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Biomedical subjects

K Christov

Publications and source records attributed to K Christov.

At least 55 records · Page 3Linked to original sources
PubMed1977

Cytochemical localization of peroxidase activity in normal, proliferating and neoplastic thyroid tissues of rats. An ultrastructural study.

In the control animals of thyroid peroxidase is localized within the membrane of rough endoplasmic reticulum, perinuclear cisternae, microvilli, lamellar structures of the GOLGI apparatus and dispersed through the cytoplasm small vesicles. 3 weeks treatment of the animals with MTU leads to disappearance of the peroxidase activity from the follicular cells. However, a prolongation of MTU administration until the 6th month and latter causes a reappearance of the peroxidase activity within the same structures of the proliferating cells as in the control animals. In the epithelial cells of follicular and papillary carcinomas the reaction product is observed predominantly within the membrane of the rough endoplasmic reticulum, perinuclear space and outher membrane of the microvilli. The changes in the inhibitory effect of MTU on the peroxidase activity during thyroid carcinogenesis are discussed.

Animals↗
PubMed1976

Transmission and scanning electron microscopy of experimentally induced thyroid tumors in rats.

Irradiation of the neck region of 10 days old Wistar rats with 300 rads X-rays and their subsequent treatment with MTU leads to the development of thyroid tumors. The ultrastructure of the thyroid tumors induced was studied by transmission (TEM) and scanning electron microscopy (SEM). In follicular carcinomas, cylindrical or high columnar cells with abundant microvilli, well-developed ergastoplasmic reticulum and a hypertrophied Golgi complex predominate. The cytoplasm of the tumor cells of papillary carcinomas was composed of large pleomorphic cisternae, irregular in shape mitochondria, dense bodies, phagolysosomes and lamellar or multivesicular structures. Scanning electron microscopy revealed in the control animals a regular pattern of thyroid follicles tied to each other by tissue bridges and covered by set of blood and lymph vessels. The relief of the follicular carcinomas was irregular indicating follicles different in size and shape. The internal surface of the neoplastic follicles was also irregular as result of deep invaginations and intrafollicular cell growth. The apical region of the normal and neoplastic thyroid follicular cells was covered with abundant microvilli protruding into the colloid.

Adenocarcinoma↗
PubMed1975

Thyroid cell proliferation in rats and induction of tumors by X-rays.

There are very few proliferating cells in the thyroid gland of normal adult rats, as measured by the labeling and mitotic index. One-tenth % 4-methyl-2-thiouracil in drinking water induced an exponential increase of thyroid weight after a lag phase of 2 days; the increase continued for 8 days and was followed by a plateau phase. The following sequence of events was found for the number of dividing follicular and stroma cells as well as for DNA synthesis: no significant changes during the 1st 2 days, a sharp increase between the 2nd and 8th days, a decrease between the 8th and 14th days, and an almost constant flow until the 24th day. Three-hundred rads of X-rays given to a nonproliferating thyroid gland induced tumor growth in 25% of the animals 18 months after irradiation. The same dose of irradiation, applied to a proliferating thyroid gland, increased the tumor incidence to 30% when administered in the lag phase, to 75% when administered at the peak of the proliferating phase, and to 62.5% when administered at the plateau phase. Subsequent treatment of irradiated animals with 4-methyl-2-thiouracil enhanced the number and the size of the thyroid tumors and lead to the occurrence of more carcinomas than appeared in animals treated with X-rays only or 4-methyl-2-thiouracil only.

Animals↗
PubMed1975

DNA measurements on cell nuclei of normal, proliferating and neoplastic thyroid tissues in rats.

Nuclear DNA content was measured in 3 normal, 9 hyperplastic and 16 neoplastic rat thyroid glands. Thyroid hyperplasia and tumor growth were induced after treatment of the animals with X-rays and methylthiouracil. In the control animals only diploid thyroid epithelial cells were observed. At the stages of diffuse and nodular thyroid hyperplasia, the total DNA content per nucleus indicated for a diploid chromosome number and only a few cells were hyperdiploid. In the thyroid adenomas and carcinomas a scattering of the diploid region and an increase in the number of hyperdiploid cells was found. Among the various types of thyroid tumors neither difference in the number of hyperdiploid cells, nor typical pattern of distribution of these cells in the histogram was found. The increased number of hyperdiploid cells in the hyperplastic and neoplastic thyroids suggest an increase in the proportion of the cells entering the cell cycle and does not indicate for appearance of a neoplastic stemline.

Adenocarcinoma↗