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Biomedical subjects

V S Turusov

Publications and source records attributed to V S Turusov.

At least 37 records · Page 2Linked to original sources
PubMed1997

[The effect of prenatal diethylstilbestrol treatment on 1,2-dimethylhydrazine-induced carcinogenesis in C3HA female mice].

C3HA female mice received 0.1-0.3 mg/g body weight diethylstilbestrol (DES) on day 17 of gestation. Their descendants received a total of 20 injections of 1.2-dimethylhydrazine (DMH), subcutaneously, weekly, starting from month 2. Prenatal DES significantly inhibited the development of DMH-induced clitoral gland tumors, particularly, hemorrhagic ovarian cysts which were the frequent cause of death due to their rupture into the abdominal cavity. A significant decrease in cyst incidence resulted in higher survival in mice receiving combined therapy. The results were attributed to DES-induced hyperestrogenization which was confirmed by vaginal smears examination.

1,2-Dimethylhydrazine↗
PubMed1997

1,2-Dimethylhydrazine carcinogenesis in C3HA and CBA female mice prenatally treated with diethylstilbestrol.

C3HA and CBA female mice received a single intraperitoneal (i.p.) injection of 0.1 or 0.3 mg/kg body weight (b.w.) of diethylstilbestrol (DES) at day 17 of pregnancy. The descendants, starting from the age of 2-3 months, were receiving weekly subcutaneous (s.c.) injections of 1,2-dimethylhydrazine (DMH) (8 mg/kg b.w.), total 20 injections. The survival of C3HA mice treated with DMH together with prenatal DES was considerably better than in mice treated with DMH alone, this being due to the strong inhibiting effect of DES on the induction by DMH of the hemorrhagic ovarian lesions (78.4% in DMH alone vs. 53.3 and 43.7% in groups with DES plus DMH), which frequently were the cause of animal death. Prenatal DES also inhibited the induction by DMH of clitoral gland tumors: 51.4% in the group with DMH alone vs. 26.6 and 28.1% in two groups of DES plus DMH, respectively. DES treatment, at the above doses, did not influence significantly the DMH carcinogenesis in CBA mice. Prenatal DES given to CBA mice at the dose of 1 mg/kg b.w. significantly increased the incidence of DMH-induced uterine sarcomas (42.8% vs. 73.3% in the group with DMH alone and the group receiving DMH together with prenatal DES, respectively) and accelerated their growth. The effects of prenatal DES on DMH-induced carcinogenesis correlated with the degree of hyperestrogenization produced in both strains of mice by DES.

1,2-Dimethylhydrazine↗
PubMed1995

Sarcomatous lesions in CBA female mice treated with 1,2-dimethylhydrazine: independent primaries or metastases?

CBA female mice treated with 1,2-dimethylhydrazine (DMH) alone or in combination with oestradiol dipropionate (EP) or ascorbic acid (AA) developed, as expected, a high incidence of uterine sarcomas. In addition, sarcomatous lesions at unusual sites (mainly in the forestomach) were evident. The incidence of sarcomatous lesions at other sites was 53/220 in mice having uterine sarcomas and 0/186 in mice treated with DMH but without uterine sarcomas. The difference between the two groups was highly statistically significant (P < 0.001) and demonstrates non-coincidental association of the above sarcomatous lesions with uterine sarcomas. Uterine sarcomas which presented in association with lesions at other sites were of a larger size than those found in isolation, and the difference in weights in three out of four groups was statistically significant (P = 0.008, 0.035 and 0.011). Histologically, sarcomatous lesions were similar in structure to those of uterine sarcomas, i.e. were of a fibroblastic-histiocytic nature with admixture of giant cells. On the basis of the above data the sarcomatous lesions described appear to represent uterine sarcoma metastases rather than independent primary tumours. AA did not have any influence on carcinogenesis induced by DMH alone but inhibited the growth of uterine sarcomas (whether or not they were associated with other sarcomatous lesions) induced by DMH combined with oestradiol dipropionate.

1,2-Dimethylhydrazine↗
PubMed1995

Perinatal lung carcinogenesis in mice: in vivo and in vitro correlation.

Perinatal lung carcinogenesis in susceptible (A) and resistant (C57B1/6J) to lung carcinogenesis mice was studied in (1) experiment in vivo and (2) in organ cultures of embryonic lung exposed to carcinogens directly (in vitro) or transplacentally (in utero): females were treated with carcinogens at 17-19 days of pregnancy, killed 1-2 days after the treatment and embryonic lungs were explanted in organ cultures. Transplacental and direct (in vitro) treatment with urethane and benz(a)pyrene (BP) induced in the explants: (1) stimulation of epithelial and mesenchymal cell proliferation; (2) increase of viability and survival as compared to the non-treated explants (growth stimulating effect); (3) morphological lesions (hyperplasia and squamous-cell metaplasia of epithelium, adenomatous growth and adenoma-like structures). All the alterations developed in treated lung explants depended both on host factors and carcinogenic treatment (type of carcinogen, dose, method of exposure, and duration of cultivation).

Animals↗
PubMed1994

Estrogen modification of 1,2-dimethylhydrazine carcinogenesis in C3HA mice.

Considerable strain differences were reported in our previous studies in the induction by 1,2-dimethylhydrasine (DMH) of uterine sarcoma and hemorrhagic ovarian lesion (HOL) in mice: the incidence of the former was high and that of the latter was low in CBA mice while the reverse was observed in C3HA mice. The present study confirmed the above observation in that C3HA mice treated with DMH developed high incidence (59%) of HOL and no uterine sarcoma. Combined treatment of C3HA mice with DMH and estradiol dipropionate (EP) completely inhibited the induction of HOL and increased the incidence of uterine sarcomas from naught to 28%. EP significantly decreased (from 61 to 19%) the incidence of clitoral gland tumors and somewhat increased the frequency of liver epithelial tumors and colon tumors. It is suggested that the strain differences in the induction by DMH of uterine sarcoma and HOL may be due rather to differences in the strain hormonal status than to the differences in the susceptibility to carcinogen.

1,2-Dimethylhydrazine↗
PubMed1994

Infrequent transforming mutations in the transmembrane domain of the neu oncogene in spontaneous rat schwannomas.

Ethylnitrosourea (ENU) given transplacentally to rats induces schwannomas of the cranial, spinal, and peripheral nerves, with a high frequency of mutations in the neu proto-oncogene. To establish the requirement for such mutations in tumorigenesis of the Schwann cell, spontaneous schwannomas from BD-VI rats were evaluated for transforming mutations in the transmembrane domain of the protein encoded by the neu proto-oncogene. While all five schwannomas induced transplacentally with ENU were shown to contain T-->A transversions in base 2012 of neu by selective oligonucleotide hybridization and dideoxy sequencing of polymerase chain reaction-amplified products from paraffin sections, only one of nine spontaneous schwannomas from untreated rats had the same mutation. Examination of tumors for mutations in codon 12 of Ki-ras revealed normal alleles. Therefore, the high frequency of mutations in neu in ENU-induced tumors may be directly attributable to the carcinogen or to the period of development at which exposure occurred, and transforming mutations of the transmembrane domain of neu are not required for tumorigenesis of the Schwann cell.

Animals↗
PubMed1994

S-100 protein and glial fibrillary acidic protein (GFAP) in experimentally induced and spontaneous tumours of peripheral nerves in BDVI rats. Light microscopic and immunohistochemical study.

Twenty-five ethylnitrosourea (ENU) induced and 24 spontaneous tumours of peripheral nerves as well as 28 spontaneous mesenchymal tumours in BDVI rats were studied by light microscopy and immunohistochemically for the presence of S-100 protein (S-100). Early ENU-induced schwannomas*) representing the thickenings of nerves showed weak or negative S-100 immunoreactivity. S-100 positivity (both in the cytoplasm and nucleus) was observed in all large ENU-induced tumours found in animals dying or killed at advanced age. Immunostaining was present in both cystic and solid areas of schwannomas. S-100 positivity was found in 20 of 24 spontaneous schwannomas: 14 of 20 positive tumours contained cysts. Twenty-seven schwannomas (12 ENU-induced and 15 spontaneous) were studied for the presence of glial fibrillar acid protein (GFAP) and 13 were positive (7 had cystic areas). GFAP-positivity was relatively high in 4 tumours (3 ENU-induced and 1 spontaneous); these tumours also showed intense S-100 reactivity. Immunoreactivity for S-100 occurred more frequently and was much more intense than that for GFAP. The incidence of spontaneous peripheral nerve tumours in BDVI males reached 4%, cystic schwannomas being the most frequent type. All spontaneous mesenchymal tumours except lipoma (S-100 positive) were negative for S-100 protein and for GFAP.

Animals↗
PubMed1993

Uterine sarcomas in CBA mice induced by combined treatment with 1,2-dimethylhydrazine and estradiol dipropionate. Light and electron microscopy.

Three uterine sarcomas induced by combined treatment (1,2-dimethylhydrazine and estradiol dipropionate) in CBA mice were examined by light and electron microscopy. Histologically the tumours consisted either of loose areas with stellate cells or of solid cellular areas. These were formed of elongated cells of the fibroblastic type and rounded cells with clear nuclei and abundant cytoplasm without clearly discernible bodies. Ultrastructurally, undifferentiated mesenchymal cells and cells with the features of fibroblasts and myofibroblasts were distinguished. The tumours described bear resemblance to human endometrial stromal sarcomas and are interpreted as sarcomas originating from immature mesenchymal cells differentiating mainly in the direction of cells of the fibroblastic type. Certain similarities with fibrous histiocytomas are noted.

1,2-Dimethylhydrazine↗
PubMed1992

Occurrence of tumours in the descendants of CBA male mice prenatally treated with diethylstilbestrol.

There is well documented evidence both in humans and in experimental animals that exposure to diethylstilbestrol (DES) during pregnancy results in an increased incidence of tumours in the progeny. The increased cancer risk has been reported to persist in the second generation descendants of DES-exposed pregnant mice. In the present experiment, female mice of the CBA strain were treated at day 17 of pregnancy with 1 microgram/g body weight of DES. The descendants of DES-treated mothers, described as F1DES, were mated among each other or with untreated animals. The F1DES females were found to be sterile when mated with either F1DES or untreated males. F1DES males were successfully mated with untreated females. In the female offspring so obtained, but not in the male, a statistically significant increased incidence of tumours was observed, in particular of uterine sarcomas, and also of benign ovarian tumours and of lymphomas.

Animals↗