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Biomedical subjects

N A Chebotar'

Publications and source records attributed to N A Chebotar'.

At least 37 records · Page 2Linked to original sources

[Correlation of tetratogenic and antimitotic activity of a number of derivatives of 2,4-diaminopyrimidine].

The effect of 6 substances, analogues of the antimalarial drug chloridine, on the mitotic activity of liver cells in rat embryos and cells of corneal epithelium in adult rats has been studied. A definite correlation was established between the antimitotic activity and the chemical structure of the drugs under study, and namely the length of alkyl radical in the position 6 of pyrimidine ring. The full correlation was noted between the teratogenic and antimitoic activities of these drugs.

Abnormalities, Drug-Induced↗

[Increase in the frequency of spontaneous chromosome aberrations with age in rats].

675 oocytes from 1294 studied were found suitable for counting chromosomes and caryotyping. 86,8% of oocytes (586) had a normal chromosome number, while aneuploidy was observed in 12,7% of oocytes (86). Among them 72 (10,67%) were with hypoploidy, while only 14 (2,07%) were hyperploid with 22 chromosomes. Structural chromosome aberrations were found in three oocytes: two of them had chromosome fragments and one had a break in the long arm of the chromosome 1.

Aging↗

[Spontaneous chromosome aberrations in the oogenesis of laboratory rats].

Cytological preparations were made by Tarkovsky's method from 2335 rat oocytes obtained after an induced superodulation. The chromosomes could be counted exactly in 861 oocytes. In 797 oocytes (92.7%) euploidy (metaphase II with 21 chromosomes) and in 64 oocytes (7.5%) aneuploidy was found. 60 oocytes were hypoploid, but only 4 oocytes (0.4%) were hyperploid (with 22 chromosomes). Hypoploidy can often be due to the presence of artefacts. Probably the rate of spontaneous aneuploidy in rat oogenesis is about 0.8%, this being significantly lower than the rate of spontaneous aneuploidy in mice oogenesis.

Aneuploidy↗

[A comparative study of the transport dynamics of the peptide moiety of the milk ceruloplasmin molecule in the body of rats with embryonic and adult types of copper metabolism].

In chase experiments, we followed the distribution of [125I]-ceruloplasmin prepared from human breast milk orally administered to young rats. Experiments were conducted using six-day-old rat pups (the embryonic type of copper metabolism) or 35-day-old ones (the adult type of copper metabolism). Using the technique of rocket immunoelectrophoresis, we have demonstrated that in six-day-old rats [125I]-ceruloplasmin was transferred from the gastrointestinal tract to the bloodstream and could be detected there over a period of 4 h. In 35-day-old rats, milk ceruloplasmin was digested in the upper part of the intestinal tract. The dynamic aspects of the distribution of labeled milk ceruloplasmin in the body of six-day old rats over a period of 4 h point out that, under the conditions of embryonic copper metabolism, it can serve as a transporter of copper ions to extrahepatic organs. We discuss the role of milk ceruloplasmin in copper metabolism in mammals during the neonatal period.

Animals↗

[Characteristics of chemical structure of analogs of the antimalarial drug chloridine (pyrimethamine), detetermining their teratogenic properties].

On an example of substituted 2,4-diaminopyrimidines containing at the 6th position hydrogen, alkyl radicals with a varying length of chains, ramified isoalkyl radicals and aromatic nuclei it is shown that the teratogenous activity is inherent only in some agents, being related to the chemical structure and conformation of the molecules. Accordingly, the principles of elective toxicity lying at the root of current chemotherapy may be extended also to teratology. From this it follows that there exists as a matter of principle the possibility of a purposeful synthesis of new medical compounds that would be devoid of teratogenous activity, but were endowed with valuable curative properties.

Abnormalities, Drug-Induced↗

[The embryo-protective action of antifein derivatives in chloridin-induced teratogenesis].

We studied the effect of propyl- and ethylnorantifein on chloridine-induced abnormalities of extremities in rat embryos. Chloridine (50 and 25 mg/kg, given through the gastric tube) was administered to rats on day 14 of pregnancy, and its embryotoxic effect was estimated from the state of fetuses and implantation sites on day 20 of prenatal development. Propylnorantifein had fetoprotective properties both after intraperitoneal (10 mg/kg) and after intraamniotic (6 and 0.06 micrograms) administration. Ethylnorantifein under similar conditions does not change the action of chloridine, and it prevents the appearance of developmental abnormalities only at the concentration of 0.06 microgram/embryo. These data are discussed in connection with different effects of antifein derivatives on chromatin proteinkinase, which phosphorylates HMG nonhistone proteins.

Abnormalities, Drug-Induced↗

[The role of the yolk sac in copper metabolism during rat embryogenesis].

Using the immunoblotting method, the synthesis of two copper-transporting P1-type ATPases, ATP7A (a candidate for the product of the Menkes disease gene) and ATP7B (presumed product of the Wilson disease gene), in the yolk sac cells of rat embryos at days 11 and 20 of embryogenesis was demonstrated. Concomitantly, yolk sac cells produce ceruloplasmin, a soluble copper-transporting glycoprotein, a proportion of which in secreted proteins progressively diminishes, attaining 5.2% at day 11 and 3.1% at day 20 of development. At different stages of embryogenesis, yolk sac cells synthesize two molecular forms of [14]C-ceruloplasmin, one of which is secreted towards the embryo, whereas the other, towards the decidual membrane. Two forms of ceruloplasmin secreted in polar directions differ in the rate of secretion. The role of the yolk sac as a key organ controlling the delivery and secretion of copper in the embryo during the postimplantation period is discussed.

Adenosine Triphosphatases↗