[Deposition of exogenous and endogenously generated unsaturated fatty acids in lipid droplets triacylglycerol as a mechanism of its sequestration in epithelial cells].

Neutral lipids are deposited in intracellular compartments called lipid droplets, which are known to be critically implicated in regulation of cellular lipid metabolism. These organelles consist of a core of neutral lipids, mainly triacylglycerol (TAG) and cholesteryl esters, surrounded by phospholipid monolayer. Using Nile red lipid staining and [3H]-arachidonic and [3H]-oleic acids as precursors for lipid biosynthesis, we have evaluated the mechanisms of lipid body induction elicited by exogenous fatty acids within primary cultured epithelial cells from the frog urinary bladder.

[Gangliosides GM1 and GD1a modulate inflammatory effect of bacterial lipopolysaccharide in epithelial cells].

It is known that exogenous gangliosides (GL) inhibit acute inflammatory signals in different cells induced by Escherichia coli lipopolysaccharide (LPS). Until now the mechanisms underlying their effect are unknown. We hypothesize that the anti-inflammatory effect of GL is caused by their ability to modify TLR4 translocation into the lipid rafts.

[Regulatory interconnections of cyclooxigenase and inducible no-synthase in urinary bladder epithelial cells of the frog Rana temporaria under action of bacterial stimuli].

Earlier we have shown that in epithelial cells of the frog urinary bladder under action of bacterial lipopolysaccharides (LPS) there is activated expression of inducible NO-synthase (iNOS) and there is increased the NO production, which can play an important role in providing protective cell reactions from pathogens. The goal of the present work consisted in study of cyclooxigenase (cOG) products and mechanisms of their regulatory effect on expression of iNOS under action of LPS. In experiments on urinary bladder epithelial cells on the frog Rana temporaria it has been shown that incubation of the cells for 21 h with LPS leads to a rise in production of PGE2 and nitrites, stable NO metabolites.

[Lipopolysaccharide E. coli inhibits the arginine-vasotocin-induced increase of osmotic water permeability in the frog urinary bladder].

Since Gram-negative bacteria are known to be present in the cavity of urinary bladders in amphibian species, it was interesting to study the effect of bacterial endotoxins on epithelial signaling network which provides the arginine-vasotocin-induced increase of osmotic water permeability (OWP). The effect of LPS E. coli on AVT-induced OWP was studied in isolated frog Rana temporaria L.

[No-synthase activity in primary cultured frog urinary bladder epithielial cells and no-dependent antimicrobial effect].

We have shown previously that endogenous NO modulates the effect of arginine-vasotocin on the increase in the osmotic water permeability of the frog urinary bladder epithelium. The aim of the present work was to develop a procedure of cultivation of epithelial cells from the frog urinary bladder as a primary culture in order to study in vitro the cellular production of NO and its regulation. Isolated cells were cultivated in modified L-15 medium with 10% FBS and gentamycin (40 microg/ml) at room temperature.

[The presence of nitric oxide synthase in mucosal epithelial cells of the frog urinary bladder].

In experiments on frog Rana temporaria L. urinary bladder, we investigated localization of NO-synthase (NOS) in urinary bladder slices and measured NOS activity in the suspension of mucosal epithelial cells. Intensive NADPH-diaphorase staining which is widely used as an indicator of NOS activity was found in mucosal epithelium.

[Atrial natriuretic factor stimulates the frog urinary bladder osmotic permeability in presence of a cyclic nucleotide phosphodiesterase inhibitor].

The role of atrial natriuretic factor (ANF) in regulation of osmotic water permeability was studied in isolated frog Rana temporaria L. urinary bladder. It was found that ANF (rANF, 1-28) added to the serosal solution at concentrations 5 x 10(-8) M and higher dosedependently stimulated the arginine-vasotocin (AVT)-induced increase of osmotic water permeability.

[Effect of cGMP-dependent signaling system in regulation of osmotic permeability in the frog urinary bladder].

In frogs' isolated urinary bladders, contribution of cytosolic guanylate cyclase and cGMP-dependent protein kinase to regulation of osmotic permeability was studied. ODQ (25-100 microM), an inhibitor of cytosolic guanylate cyclase induced an increase of vasotocin-activated osmotic permeability but had no effect on the hormone-activated transepithelial urea transport. In isolated mucosal epithelial cells ODQ (50 microM) decreased the concentration of intracellular cGMP.

[Various effects of prostaglandin E2 on reabsorption of water and urea in the amphibia osmosis-regulating epithelium].

Principal similarities between molecular pathways providing the enhancement of water and urea reabsorption under the action of argininvasotocin (AVT) in amphibian urinary bladder suggest that prostaglandin E2 (PGE2) could be a negative regulator of urea transport. To analyse this hypothesis, the role of PGE2 in regulation of urea transport was studied in isolated frog (Rana temporaria L.) urinary bladder.

[Comparative study of the action of antineoplastic platinum compounds with varying nephrotoxic effects].

Studying the action of the two antitumour platinum compounds--cisplatin capable of exerting a nephrotoxic action and cycloplatam which has no damaging effect on the kidney, it was found that 3 h after the administration of cycloplatam the content of platinum in the kidney was 2 times lower than in the cfse of cisplatin. Due to different dynamics of the excretion of platinum compounds from the kidney 5 lays after their addition the content of platinum in the kidney was the same in both cases. The content of platinum in the nuclei, mitochondria and supernatant with respect to a total content in the kidney cortex was almost equal for both compounds.

Renal failure and nephrotoxic drug-induced disturbances in rat kidney tissue.

The injection to rats of glycerol, cisplatin, uranyl acetate, sodium dichromate, and mercuric chloride is followed on the third day by acute renal failure. A new approach for quantitative estimation of disturbance of excretory renal function is presented. The decrease in renal function due to uranyl acetate was 77%; sodium dichromate, 71%; mercuric chloride, 52%; cisplatin, 25%; and glycerol, 10%.

[The use of prednisolone for the attenuation of the nephrotoxic effect of cisplatin].

Rats experiments have indicated that prednisolone significantly decreases the nephrotoxic effect of the antitumor drug cisplatin. A single injection of the agent in a dose of 5 mg/kg body weight was followed by acute renal failure, which led to an increase in serum levels of creatinine and urea, to a rise in kidney weight, changes in renal water and ion content. The injection of prednisolone (5 mg/kg body weight) 3 hours prior to cisplatin administration resulted in a two-fold decrease in the concentration of nitrogen metabolic end products, without any effects on renal tissue.

[The stimulation of organic acid secretion in the kidneys of the frog Rana temporaria with the repeated administration of para-aminohippurate and triiodothyronine].

Investigating possible ways of the increase in the rate of organic acid transport in the kidney of frogs, it has been demonstrated that animals which passed hypobiosis exhibit the increase in maximum capacity of the kidney to secretion of paraaminohippurate during substrate stimulation evoked by the injection of this salt twice a day within three days, as well as by the injection of triiodthyronine once a day within three days. The effect produced is similar to kidney reaction in adult mammals.

[The water-salt metabolic state of guinea pigs after a prolonged stay at different temperatures of a hyperbaric environment].

Guinea-pigs were exposed for 6-10 days to a helio-oxygen mixture with the pressure 6 x 10(5) and 36 x 10(5) Pa and temperature 30.5 degrees C to 34.5 degrees C.

Triiodothyronine (T3) increases cisplatin nephrotoxicity in young and adult rats.

The influence of pretreatment with triiodothyronine (T3) on cisplatin (CP)-induced nephrotoxicity was investigated in 10- and 55-day-old rats. Triiodothyronine pretreatment enhanced CP proteinuria in young and adult rats, and increased blood urea nitrogen concentration in 55-day-old rats. As T3 decreased Pt concentrations in renal tissue, the enhanced nephrotoxicity of CP by T3 must have another mechanism.

[The action of cisplatin on the developing meso- and metanephros of chick embryos].

Injection of various doses of cisplatin to 2-14-day chick embryos showed that within 2-8 days of incubation cisplatin produces total toxic effect, the number of dead embryos being dependent on a dose of the drug. Within 9-16 days of incubation, i.e.

Cisplatin: nephrotoxic action in vertebrates and its prevention.

1. The kidney of frog and black sculpin appeared to be much less sensitive to the toxic action of CP in comparison with rat and pigeon. 2.

[Morphofunctional correlates of the nephrotoxic action of cis-platin].

A single injection of 5 mg/kg cisplatin causes (in 2 days) focal changes in rat renal parenchyma. These changes correlate well with the decrease in glomerular filtration rate, increase in blood urea concentration, decrease in water load excretion. Cellular dystrophy was found in the convoluted and straight proximal renal tubules, in line with a marked thickening of basal membrane in damaged cells, that appears to account for the impairment of paraaminohippurate secretion, the increase of kidney mass and its swelling.

[Pharmacological blockade of the nephrotoxicity of cisplatin in rats].

Cisplatin injection (0.5 mg/100 g body weight) induced 5 days later an increase in serum urea concentration from 3.31 +/- 0.

[Glucose reabsorption in the kidneys of rats after insulin administration against a background of stabilized hyperglycemia].

In rat with constant i. v. infusion of 40% glucose solution, administration of insulin (0.

[Succinate dehydrogenase activity in the mesonephros in the process of development of chick embryos].

The activity of succinate dehydrogenase in the mesonephros tissue of chick embryos is rather high on the 6th day of embryonal development and is not subjected to significant changes up to the 17th day. The absence of wide variations in the activity of this enzyme during the period of degeneration of the mesonephros may be due to a parallel decrease in the organ's mass and in the number of its mitochondria.