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Biomedical subjects

I Ia Kon'

Publications and source records attributed to I Ia Kon'.

At least 37 records · Page 2Linked to original sources
PubMed1996

[Selenium status of healthy children under 1 year of age dependent on the type of feeding].

Selenium status was studied in 70 healthy children under 1 year of age being on breastfeeding or bottle feeding. Selenium status was determined by analysis of selenium in baby's hairs and nails. Selenium was also analyzed in breast milk in course of the lactation and in breast milk substitutes. The selenium status was better in breastfed children than in bottle fed ones. The most high level of selenium was found in breast milk in first month of lactation. Selenium status of bottle fed children was depended on selenium level in milk substitutes. It is necessary further investigations on selenium status of children under 1 year age to elaborate and suggest the standard level of selenium contents in milk substitutes.

Age Factors↗
PubMed1996

[Connection between the level of transferrin in blood plasma and the level of malondialdehyde in mouse liver].

To study possible correlation between plasma transferrin content and level of 2-thiobarbituric acid-reactive substances (malonic dialdehyde (MDA)) in the liver of mice, these parameters were assayed during brombenzol-induced lipid peroxidation and when this process was inhibited by zinc-metallothionein (zinc-MT). In 24 h after brombenzol injection (0.5-2 g/kg intraperitoneally), mice had decreased blood transferrin concentration and increased MDA level in the liver. On the contrary, in 24 h after the zinc-MT injection (1-4 mg/kg intraperitoneally), blood transferrin concentration was 2-3-fold increased and liver MDA content was 2-3-fold decreased. The effects of zinc-MT were observed even in brombenzol-injected animals. Zinc-MT injection increased total transferrin content in the blood and decreased glycosylation of this glycoprotein. Changes in blood transferrin content negatively correlates (r = -0.75) with changes in liver MDA. The data confirm that plasma transferrin can participate in regulation of tissue lipid peroxidation.

Animals↗
PubMed1996

[Effects of vitamin D on protein turnover in children with renal osteopathy].

Amino acid analysis and investigation of nitrogen balance were done in 2 groups of the patients with renal failure and osteodystrophy on the diet and vitamin D treatment. The results of the investigations confirm vitamin D influence on free amino acid turnover. We observed significant elevations of plasma amino acids in patients treated with the diet and vitamin D in comparison with the patients without vitamin D supplementation. Vitamin D didn't influence on the retention, urinary and fecal excretion of endogenous nitrogen in patients with renal failure

Adolescent↗
PubMed1990

[Vitamin A and microsomal membranes: the effect of retinol deficiency on lipid microviscosity and phospholipid turnover in rat liver microsomes].

Studies with the use of the fluorescent probe pyrene revealed that vitamin A deficiency in maturing male rats results in the increased microviscosity of liver lipids. This effect seems to be due to changes in the lipid composition of microsomal membranes (increased cholesterol/phospholipid ratio and lowered polyunsaturated fatty acid content) as well as to the low level of retinol. Analysis of microsomal phospholipids labeled with [3H]palmitate and [14C]glycerol revealed that vitamin A deficiency accelerates the turnover of the glycerol skeleton but sharply decelerates that of fatty acid residues. It is concluded that the observed effect of retinol on the structural and functional properties of biological membranes is due to its ability to control the microviscosity and turnover of membrane lipids.

Animals↗
PubMed1987

[Effect of vitamin A on the adhesive interaction of cells in epithelial tissue].

Both the increasing and decreasing contents of vitamin A in rats induced a lowering of cell adhesion in the skin multilayer epithelium, and that of their packing density. However, the same stimulus did not alter cell adhesion in the small intestinal monolayer epithelium. The data obtained show that vitamin A may serve as a factor modulating intercellular adhesive interactions with tissue specificity.

Animals↗
PubMed1987

[Liver cytochrome P-450 induction in rats by drug preparations and the body vitamin A allowance].

The content of P-450 cytochrome and vitamin A was determined in the liver of mature male rats who received for a month daily parenteral administrations of phenobarbital solutions (Pb; 40 mg/kg), rheopyrine (a mixture of equal aliquots of amidopyrine and butadione; 200 mg/kg), amidopyrine (100 mg/kg) or water (control). The animals were kept on a semisynthetic diet, receiving once, every week 400 IU of retinol-palmitate per rat. Pb administration markedly (more than threefold) increased P-450 cytochrome content in the liver. Rheopyrine and amidopyrine also elevated its level, but to a lesser extent than Pb. Pb and rheopyrine also depressed vitamin A levels in the liver and caused either a trend towards its decrease (Pb) or a significant decrease (rheopyrine) of its overall content in the liver. The effect of amidopyrine on the concentration and storage of retinol in the liver was less pronounced. The data obtained suggest that the drugs inducing P-450 cytochrome are capable of disturbing vitamin A content in the body.

Aminopyrine↗
PubMed1987

[Effect of vitamin A deficiency on the macromolecular permeability of small intestine mucosa in the adult rat].

Adult rats with experimental vitamin A deficiency and control animals were intraperitoneally injected with chicken ovalbumin (OA) solution and the entrance of native OA into the blood was assessed 3 hours later by competitive radioimmunoassay. The OA amounts circulating in the blood of control animals averaged (0.39 +/- 0.06) X 10(-4)% of the consumed dose, while in the experimental group it averaged (1.33 +/- 0.42) 10(-4)%. Electron microscopy, using colloid lanthanum hydroxide, has shown vitamin A deficiency to give rise to an abrupt reduction in glycocalix layer, as compared to the control, without increasing erythrocyte membrane permeability for tracer particles. It is concluded that vitamin A deficiency leads to a considerable damage of small intestinal permeability for protein macromolecules.

Animals↗
PubMed1986

[Vitamin A and lipid peroxidation: effect of retinol deficiency].

The effect of alimentary vitamin A deficiency on some parameters of lipid peroxidation (LPO) in young rats was studied. It was found that under vitamin A deficiency the content of diene conjugates in liver homogenates and microsomes diminishes, whereas that of malonic aldehyde in small intestinal mucosa, liver and testis homogenates is unaffected. However, the malonic aldehyde production in liver homogenates and microsomes decreases after 60 min incubation at 37 degrees C without addition of prooxidants. At the same time, enzymatic NADPH-dependent and nonenzymatic ascorbate-dependent LPO in liver microsomes of vitamin A-deficient rats does not change significantly. The decrease of LPO intensity in vitamin A-deficient animals may be due to the reduced content in liver microsomes of the main LPO substrates, i.e., arachidonic and linoleic acids, as well as to the decrease of cytochrome P-450 level in rat liver.

Animals↗
PubMed1985

[Action of retinoic acid on lipid peroxidation in rat liver microsomes in vitro].

It has been shown in experiments in vitro that preincubation of rat liver microsomes with an ethanol solution of all-trans-retinoic acid in the final concentration 7.0 X 10(-5) M results in a decrease of both NADPN-dependent and spontaneous lipid peroxidation (to 53 and 70% of control, respectively) but did not influence ascorbate-dependent lipid peroxidation. Retinol at the same concentration induces more pronounced inhibition of all types of microsomal lipid peroxidation. The rate of NADPN-dependent lipid peroxidation decreases linearly as the retinoic acid concentration in the incubation medium is raised, whereas the rate of ascorbate-dependent lipid peroxidation drastically lessens only after the retinoic acid concentration in the medium is increased to 1.4 X 10(-4) M. The data obtained provide evidence in favour of the concepts of a possible role of vitamin A in LPO regulation in the body and point to the necessity of taking into consideration the antioxidant properties of retinol and retinoic acid while analysing their pharmacological action.

Animals↗
PubMed1984

[Effect of hypervitaminosis A on the rat small intestine epithelium].

The excess of vitamin A, orally administered to young albino male rats (during 8 days, per os, in total dose of 400000 ME per rat) induced a considerable decrease in the number of mitoses in the small intestine crypt glands of both its distal and proximal parts. This treatment also led to changes in the intestine mucosa morphology (decrease of the crypt depth and number of epithelial cells, lining crypts) and to the loss of the RNA content gradient along the villus. It is concluded, that in rats the small intestine mucosa is an organ-target for vitamin A, and its excess induce the inhibition of enterocyte proliferation and impairment of their differentiation.

Animals↗
PubMed1984

[Effect of vitamin A excess and T-2 toxin on the enzyme system activities of the second phase of xenobiotic metabolism in the rat liver].

Oral administration of retinyl palmitate to young Wistar rats during 7 days (70,000 IU of vitamin A per 100 g of body weight daily) caused a decrease in the liver UDP-glucuronosyl transferase and glutathione transferase activities and a significant decrease in the liver glutathione-SH content. A single administration of T-2 toxin (3 mg per kg of body weight) to rats after the treatment with high doses of vitamin A was accompanied by an increase in T-2 toxicity. The rat mortality was doubled and the decrease in UDP-glucuronosyl transferase and glutathione transferase activities was more distinct as compared with the rats treated with T-2 toxin only. Vitamin A excess appears to decrease the phase II drug-metabolizing enzyme activities and glutathione-SH content in rat liver tissue. Excess of vitamin A may be responsible for an increase of T-2 toxicity in rats.

Animals↗
PubMed1981

[Vitamin A and NADP-dependent isocitrate dehydrogenase: difference in activity of mitochondrial and cytoplasmic isoenzyme fractions].

The effects of vitamin A excess on the activity of isoenzyme fractions of NADP-dependent isocitrate dehydrogenase from rat liver separated by polyacrylamide gel disc-electrophoresis was studied. Vitamin A was shown to activate mitochondrial isoenzyme of NADP-dependent isocitrate dehydrogenase and had but very slight effect on the cytoplasmic isoform. This effect was observed already after 24 hrs following the injection and was enhanced at increasing doses of the vitamin. The data obtained suggest that NADP-dependent isocitrate dehydrogenase is controlled by complex mechanisms. The possibility of independent regulation of activity of mitochondrial and cytoplasmic isoenzymes and a possible involvement of retinol in the regulation of activity of its mitochondrial isoform are postulated. It is assumed that vitamins, similar to hormones, can selectively influence individual isoenzymes.

Animals↗