THE HISTOLOGICAL AND BIOCHEMICAL STUDY OF THE EFFECT OF PURE FLAX SEED LIGNIN ON THE MAMMARY GLAND IN FEMAL RABBITS

The mammary gland ultrastructure in various functional states is the object of our investigations. The material prepared for electron microscopic examination by the conventional chemical methods has several limitations, the most important are the protein denaturation processes and the loss of large amounts of chemical constituents from the cells. In relevance to this,one can't be sure about a degree the observed images are adequate to the realy ultrastructure of a living cell. To avoid the disadvantages of the chemical preparation methods,some autors worked out alternative physical methods based on tissue freezing / freeze-drying, freeze-substitution, freeze-eatching techniqs/; actually the technique of cryoultraraicrotomy,i,e.cutting ultrathin sections from deep frozen specimens is assented as a complete alternative method. According to the limitations of the routine plastic embbeding methods we were interested to analize the mammary gland ultrastructure during lactation by the cryoultramicrotomy method.

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The effect of bromocriptine on mammary-gland ultrastructure of hyperprolactinemic rats

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100111136 ◽

1984 ◽

Vol 42 ◽

pp. 204-205

Author(s):

I.C. Murray

Keyword(s):

Mammary Gland ◽

Dopamine Agonist ◽

Alveolar Epithelium ◽

Mammary Glands ◽

Female Rats ◽

Control Group ◽

Cell Hyperplasia ◽

Once Daily ◽

Long Evans

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.

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Ultrastructural Changes in the Mammary Epithelial Cell Population During Neoplastic Development Induced by A Chemical Carcinogen.

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100091238 ◽

1976 ◽

Vol 34 ◽

pp. 250-251 ◽

Cited By ~ 2

Author(s):

J. Russo ◽

W. Isenberg ◽

M. Ireland ◽

I.H. Russo

Keyword(s):

Mammary Gland ◽

Cell Population ◽

Virgin Female ◽

Histological Change ◽

Mammary Epithelial ◽

Female Rats ◽

Ultrastructural Changes ◽

Post Inoculation ◽

Chemical Carcinogen ◽

Sprague Dawley

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.

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Potentiation of bromotrichloromethane hepatotoxicity in male rats exposed to 10 ppm dietary chlordecone: Electron Microscopic and biochemical study

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100158972 ◽

1990 ◽

Vol 48 (3) ◽

pp. 284-285

Author(s):

O. M. Faroon ◽

R. W. Henry ◽

M. G. Soni ◽

H. M. Mehendale

Keyword(s):

Free Radical ◽

Biochemical Study ◽

Prior Exposure ◽

Male Rats ◽

Cellular Injury ◽

Low Doses ◽

Mixed Function Oxidase ◽

Electron Microscopic ◽

Potent Inducer ◽

Cellular Energy

Previous work has shown that mirex undergoes photolytic dechlorination to chlordecone (CD) (KeponeR) in the environment. Much work has shown that prior exposure to nontoxic levels of CD causes potentiation of hepatotoxicity and lethality of CCl4, BrCCl3 and other halomethane compounds. Potentiation of bromotrichloromethane hepatotoxicity has been associated with compounds that stimulate the activity of hepatic mixed-function oxidase (MFO). An increase in the metabolism of halomethane by the MFO to a free radical initiates peroxidative decomposition of membranal lipids ending in massive cellular injury. However, not all MFO inducers potentiate BrCCl3 hepatotoxicity. Potentiation by much larger doses of phenobarbital is minimal and th at by a more potent inducer of MFO, mirex, is negligible at low doses. We suggest that the CD and bromotrichloromethane interaction results in a depletion of cellular energy and thereby reducing the cellular ability to undergo mitosis.

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