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Biomedical subjects

I A Ostapenko

Publications and source records attributed to I A Ostapenko.

At least 19 recordsLinked to original sources
PubMed1989

The influence of the lipid bilayer phase state on the p-aminohippurate (PAH) transport and the activity of the alkaline phosphatase in brush-border membrane vesicles from normal and mutant rats.

The kinetic parameters of p-aminohippurate transport and activity of the alkaline phosphatase were studied using brush-border membrane vesicles isolated from the kidney cortex of normal and mutant (strain of Campbell) rats. p-Aminohippurate (PAH) transport of both normal and mutant animals was carried out by the mechanism of facilitated diffusion. The apparent Michaelis constant at 36 degrees C was equal to 7 mM, the maximal rate of PAH transport was 15 nmol/min per mg protein and the constant of inhibition by probenecid was 0.5 mM for normal rats and, respectively, 29 mM, 62 nmol/min per mg protein and 1.4 mM for mutant rats. The Arrhenius plot for the PAH transport and activity of the alkaline phosphatase showed the breakpoints at 28-30 degrees C for normal rats and at 36-38 degrees C for the Campbell strain rats. The thermotropic phase transitions detected by the EPR method with 5-doxylstearate as a probe were recorded at 21-30 degrees C and 30-35 degrees C for normal and mutant rats, respectively. Therefore, characteristic features of the PAH carrier and alkaline phosphatase activity in normal and Campbell strain rats are determined by the difference in the phase state of their membrane lipid bilayers. We suppose that mutation in the Campbell strain gives rise to a membrane pleiotropic effect which enables us to understand the mechanism of genetic control of the lipid structure and membrane fluidity.

Alkaline Phosphatase↗
PubMed1989

[Age-related features of the state of plasma lipoproteins in rats with hereditary retinal degeneration].

The content of lipids and lipoproteins was determined in the blood plasma of Campbell rats with inherited retina degeneration and Wistar rats used as control. It was shown that in the 30-day old Campbell rats the content of cholesterol in high density lipoproteins sufficiently exceeded that of control. When the distribution of lipoproteins particles in the density gradient was studied after ultracentrifugation, some "anomalous" particles were revealed in the 30-45 day old rats with inherited retina degeneration, which with respect to the flotation rate occupy intermediate position between the low and high density lipoproteins. The obtained data show that the development of inherited retina degeneration in rats involves a disturbance, of the lipoprotein spectrum of blood plasma.

Age Factors↗
PubMed1983

[The system of active transport of organic acids in the proximal tubules of rats with hereditary retinal degeneration (Campbell strain)].

Active transport of organic acids (ATOA) in proximal renal tubules of Campbell, Wistar and random-bred rats was studied by contact microfluorometry with anion fluorescein as a marker. Beginning with the 60th day of life this transport in Campbell rats was characterized by a lower equilibrium uptake of fluorescein by the tubules, by altered sensitivity to AMP and adenosine, and by no response to unilateral nephrectomy. It is assumed that ATOA in Campbell rats plays a certain role in the pathogenesis of retinitis pigmentosa.

Adenosine↗
PubMed1982

[Changes in the blood uric acid levels in patients with retinitis pigmentosa and in rats with hereditary retinal degeneration].

The content of uric acid was measured in the blood of patients suffering from retinitis pigmentosa, as well as in the blood, retina, brain, liver and urine of rats with inherited retinal degeneration in the course of postnatal development. It was found that in the patients with retinitis pigmentosa, the concentration of uric acid in the blood serum was 50% higher as compared to normals. On the 8th day of life the content of uric acid in the blood of the sick rats was equal to 150% as compared to the normal animals. This difference persisted during the subsequent postnatal life. In the rats with inherited retinal degeneration, the content of this purine in the retina, brain and liver was approximately the same as that seen in the normal animals in all the studied periods of life. Meanwhile statistically significant changes in the uric acid content in the sick animals' urine appeared at an age of 1.5-2 months. It is believed that the identical line of changes in the uric acid content in the blood of the sick persons and rats points to similarity of the experimental disease of the animals to the disease in humans.

Animals↗
PubMed1981

[Biochemical disorders in hereditary retinal degeneration: changes in cyclic nucleotide phosphodiesterase activity and rhodopsin concentration in the retinas of Campbell rats].

A correlation was noted between alterations in activity of cGMP phosphodiesterase /PDE/ and in content of rhodopsin /R/ from rats of the Campbell strain with hereditary retina degeneration as well as from control animals of the Wistar strain. Dynamics of alterations in the PDE/R ratio was similar to both in impaired and healthy animals within the first 35 days of life. These data suggest that the decrease of the PDE activity in retina of the Campbell rats occurred due to destruction and removing of outer layer of photoreceptor cell segments, i.e. it was of the secondary nature rather than of primary pathogenetic importance. After 1.5 month of the life retina aqueous extract activated PDE of cyclic nucleotides in impaired rats, but did not cause inhibition as it was observed in healthy animals. The phenomenon appears to be due to various localization of PDE inhibitors and activators in retina as well as to destruction of the layer of rod outer segments in retina of impaired rats.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1981

[Early changes in retinal 5'-nucleotidase activity in hereditary retinal degeneration].

Activity of soluble cGMP phosphodiesterase (PDE) and of two membrane enzymes, 5'-nucleotidase and Na,K-ATPase, was studied in the developing retina of rats with inherited retinal degeneration. It was found that by day 10 of life, the content of 5'-nucleotidase in the afflicted rats was significantly reduced as compared with controls. This difference was unchanged throughout the subsequent animals' life. Na,K-ATPase activity in the afflicted and normal animals was the same. Within the first 45 days of life, PDE calculated with respect to the rhodopsin content was not different as regards both the afflicted and normal rats. When calculated with respect to protein, the changes in PDE corresponded with the reported data. The data obtained allowed a suggestion to be made that changes in 5'-nucleotidase in inherited retinal degeneration are disease-specific. They are accounted for by changes in the enzymes of nonphotoreceptor retinal membranes. The changes in PDE may be regarded as secondary, correlating with variation in the number of the photoreceptor membranes.

5'-Nucleotidase↗
PubMed1980

[Proteins of the retina and its pigmented epithelium in hereditary retinal degeneration].

Water-soluble and membranous proteins of the retina and pigment epithelium were studied by electrophoresis in polyacrylamide gel in Campbell albino rats with inherited retinal dystrophy and in Wistar rats that served as control. It was shown that early changes in abnormal animals were characteristic of retinal proteins. The proteins affected in the first turn proved to be other than cyclic nucleotide phosphodiesterase or opsin. The changes in pigment epithelium were recorded to take place much later.

Animals↗
PubMed1978

[Rhodopsin regeneration: role of interaction between the photoreceptors and pigment epithelium cells].

Regeneration of rhodopsin has been studied in the eyecup, isolated retina and retinal homogenate of frog Rana temporaia as well as in the eyecup and isolated retina of fish-flounder Limanda aspera (Pallas). Rhodopsin has been found to regenerate only in the eyecup of frog, while isorhodopsin appeared to be the final product in the frog retinal homogenate. Decrease in rhodopsin regeneration level has been resulted from addition of inhibitors--theophyllin (2.10-2 M), papaverine (10-4--10-3 M) and strophantin (2.10-4 M) To the eyecup preparations (60, 20, 23%, consequently). A conclusion is made that structural connection between pigment epithelium cells and photoreceptors is necessary to provide regeneration of native rhodopsin.

Animals↗
PubMed1978

[Resynthesis of rhodopsin in rats with hereditary retinal dystrophy].

Resynthesis of rhodopsin both in the retina and the eye cup was studied in albino rats (Campbell line) and in rats with pigmented eyes (Hunter line) with hereditary retinal dystrophy. Wistar rats and those of MSU line were used as controls, respectively. The rate of resynthesis of rhodopsin after its bleaching in the retina of dystrophic animals appeared to be much less than that in the normal ones, and decreased during the disease. When clear morphological changes were seen, only 50% of the previously bleached pigment was capable of regeneration during 2 hours of dark adaptation, the time being quite adequate for complete regeneration of rhodopsin in normal animals. It was found that in Campbell and Hunter rats breakdown and resynthesis of rhodopsin takes place not only in the retina but also in the layer of outer segment debris of photoreceptors located between the pigment epithelium cells and the retina.

Animals↗
PubMed1977

[Changes in the electroretinogram and concentration or rhodopsin in the Hunter strain of rats during development of hereditary retinal degeneration].

Electroretinographic changes as well as rhodopsin content in the isolated retina and the eye cup in Hunter rats were studied during inherited retinal degeneration. The concentration of rhodopsin in the eye cup increases for the first 45 days after birth and then decreases slowly; the visual pigment concentration in the retina reaches its maximum by the 25th day and drops abruptly after the 35th day. The amplitude of the electroretinographic b-wave evoked by near-threshold and saturating stimuli decreases evenly till 35th day. After this day the threshold drastically increases and a-wave disappears. Thus, the 35th day is crucial in the degeneration process. The possible role played by abnormal rhodopsin metabolism in the changes observed is discussed.

Animals↗
PubMed1975

[Localization of several rhodopsin regeneration enzymes in retinal rods].

The distribution of NAD kinase and glucose-6-phosphate dehydrogenase within membranes of both outer and inner retina rod segments was studied by the sucrose gradient centrifugation of crude outer segment preparations. Rhodopsin and retinoldehydrogenase served as markers for outer segment membranes, whereas succinate dehydrogenase was a marker for inner ones. It is shown that NAD kinase and glucose-6-phosphate dehydrogenase are localized within inner segment membranes of the photoreception cell and that the activity of these enzymes in the crude preparations is due to contamination of the inner segments.

Alcohol Oxidoreductases↗