Biomedical subjects

I A Khodosova

Publications and source records attributed to I A Khodosova.

At least 19 recordsLinked to original sources

PubMed1989

[The role of protein kinase C in tumor growth].

A review of recent papers dealing with the role of protein kinase C (PK C) in regulation of normal and tumour cell proliferation contains the data on the interaction of PK C with the tumour promoters and oncoproteins as well as the data which characterize changes of the PK C activity in tumour cells and during carcinogenesis. Probable mechanisms of the PK C influence on the functioning of the growth factors receptors are discussed. It is proposed that one of the PK C functions which is substantial for induction of the mitogenic signal is the polyamine synthesis stimulation. Participation of PK C in the tumour promotion may play a key role in multistep processes of the carcinogenesis.

Animals↗

PubMed1988

[Comparative study of protein kinase C in the normal rat liver and in Zajdela's hepatoma. I. Electrophoretic analysis].

The heterogeneity of protein kinase C (PKC) derived from rat liver and the Zajdela hepatoma was studied by sodium dodecyl sulfate electrophoresis in polyacrylamide gel. Proteins with PKC-activity of molecular weight equal to 67,000 Da and 80,000 Da and an active fragment of 50,000 Da were detected in samples from the normal rat liver. The samples from the Zajdela hepatoma contained PKC with molecular weight equal to 67,000 Da and the active fragment of 50,000 Da. PKC with molecular weight of 80,000 Da was absent.

Animals↗

PubMed1986

[Morphometric and immunomorphological characteristics of the liver cells of rats after a single DAB exposure].

The paper deals with characterization of hepatocytes isolated by sodium perchlorate from livers of rats both intact and given a single intraperitoneal injection of a carcinogen--4-dimethylaminoazobenzene (DAB). 7 days after DAB injection a decrease in the number of large hepatocytes (600-900 microns2) and the appearance of "small" hepatocytes (64-128 microns2) were observed; an increased accumulation of glycogen was shown in certain hepatocytes. By the 30th day the picture was almost normal. Following the injections of phenobarbital (6 times) the population of "small" hepatocytes and abnormal distribution of glycogen persisted for 45 days after the carcinogen injection. By the indirect immunofluorescence reaction hetero-organic antigens of kidney nature were found in the outer membranes of hepatocytes on the 1st to 12th days after the DAB injection. The synthesis of these proteins is characteristic of rat hepatocellular tumours.

Animals↗

PubMed1986

[Detection of cells resistant to the cytotoxic action of CCl4 in rat hepatocyte populations following a single exposure to diethylnitrosamine and subsequent injections of phenobarbital].

A single intraperitoneal injection of hepatocarcinogen diethylnitrosamine induced emergence of a new subpopulation of "small" hepatocytes (64-128 mkm2), disappearing by the 30th day after carcinogen injection. But 5 injections of the tumor promotor phenobarbital 7 days after carcinogen treatment prolonged the existence of such "small" hepatocytes up to 3 months. The quantitative cytochemical measurement of succinic dehydrogenase activity (respiratory enzyme of mitochondria) showed these cells to be resistant to cytotoxic action of CCl4. These data are consistent with the earlier reported results obtained in analogous experiments with 4-dimethylaminoazobenzene and phenobarbital.

Animals↗

PubMed1985

[Role of enzymatic DNA methylation in cell differentiation and carcinogenesis].

The enzymatic methylation of specific cytosine residues in DNA plays a part in controlling gene expression. Low methylation levels may be a necessary condition for gene expression. The chemical carcinogens exert their effect on the enzymatic methylation of mammalian DNA and can cause hypomethylation. Demethylated sites do not become remethylated in the subsequent cell cycles. The consequence of DNA hypomethylation may be both stimulation of cell differentiation and initiation of carcinogenesis.

Animals↗

PubMed1985

[Detection of cells resistant to the cytotoxic action of CCl4 in the hepatocyte populations of rats following a single exposure to 4-dimethylaminoazobenzene combined with subsequent injections of the tumor promoter phenobarbital].

It is found that hepatic cells of intact rats measuring 129-192 mcm2 are resistant to cytotoxical action of carbon tetrachloride (CCl4). After a single interperitoneal injection of the carcinogen 4-dimethylaminoazobenzene, small hepatocytes (64-128 mcm2) appear to be maintained for one month following five injections of phenobarbital. These small hepatocytes are resistant to cytotoxical action of CCl4. The resistance was studied using a cytochemical test on succinate dehydrogenase. A direct dependence exists between the cell size and the sensitivity to CCl4 among large sized hepatocytes.

Animals↗

PubMed1984

[Glycogen distribution in rat hepatocyte populations after a single exposure to 4-dimethylaminoazobenzine and subsequent injections of phenobarbital].

7 day after a single interperitoneal injection of carcinogen 4-dimethylaminoazobenzen (DAB), a little number of cells with high glycogen contents was found in parallel with a decreased glycogen content in most isolated hepatocytes. 1.5 months after DAB injection, the normal distribution of glycogen content was seen restored in hepatocytes. The treatment of rats with phenobarbital (6 PhB injections 7 days after DAB application) blocked the restoration of the normal glycogen distribution. 2 months after the last PhB injection (3 months after DAB injection) an increased glycogen content was found in the smallest hepatocytes.

Animals↗

PubMed1983

[Morphometric and cytochemical characteristics of the hepatocytes isolated from the liver of rats after a single exposure to 4,dimethylaminoazobenzene].

Hepatocytes have been characterized that were isolated with sodium perchlorate from the livers of rats both intact and given a single injection of a carcinogen--4-dimethylaminoazobenzene. A decreased number of big hepatocytes (600-900 mkm2) and the appearance of small hepatocytes (75-120 mkm2) were observed 7 days after the carcinogen injection. An excessive accumulation of glycogen was shown in certain hepatocytes. By the 30th day the picture was nearly normal.

Animals↗

PubMed1980

[Localization of embryonic aldolase isoenzyme in rat liver cells after a single injection of the carcinogen, 4-dimethylaminoazobenzene, and its noncarcinogenic analog].

The localization of a fetal isoenzyme of aldolase (A) in rat liver cells early after a single injection of carcinogen 4-dimethylaminoazobenzene and its noncarcinogenic analog 4-diethylaminoazobenzene has been studied using the immunofluorescent method. Aldolase A was found in the cytoplasm of oval and "transition" cells. These cells appeared in rat liver as a result of treatment with carcinogen and its analog. In mature hepatocytes aldolase A was not found either in intact rat liver, after the treatment with carcinogen or its analog.

Animals↗

PubMed1978

[Effect of single exposure to the carcinogen 4-dimethylaminoazobenzene on several properties of rat liver mitochondria].

The hepatospecific carcinogen 4-dimethylaminoazobenzene (DAB), applied as a single interperitoneal injection, induced no changes in the activity of mitochondrial and cytoplasmic malate-dehydrogenase in the rat liver. The same carcinogen and non-carcinogenic isomer 4-diethylaminoazobenzene brought about decreased activity of cytochromeoxidase in isolated rat liver mitochondria. During 18 days after a single interperitoneal injection of DAB the swelling-contraction properties of isolated liver mitochondria were seen altered in the presence of succinate and ATP whereas DAB exerted no influence on mitochondria from the kidney, which organ is not a target-tissue for carcinogenic action.

Animals↗

PubMed1977