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Biomedical subjects

L Tomatis

Publications and source records attributed to L Tomatis.

At least 127 records · Page 7Linked to original sources
PubMed1977

[Blastomogenesis in mice due to postnatal effect of N-nitrosoethylurea and x-ray irradiation].

N-nitrosoethylurea (NEU) is found to show an intensive transplacental carcinogenic effect inducing in mice different neoplasms, mainly lung adenomas. Postnatal x-ray irradiation of control animals resulted in the occurrence of ovarian tumors in some female mice. Delivary and feeding of the progeny would lead to the development of mammary gland tumors in a number of control female animals. Postnatal exposure to x-rays of mice exposed to transplacental effect of NEU resulted in the increased incidence of lung neoplasms, mainly adenocarcinomas.

Adenocarcinoma↗
PubMed1977

[Effect of N-nitrosoethylurea dosage and postnatal x-ray irradiation on transplacental blastomogenesis in mice].

In transplacental exposure to nitrosoethylurea in a dose of 2 mg/Kg the frequency of occurrence of different neoplasms in mice would not change as compared with a dose of 20 mg/Kg. However, in a dose of 2 mg/Kg the time of lung tumor development was prolonged. Postnatal roentgen irradiation increased the incidence of lung adenomas and ovarian tumors in female mice, exposed in embryogenesis to NEU effect in a dose of 2 mg/Kg; male mice showed a somewhat delayed development of tumors. In animals, subjected to NEU effect transplacentally in a dose of 20 mg/Kg, postnatal roentgen irradiation resulted in the appearance of lung adenocarcinomas, tumors of other lacolizations being developed neither in female nor in male mice.

Adenoma↗
PubMed1977

[Tumors in BALB C mice after transplacental exposure to N-nitrosoethylurea in progenesis].

In the experiments with transplacental exposure of mice to N-nitrosoethyl urea (NEU) an enhanced carcinogenesis was noted not only in the first but also in the second generation. This effect in mice of the second generation was manifested in earlier development, as compared with control animals, of different neoplasms as well as in somewhat increased frequency of their detection. Postnatal exposure to NEU would enhance carcinogenesis in mice of both experimental and control groups, whereas no enhancement of carcinogenesis was observed in animals exposed to NEU in progenesis, compared with control mice. Postnatal x-ray irradiation also failed to produce enhanced carcinogenesis, compared with control animals i.e. those exposed to NEU in progenesis. While in female mice of the same group, contrary to the control, ovarian tumors under the effect of irradiation did not arise. It is suggested that there is a pathogenic connection between the inheritance of carcinogenic effect by oocytes and the loss by the ovary its capacity to produce neoplasms in response to irradiation.

Adenocarcinoma↗
PubMed1976

The IARC program on the evaluation of the carcinogenic risk of chemicals to man.

The International Agency for Research on Cancer has initiated a program to evaluate the carcinogenic risk of chemicals to man. This program is centered on the production of monographs on individual chemicals, consisting of data on use and production, carcinogenicity in experimental animals, epidemiological studies and case reports, and other biological data such as metabolism and mutagenicity, and ending with a balanced evaluation of all the data made by an international group of experts. Chemicals to be surveyed for the preparation of monographs have so far been selected among those for which some evidence or suspicion of carcinogenicity in experimental animals and/or man exists and for which human exposure is known to occur. Of the 196 compounds already evaluated, 17 have been found to be associated with cancer in man. Ninety-four compounds were definitely carcinogenic in experimental animals, and 41 were shown to have a limited carcinogenic effect in experimental animals. A number of the chemicals found to be carcinogenic in experimental animals are produced in very large quantities. The type of exposure to the 17 chemicals found carcinogenic to man was occupational for fourteen, medicinal for two, and dietary for one.

Animals↗
PubMed1976

Mutagenicity and metabolism of vinyl chloride and related compounds.

The various adverse biological effects of vinyl chloride appear to be dependent upon the metabolic conversion of this compound into chemically reactive metabolites. The metabolism of vinyl chloride in mammals and in man, including the formation of monochloroacetic acid and some identified sulfur conjugates is reviewed. Hepatic microsomal mixed function oxidases from rats, mice, and humans were equally effective in transforming vinyl chloride into alkylating agents in vitro. Two of the enzyme reaction products, i.e., chloroethylene oxide and 2-chloroacetaldehyde, showed potent genetic activity in microorganisms and Chinese hamster V79 cells. The role of liver microsomal enzymes in the generation of electrophilic mutagenic vinyl chloride metabolites is discussed.

Animals↗
PubMed1975

Production of epithelial and mesenchymal tumours with rat liver cells transformed in vitro.

Epithelial-like cells originating from the livers of 10-day and 8-week-old BD rats were established in culture. The cells were treated in vitro for 1 or 4 weeks with dimethylnitrosamine (DMN) or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Although some structural changes were observed in treated cells, it was not possible to score for morphological transformation in vitro. Newborn syngeneic rats were injected with 1.5-2 times 10(6) treated or 1.5-5 times 10(6) control cells at various times up to 38 weeks from the beginning of treatment with the carcinogen. Following the injection of DMN-treated cells, a total of 32 of the 42 injected rat developed tumours, of which 17 were epithelial, 10 carcinosarcomas and 5 fibrosarcomas. Following the injection of the MNNG-treated cells into 61 rats, a total of 30 tumours were observed, including 8 carcinomas, 9 carcinosarcomas and 13 fibroscarcomas. Tumours, mainly of the mesenchymal type, were also observed in rats inoculated with control cells but at a lower frequency. The observation observed in rats inoculated with control cells but at a lower frequency. The observation of mesenchymal tumours is attributed to the presence of a mixed population of epithelial and mesenchymal cells in the orginal culture.

Animals↗
PubMed1975

The occurrence of tumours in F1, F2 and F3 descendants of bd rats exposed to N-nitrosomethylurea during pregnancy.

N-nitrosomethylurea (NMU) was administered once IP at a dose of 20 mg/kg to BD female rats on the 18th day of pregnancy. The first generation descendants (F1) were mated to produce a second generation (F2), which were then mated to produce a third generation (F3). While F1 rats were exposed directly to NMU during intrauterine life, it can be reasonably excluded that F2 and F3 descendants were exposed to NMU or its metabolites. F2 and F3 rats received no other treatment and untreated rats served as controls. Kidney and nervous-tissue tumours were observed in F1 descendants and, with a lower incidence, in F2 descendants. In F3 rats, tumours of nervous tissue, but not of kidneys, were observed. These results confirm previous observations that exposure to a carcinogen during prenatal life results in an increased cancer risk which may persist for more than one generation.

Animals↗