Basal Lamina Formation in DMBA Induced Mammary Carcinoma

Author(s):  
I. Russo ◽  
J. Saby ◽  
J. Russo

It has been previously demonstrated that DMBA-induced rat mammary carcinoma originates in the terminal end bud (TEB) of the mammary gland by proliferation of intermediate type cells (1). The earliest lesion identified is the intraductal proliferation (IDP), which gives rise to intraductal carcinomas. These evolve to cribriform, papillary and comedo types (2). In the present work, we report the ultrastructural changes that take place in the IDP for the formation of a cribriform pattern.Fifty-five-day-old Sprague Dawley virgin female rats were inoculated intra- gastrically with 20 mg 7,12-dimethylbenz(a)anthracene (DMBA) in 1 ml sesame oil. Non-inoculated, age-matched females were used as controls. Mammary glands from both control and experimental rats were removed weekly from the time of inoculation until 86 days post-inoculation. The glands were fixed and processed for electron microscopy (2).The first change observed in IDP's was the widening of intercellular spaces and the secretion of an electron dense material into these spaces (Fig. 1).

Author(s):  
J. Russo ◽  
W. Isenberg ◽  
M. Ireland ◽  
I.H. Russo

The induction of rat mammary carcinoma by the chemical carcinogen DMBA is used as a model for the study of the human disease (1). We previously described the histochemical changes that occur in the mammary gland of DMBA treated animals before the earliest manifested histological change, the intraductal proliferation (IDP), was observed (2). In the present work, we demonstrate that a change in the stable cell population found in the resting mammary gland occurs after carcinogen administration.Fifty-five day old Sprague-Dawley virgin female rats were inoculated intragastrically with 20mg of 7,12-dimethylbenz(a)anthracene (DMBA) in 1ml sesame oil. Non-inoculated, age-matched females were used as controls. Mammary glands from control and inoculated rats were removed weekly from the time of inoculation until 60 days post-inoculation. For electron microscopy, the glands were immersed in Karnovsky's fixative, post-fixed in 1% OsO4, dehydrated, and embedded in an Epon-Araldite mixture. Thick (lμ) sections were stained with 1% toluidine blue and were used for selecting areas for ultrastructural study.


2001 ◽  
Vol 280 (3) ◽  
pp. H956-H961 ◽  
Author(s):  
Yunlong Zhang ◽  
Ken G. Stewart ◽  
Sandra T. Davidge

The role of estrogen in the maternal systemic cardiovascular adaptations during pregnancy is still controversial. Female Sprague-Dawley rats were implanted at day 14 of pregnancy with either a 50-mg tamoxifen pellet (estrogen receptor blocker, n = 10) or placebo pellet ( n = 10). Virgin female rats were a nonpregnant control ( n = 7). At days 20–22 of pregnancy, resistance-sized mesenteric arteries were mounted onto a dual-chamber arteriograph system. Pregnancy significantly blunted the pressor response to phenylephrine [measurement of the effective concentration that yielded 50% maximum response (EC50) values were 1.5 ± 0.22 vs. 0.69 ± 0.16 μM ( P < 0.05)] and enhanced vasodilation to ACh [EC50 = 1.13 ± 2.53 vs. 3.13 ± 6.04 nM ( P < 0.05)] compared with nonpregnant rats. However, tamoxifen treatment during pregnancy reversed these effects. Inhibition of nitric oxide (NO) synthase with N G-monomethyl-l-arginine (250 μM) shifted only the responses of the placebo-treated pregnant group to both phenylephrine and ACh. Arterial distensibility in the placebo-treated pregnant group was also significantly increased ( P < 0.05) compared with nonpregnant and tamoxifen-treated pregnant animals. In summary, endogenous estrogen during pregnancy increases NO-dependent modulation of vessel tone and arterial distensibility.


2004 ◽  
Vol 59 (5) ◽  
pp. 257-261 ◽  
Author(s):  
Alfredo Carlos S. D. Barros ◽  
Elisa Naomi K. Muranaka ◽  
Lincon Jo Mori ◽  
Christina Helena T. Pelizon ◽  
Kyoshi Iriya ◽  
...  

PURPOSE: To test an experimental model of chemical mammary carcinogenesis induction in rats. METHODS: Twenty young virgin Sprague-Dawley female rats, aged 47 days, received 20 mg of 7,12-dimethylbenz(a)anthracene (DMBA) intragastrically by gavage. Afterwards, at 8 and 13 weeks, their mammary glands were examined. At the end of the experiment, the animals were sacrificed, and the mammary tumors were measured and weighed. Tumor fragments were analyzed using light microscopy. RESULTS: Eight weeks after DMBA injection, 16 rats presented at least 1 breast tumor (80%). After 13 weeks, all of them (100%) developed breast carcinomas that were confirmed by histopathological analysis. CONCLUSION: This experimental animal model of chemical mammary induced carcinogenesis is feasible and can be used in further experiments on the role of tumorigenic biomodulator substances.


2020 ◽  
Vol 28 (4) ◽  
pp. 429-436
Author(s):  
Svetlana A. Anisimova ◽  
Janna A. Svirina ◽  
Denis A. Maksaev

Nowadays, hormonal imbalance is proven to be a factor that influences initiation of malignant and benign breast tumors. To study the aspects of participation of sex hormones in damage to organs and tissues, it may be necessary to model a common womens pathology fibrocystic disease of mammary glands characterized by the most pronounced effects of this pathogenetic factor, on experimental animals. Aim. To create a model of fibrocystic disease of mammary gland with the subsequent possibility of studying morphological manifestations of the disease in natural and drug-induced pathomorphism. Materials and Methods. The pathology was induced by intramuscular injection of 0.5 ml of 2% synestrol and 0.5 ml of 2.5% progesterone to virgin female rats on the 1st, 7th, 14th, 21st, 28th and 35th days of the experiment. For examination, histological preparations of inguinal mammary glands were made. The preparations were described and studied using morphometric analysis. Results. In the result of the experiment, pronounced macro- and microscopic alterations of mammary glands were found. Microscopic picture was similar to that observed in fibrocystic mastopathy in women. Almost all the morphometric parameters underwent reliable alterations in correspondence with the given pathology. Conclusion. A model of fibrocystic disease of mammary gland was obtained that may be used for further study of morphogenesis and methods of correction.


Author(s):  
I.H. Russo ◽  
M. Ireland ◽  
W. Isenberg ◽  
J. Russo

The mammary gland is composed of epithelial and myoepithelial cells. In the present work, we show that the epithelial component is composed of three types of cells differing in their ultrastructural profiles.Sprague-Dawley virgin female rats, 60 to 100 days old, were sacrificed during estrus. The mammary gland was fixed in Karnovsky's fluid (1), embedded in Epon-Araldite (2), thin-sectioned, stained with uranyl acetate and lead citrate, and examined in an Hitachi HU-11A or a Siemens Elmiskop 1A. To see whether ultrastructural differences correspond to size differences, the nuclear and cytoplasmic areas of 1000 cells were determined from photographs at 10,000X, using a compensating polar planimeter.The population of epithelial cells in the mammary gland is comprised of three different cell types (Fig. 1): a) light cells, b) dark cells, and c) intermediate cells.


1953 ◽  
Vol 31 (2) ◽  
pp. 95-98
Author(s):  
Jules Tuba ◽  
Herbert E. Rawlinson ◽  
M. Shirley Fraser ◽  
Irmgaard Jeske

Virgin female rats did not respond to dietary 4-acetylaminobiphenyl by the production of tumors in mammary glands. This is attributed to some anticarcinogenic factor(s) in the stock laboratory diet of Purina Fox Checkers, which are composed of natural foodstuffs. However, the carcinogen did stimulate gland development, and after eight months, hyperplastic nodules appeared in almost all the experimental animals but not in the controls. This indicates that suspected carcinogens may be having an effect on mammary tissue even though visible tumors may not be present.


1966 ◽  
Vol 34 (4) ◽  
pp. 491-496 ◽  
Author(s):  
D. Y. WANG ◽  
STRETTON YOUNG ◽  
R. D. BULBROOK

SUMMARY (1) The incorporation of [1,2-3H]testosterone in vivo into various tissues of virgin, pregnant, post-partum and tumour-bearing female rats was studied. (2) In virgin female rats the clearance of radioactivity from mesenteric fat, mammary gland, uterus, spleen, lung and blood was similar. This similarity in the rates of clearance of radioactivity for all the tissues examined was also found for the tissues of pregnant, post-partum, and tumour-bearing rats. (3) After the administration of [1,2-3H]testosterone different amounts of radioactivity were found in each of the tissues examined. In virgin rats the levels of incorporation were fat > uterus ≥ mammary gland > lung > blood ≥ spleen. This pattern was also obtained in post-partum and tumour-bearing animals; the tumours in the latter behaved in a similar way to normal mammary glands. In the pregnant rat, the foetus incorporated the least amount of radioactivity.


1960 ◽  
Vol 198 (5) ◽  
pp. 1103-1106 ◽  
Author(s):  
Charles S. Nicoll ◽  
P. K. Talwalker ◽  
Joseph Meites

Sixty mature, virgin female rats were divided into six groups of 10 each and injected subcutaneously for 10 days with 10 µg estradiol in 0.1 cc corn oil. For the following 5 days the groups were treated as follows: 1) controls, 0.1 cc saline injected subcutaneously once daily; 2) severe cold (0°C) 24 hr/day; 3) intense light and heat for 12 hr/day; 4) restraint, 12 hr/day; 5) starvation, no food or water for 5 days; 6) subcutaneous injection of 0.1 cc or 0.2 cc of 10% formaldehyde once daily. The mammary glands of the control rats regressed from a lobulo-alveolar system to a bare duct system during the period of saline injections. The stressed groups all showed variable degrees of lactation after treatment. It is concluded that nonspecific stresses can promote the secretion of prolactin and ACTH from the anterior pituitary in amounts adequate to induce lactation in estrogen-primed rats. The possible role of stresses in initiating lactation at parturition and under other circumstances is considered, and a common mechanism controlling the secretion of ACTH and prolactin is postulated.


Author(s):  
R.P. Apkarian ◽  
J.S. Sanfilippo

The synthetic androgen danazol, is an isoxazol derivative of ethisterone. It is utilized in the treatment of endometriosis, fibrocystic breast disease, and has a potential use as a contraceptive. A study was designed to evaluate the ultrastructural changes associated with danazol therapy in a rat model. The preliminary investigation of the distal segment of the rat uterine horn was undertaken as part of a larger study intended to elucidate the effects of danazol on the female reproductive tract.Cross-sections (2-3 mm in length) of the distal segment of the uterine horn from sixteen Sprague-Dawley rats were prepared for SEM. Ten rats in estrus served as controls and six danazol treated rats were noted to have alterations of the estrus cycle i.e. a lag in cycle phase or noncycling patterns. Specimens were fixed in 3% glutaraldehyde in 0.05M phosphate buffer containing CaCl2 at pH 7.0-7.4 and chilled to 4°C. After a brief wash in distilled water, specimens were passed through a graded series of ethanol, critical point dryed in CO2 from absolute ethanol, and coated with 6nm Au. Observations were made with an IS1-40 SEM operated at 15kV.


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