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V S Turusov

Publications and source records attributed to V S Turusov.

At least 91 records · Page 5Linked to original sources
PubMed1984

[Effect of dose fractionation on the carcinogenicity of chemical substances].

Interrelations between single and total doses of chemical carcinogens are considered. On the basis of the data published and the author's own works a conclusion is drawn on the single dose as a decisive factor determining the organotropism (cytotropism) of certain pluripotential carcinogens (DMNA, DENA, DMH). Fractionation of the dose enhances the effect of polycyclic aromatic hydrocarbons, probably decreases the effect of directly acting carcinogens. Tumours of different histogenesis may respond to the dose fractionation in a different way.

1,2-Dimethylhydrazine↗
PubMed1984

[Analysis of uterine sarcoma induced in mice in terms of the two-staged development of tumors].

The results of combined treatment of CBA female mice with 1,2-dimethylhydrazine (DMH) and estradiol dipropionate (EP) are discussed in terms of a two-stage carcinogenesis hypothesis. 20% of mice treated with DMH alone developed uterine sarcomas. EP given after the cessation of DMH-treatment increased sarcoma incidence as high as 60.6% (5 micrograms EP) or 66.7% (10 micrograms EP) and significantly decreased the time of the first tumour appearance. From the standpoint of the two-stage carcinogenesis it is considered possible for EP to influence the tumour-initiating stage.

1,2-Dimethylhydrazine↗
PubMed1983

[Role of exogenous and endogenous factors in the etiology of human tumors].

The factors of major importance in the development of human tumors: exogenous chemical carcinogens, endogenous carcinogens, hormones, radiation, immunity disorders, heredity, nutrition, harmful habits are analysed on the basis of epidemiological and experimental evidence. Close interaction of exogenous and endogenous factors in the process of tumor development is demonstrated. Occupational carcinogens affecting at high doses small human contingents are frequently the major etiological cause of tumor development. In the general population exposed to the effect of quite low doses of carcinogens the latter are probably only initiators of neoplastic process completed by specific and nonspecific stimulators of carcinogenesis (cocarcinogens, promoters). The mechanisms of action of modifying factors on carcinogenesis (the effect of carcinogens on endogenous synthesis and metabolism, their interaction with cell macromolecules, tumor growth) are discussed.

Air Pollutants, Occupational↗
PubMed1983

[Effect of testosterone propionate on the induction by 1,2-dimethylhydrazine of angiosarcomas of the renal capsule in castrated mice].

Administration of 1,2-dimethylhydrazine (DMH) produced 83% (15/18) of renal capsule angiosarcomas in CBA mice. Castration that preceded the DMH-treatment reduced tumor incidence to 7% (2/29). Simultaneous administration of DMH and testosterone propionate (TP) to castrated males restored the tumor frequency (100%, 24/24). Castrated males that received TP after the cessation of the DMH treatment developed tumors in 10% (3/31). Combined treatment of castrated females with DMH and TP resulted in the development of angiosarcomas in 92% animals (22/24). It is concluded that TP enhances the stage of sarcomogenesis initiation induced by DMH.

Animals↗
PubMed1983

[Influence of the rhythm and route of 1,2-dimethylhydrazine administration on its carcinogenic effect in mice].

Effects of route of administration (subcutaneous, intraperitoneal, by stomach tube and with drinking water) and dose fractionation on the carcinogenicity of 1,2-dimethylhydrazine (DMH) were studied in CBA and (C57B1/6j X CBA)F1 mice. Fractionation of DMH dose given subcutaneously exerted different effects on tumors at various sites: decrease of colon and anal tumor incidence, increase of vascular liver tumors and renal adenomas and no influence on hepatoma, lung adenoma and uterine sarcoma induction. When given with drinking water, DMH did not induce colon and anal tumors but produced high incidence of vascular neoplasms. No such effect was observed when DMH was administered weekly by stomach tube. Alteration of the organotropism of DMH given with drinking water is attributed by authors to the decrease of single DMH dose and not to peroral route of administration.

1,2-Dimethylhydrazine↗
PubMed1982

Strain differences in susceptibility of female mice to 1,2-dimethylhydrazine.

C3H, CBA, C57BL/6j, (CBA x C57BL/6j)F1, BALB/c, DBA/2, C3HA and AKR female mice were treated with 25 weekly s.c. injections of a solution of 1,2-dimethylhydrazine (DMH) in water at a dose level of 8 mg/kg body weight. BALB/c mice appeared to be most sensitive to the induction of epithelial colorectal (93.3%) and anal tumours by DMH. There was, however, a dissociation between the severity of the macroscopical tumour lesions in the colon of BALB/c mice and their relatively weak tendency to infiltrative growth. C3HA mice were more resistant to the induction of intestinal tumours (30.9%) but the tumours showed a deep invasion into the intestinal wall. There was no correlation between the strains and within a given strain between the development of colorectal and anal neoplasms. C3H and CBA mice strains developed a high incidence of uterine sarcomas (37.5 and 40.7%, respectively) which were not found at all in BALB/c, DBA/2 and C3HA mice and which appeared in C57BL/6j and AKR mice at low frequency (2.7 and 7.7%, respectively). C57BL/6j, BALB/c, DBA/2 and C3HA mice developed haemorrhagic lesions of the ovaries (35.1, 46.7, 62.9 and 85.7%, respectively). These lesions, which led to peritoneal haemorrhage, were one of the main causes of death in C3HA and DBA/2 strains. It seems that, with the exception of AKR mice, an inverse relationship exists between the occurrence of haemorrhagic ovarian lesions and development of uterine sarcomas in female mice treated with DMH.

1,2-Dimethylhydrazine↗
PubMed1982

[Morphogenesis of experimental cancer of the large intestine (according to the results of scanning electron and light microscopy)].

Colon tumors induced by 1.2-dimethylhydrazine in mice were studied by scanning electron microscopy followed by light microscopy. The following morphological types of tumors were demonstrated: adenomatous polyps (82%) with folded and smooth patterns of the surface structure, hyperplastic polyps (13.8%), endophytic carcinoma (3.7%), and few villous tumors. In the majority of the cases carcinoma developed due to malignisation of morphologically benign adenomatous and more rarely hyperplastic polyps. Endophytic carcinoma developed without benign precursors. Villous tumors had a high potential for malignisation. All these kinds of tumors arose in diffuse hyperplastic colon mucosa.

1,2-Dimethylhydrazine↗
PubMed1982

[Effect of castration and mouse strain on 1, 2-dimethylhydrazine induction of pararenal angiosarcomas and kidney adenomas].

Castration preceding the administration of 1, 2-dimethylhydrazine (DMH) to CBA male mice inhibits the induction of pararenal angiosarcomas (from 76% to naught) and renal adenomas (from 89 to 57%). Male mice of different strains treated with DMH developed the following incidences of pararenal angiosarcomas and renal adenomas: C3H - 35.5 and 13%, respectively, CBA - 97 and 78.8%,m (CBA X C57B1) F1-36.1 and 30%. C57B1-4.2 and 23.4%, BALB/c-13 and 43.4%, C3HA -7.1 and 14.3%. Pararenal angiosarcoma develops most likely from vascular bed of renal capsula. The mechanisms of androgen stimulation of renal adenoma and pararenal angiosarcoma induction are discussed.

1,2-Dimethylhydrazine↗
PubMed1981

Modifying effect of aging on chemical carcinogenesis. A review.

The age-associated elevation in tumor incidence is generally attributed to the age-related accumulation of a total effective dose of carcinogenic agents and/or time of exposure, or is regarded as a consequence of disturbances of the hormono-metabolic pattern and the decline in immunity vigor with increasing age. This review deals with the data available on the peculiarities of realization of the effect of different carcinogenic chemicals in various tissues of young mature and old animals. The results of the analysis of the literature data show that aging may involve either an increase or a decrease in the sensitivity of tissues and the whole organism to the action of carcinogenic chemicals or no changes at all. These differences are due to the specific characteristics of the age-associated dynamics of activity of drug-metabolizing enzymes and the proliferative activity of target tissue controlled by hormonal factors and chalones.

Aging↗
PubMed1981

[Effect of age on induction of intestinal tumors in mice by 1,2-dimethylhydrazine].

1,2-Dimethylhydrazine was administered subcutaneously in a dose of 8 mg/kg bw to 2-, 8- and 12-month-old female CBA mice for 25 weeks. The animals were serially killed 26-35 weeks after the beginning of treatment. The incidence of colon tumors in 2-month-old mice was always significantly lower (P less than 0.001) than in 8- or 12-month-old mice. The incidence of tumors with invasive growth in 12-month-old mice was significantly higher (P less than 0.05) than in 8-month-old mice. Mathematical evaluation allowed the conclusion about the 1.8-fold shortening of the colon tumor latency period in old mice as compared to the young mice.

1,2-Dimethylhydrazine↗
PubMed1980

[Experimental models of embryonic nephroblastomas (Wilms' tumor)].

Histological structure and histochemical characteristics of renal tumours induced in rats either by N-nitrosodimethylamine (DMNA) or N-nitrosoethylurea (NEU) are described. The rats treated with oral administration of DMNA developed 1 nephroblastoma and 176 mesenchymal tumours similar to mesoblastic nephroma. In rats receiving the transplacental treatment with NEU 24 mesenchymal tumours and 5 nephroblastomas corresponding to the epithelial variant of human Wilms' tumour occurred. Histologic and histochemical findings show that the mesenchymal neoplasms contain the epithelial component in the form of preexisting renal tubules. These tubules are similar to those of the normal kidney and strongly differ from the primitive tubular structures of embryonic rat kidneys and nephroblastomas.

Animals↗
PubMed1980

Nephroblastoma and renal mesenchymal tumor induced in rats by N-nitrosoethyl- and N-nitrosomethylurea.

Rats treated prenatally with N-nitrosoethylurea or with N-nitrosomethylurea developed nephroblastomas, renal mesenchymal tumors and epithelial tumors (adenomas and carcinomas) of the kidneys. 15 nephroblastomas and 59 mesenchymal tumors were examined histologically. Nephroblastomas were encapsulated growths composed of dark cells, forming primitive tubules similar to those seen in the rat embryonal kidney and in human Wilms' tumor. Mesenchymal renal tumors showed an infiltrative growth and consisted of fibroblast-like cells, smooth muscles and angiomatous areas with the engulfed pre-existing tubules. These growths are similar to the mesenchymal renal tumors induced in the rat by N-nitrosodimethylamine. Nephroblastoma and mesenchymal renal tumor are considered to be separated entities, the first corresponsing to the epithelial variant of human Wilms' tumor and the second to congenital mesoblastic nephroma.

Animals↗