to improve resistance of the animals to intercurrent infections.
The effect of lithium carbonate on promotion of N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced bladder tumors in rats was studied. Lithium carbonate acted as promoter in bladder carcinogenesis resulting in a 6-fold increase in the tumor occurrence as compared to controls. The experiments with sequential injection of the agent showed its promoting effect to be most apparent within 3-6 months following exposure to the carcinogen.
Continuous administration of neozone D to dogs and rats failed to reveal its carcinogenicity. Nor did the agent potentiate the carcinogenic effect of 2-naphthylamine and benzidine in rats. Conversely, neozone D was found to inhibit benzidine-induced carcinogenesis in female rats.
The effect of sodium nitrite on promotion of N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced tumors of the bladder in rats was studied. Sodium nitrite was found to promote bladder carcinogenesis, raising the occurrence of carcinomas threefold as compared to controls.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The study was concerned with the effect of forced diuresis on the frequency and morphologic pattern of bladder cancer induced with butylbutanolnitrosamine in rats. An 1.6 times increase in diuresis was followed by inhibition of bladder carcinogenesis, resulting in a 2.5-fold decrease in the tumor rate as compared to controls. The data obtained confirm the earlier suggested hypothesis of "urothelial contact" as well as epidemiologic data.
The dependence of gastrocarcinogenesis on biochemical and morphological disorders of the stomach mucous membrane, i.e. epimolecular alteration of chromatin structure, inhibition of pepsinogen synthesis, alteration of ontogenetic heritage of glandular epithelium was studied in 450 random-bred white rats with the aid of a model of gastrocarcinogenesis induced with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). This agent weakened the DNA-protein linkage in the chromatin. The irreversibility of this phenomenon coincided with the crucial point of the MNNG gastrocarcinogenesis (precancer sign appearance). The consequences of MNNG-induced specific alteration of epithelial stem cells became inherited (stomach adenocarcinoma development). In parallel with gastrocarcinogenesis, concomitant deficiency of pepsinogen-pepsin in the mucous membrane also developed. The data suggest that deficiency of the enzyme was in some degree obliged to alteration of pepsinogen mRNA synthesis.
Dichlorobromomethane (DCMB) and dibromochloromethane (DBCM) isolated from chlorinated drinking water were tested for toxicity, mutagenicity and carcinogenicity. Both agents proved mutagenic in a "dessicator" modification of the Ames test using Salmonella typhimurium TA98 and TA100 in the presence of exogenous metabolic activation. In aquarium Danio rerio fish tests, LD50/30 was 250 mg/l for both compounds. Both agents induced hepatocellular carcinoma in fish: DCMB--in 11 out of 29 animals (at 16.5 weeks) and DBCM--in 3 out of 16 (at 26.5 weeks). These data merit further investigation of the agents' carcinogenicity in chronic experiments in rodents.
The paper discusses spontaneous tumor profile in albino rats bred at the N. N. Petrov Research Institute of Oncology of the USSR Ministry of Health (1981-1984). The overall incidence of tumors and that of malignant ones were shown to be 27.2 and 12.5%, respectively, in males and 47.4 and 16.4%, respectively, in females. Pituitary and hemopoietic tumors most frequently occurred in males (67%). Female rats most often revealed tumors of the pituitary, breast and hemopoietic system (90%). On the whole, the tumor profile proved identical in the animal population studied and that of Rappolovo farm of the USSR Academy of Medical Sciences. However, infection resistance in the former population was superior.
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The pathologic characteristics of gastric tumors induced by single injections of N-methyl-N'-nitro-N-nitrosoguanidine (15 mg) solution and N-methyl-N-nitrosourea (10 mg) solution in 0.1 ml dimethylformamide were studied in 23 noninbred rats. The chemicals were injected into the antropyloric segment of the stomach. By months 11-15, specific changes in the glandular epithelium had developed at that site in 20 rats: dysplasia--in 6, precancer--7, and adenocarcinoma in 7 animals. Also, there were papillomas (6), squamous cell carcinoma (3), precancer and sarcoma (4) in various segments of the organ.
In the experiments carried out on white male rats the effect of vinblastine on the development of malignant stomach tumours induced with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) has been studied. The combined administration of MNNG and vinblastine inhibits the experimental carcinogenesis at the stage of "intestinalization" and decreases the indicence of stomach adenocarcinomas by 3-fold. Pharmacological analysis using the application of apomorphine stereotypy showed the antagonism of MNNG and vinblastine at the level of central parts of the autonomic nervous system due to the inhibition of axoplasmic transport of catecholamines. These results confirm the earlier data on the essential role of catecholamines in the mechanisms of carcinogenic action of nitrosamines.
126 chemical compounds were tested in the Ames assay with bacterial Salmonella typhimurium of 8 various strains (mainly TA 98 & TA100). For metabolic activation liver S9 from arochlortreated rats was used. In the first group of substances tested (51 compounds with confirmed carcinogenicity for animals) 45 agents possessed mutagenicity and 6 gave false-negative response (1.2-dimethylhydrazine, urethane, DDT, chloroform, carbon tetrachloride, 1.4-dioxane). In group 2 (27 compounds which did not possess carcinogenic activity) 22 agents were correctly identified and the rest 5 gave false-positive response (acrolein, styrene-oxide, acridine-orange, 1-naphtylamine, dichlormethane). After summation of data obtained test sensitivity for both groups together made 88.2%, specificity--81.5%, and predictive value--90%. In group 3 (48 compounds, presented by chemical, pharmaceutical and food industries, in respect of which either there are insufficient data on their carcinogenicity, or they were tested for the first time), 8 appeared mutagenic (1-aminoanthraquinone, 2-aminoanthraquinone, 1-amino-4-chloranthraquinone, 2-amino-3-oxyanthraquinone, Rhodulin blau 5B, dinitrochlorbenzene, nitrosodiphenylamine and 2,3,5-trinitronaphthalene).
One-hundred and six chemical compounds were tested in Ames test with bacteria Salmonella typhimurium. Eight different strains (mainly, TA98 and TA100) were used. Liver S9 from Aroclor-treated rats was employed for metabolic activation. In group I comprising 51 compounds with sufficient evidence of carcinogenicity for animals, 45 were mutagenic while 6 (urethane, 1,2-dimethylhydrazine, DDT, chlorophorm, 1,4-dioxane and carbon tetrachloride) were not. In group 2 (27 noncarcinogenic compounds), 22 agents failed to exhibit mutagenicity whereas 5 (acrolein, styrene-oxide, acridine orange, I-naphthylamine and dichlormethane) revealed such activity. In groups 1 and 2, the sensitivity was 88.2, specificity--81.5 and predictive value--90%. In group 3 consisting of 28 agents used in chemical, pharmaceutical and food industries but not yet tested for mutagenicity and for the carcinogenicity of which no conclusive data are available, seven appeared to be mutagens (1-aminoanthraquinone, 2-aminoanthraquinone, 1-amino-4-chloranthraquinone, based blue, dinitrochlorbenzene, nitrosodiphenylamine and 2,3,5-trinitronaphthalene).