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Biomedical subjects

I S Chelnakova

Publications and source records attributed to I S Chelnakova.

At least 19 recordsLinked to original sources
PubMed1992

Trophic effect and modulation of ACTH-dependent stimulation of steroidogenesis by prolactin in guinea pig adrenal cortex.

The effect of PRL in intact guinea pig on the incorporation of specific labelled precursors into DNA, RNA, proteins and corticosteroids in adrenocortical tissue of intact guinea pig at different levels of activation of the gland were studied. PRL (2 IU/100 g daily) did not cause any significant changes until 3 days of treatment. PRL administered alone for 3 days caused significant elevation of 3H-thymidine incorporation into DNA in adrenocortical slices and no significant changes in labelling of RNA, protein and corticosteroids. In contrast, PRL administered together with ACTH (0.5 IU/100 g) for 3 days did not affect DNA synthesis but caused increase of 3H-cholesterol incorporation into cortisol and cortisone additionally to the ACTH action. Labelling of 17-deoxycorticosteroids in adrenocortical slices from animals of ACTH+PRL group either did not change significantly (aldosterone) or decreased (corticosterone).

Adrenal Cortex↗
PubMed1989

[Chloditan-induced changes in lipid peroxidation in the adrenals of dogs and guinea pigs].

The effect of adrenocorticolytic drug chloditan (1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane;) on the content and the rate of lipid peroxidation in dog and guinea pig adrenals was studied. In adrenals of dogs and guinea the amount of malondialdehyde (MDA) was increased. In vitro spontaneous lipid peroxidation was delayed in adrenal homogenate of DDD-treated dogs. Spontaneous lipid peroxidation in adrenal homogenate was not decreased by feeding DDD in the guinea pig. DDD consumption did not affect on lipid peroxidation promoted by ascorbic acid and ferrous iron. The accumulation of MDA in dog and guinea pig adrenal homogenates was inhibited by NADPH.

Adrenal Glands↗
PubMed1978

[Effect of O,N'=dichlorodiphenyldichloroethane and pertan in vitro on glutathione reductase activity in the adrenals of dogs and guinea pigs].

Glutathione reductase is activated by o,p'-dichlorodiphenyldichlorethane (o,p'-DDD) and pertan added in a concentration of 312 micrometer to the homogenate and cytoplasmic fraction of the dog adrenals. At a concentration of 156 micrometer o,p'-DDD and pertan failed to influence the glutathione reductase activity of the dog adrenal glands. Added in vitro, o,p'-DDD and pertan activate glutatione reductase of the quinea pig adrenal glands. O,p'-DDD does not affect the glutathione reductase activity of the liver and kidney cytoplasmic fraction in dogs. This observation confirms the high specificity of o,p'-DDD action on the adrenal glands.

Adrenal Glands↗
PubMedDate not supplied

[Effect of N-acylethanolamines on adrenal cortex function].

The possibility of NAE to take part in the regulation of the function of adrenal glands was studied. It was shown that two times NAE (18:0) injection in a dose 5 mg/kg of weight increased the content of 11-hydroxysteroids in blood of intact male rats. NAE caused the raise of the blood hormone content by 4 times under the immobilization stress. It is apparent that augment of stress response under the influence of NAE in vivo is explained by the activation of hypophysis-adrenal cortex system. In vitro NAE lowered steroidogenesis by near 40%. One can suggest that this decrease is caused by membranotropic properties of NAE.

Adrenal Cortex↗
PubMedDate not supplied

[Investigation of N-acylethanolamines on adrenal cortex function].

The possibility of NAE to take part in the regulation of the function of adrenal glands was studied. It was shown that two times NAE (18:0) injection in a dose 5 mg/kg of weight increased the content of 11-hydroxysteroids in blood of intact male rats. NAE caused the raise of the blood hormone content in 4 fold under the immobilization stress. It is apparent that augment of stress response under the influence of NAE in vivo is explained by the activation of hypophysis-adrenal cortex system. In vitro NAE lowered steroidogenesis by near 40%. One can suggest that this decrease is caused by membranotropic properties of NAE.

Adrenal Cortex↗
PubMedDate not supplied

[Activity of glutathione reductase and glutathione-S-transferase in rabbit brain tissue in the long-term post-traumatic period].

The glutathione-reductase and glutathione-S-transferase activities in the cortex and brain stem tissues of rabbits with post-traumatic epileptic reality (1 year after the light brain injury) was defined. An increase of glutathione-reductase activity in the cortex microsomal and stem mitochondrial fractions, and increase of glutathione-S-transferase activity in cortex and stem mitochondrial fractions was obtained. The conclusion is made that the activation of the anti-oxidant glutathione fermentative system is a long-term metabolic CNS adaptation in the case while mitochondrial oxidation and oxidative phosphorilation are disturbed.

Adaptation, Physiological↗
PubMedDate not supplied

[Regulation of hormone biosynthesis in guinea pig adrenal glands by potassium ions as affected by dihydropyridines. 1. Analysis of changes in steroidogenesis evoked by dihydropyridines].

Influence of Ca2+ channel modulators BAY K 8644, nitrendipine and newly synthesized derivative of 1,4-dihydropyridine: 4-(3', 4'-dimethoxyphenyl)-2,6-dimethyl-3,5- diethoxy-carbonyl-1,4-dihydropyridine-(DHP-51) on aldosterone production by adrenocortical slices depends on K+ content in the incubation medium. The modulators only slightly influence the hormone output at low K+ level in the medium. Intensive synthesis of aldosterone at high level of potassium in the medium was prevented in the presence of DHP-51 and low concentration of BAY K 8644. DHP-51 inhibited [3H]-cholesterol incorporation into all main corticosteroids in the high-potassium medium.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

[Regulation of hormone biosynthesis in guinea pig adrenal glands by potassium ions as affected by dihydropyridines. 2. Possible mechanisms of changes in steroidogenesis induced by 1,4-dihydropyridines in dispersed adrenocorticocytes].

Formation of aldosterone, corticosterone, cortisol and cortisone of labelled cholesterol in the dispersed adrenocorticocytes significantly intensifies at high potassium concentrations in the incubation medium. Labelling of aldosterone and corticosterone in the presence of DHP-51 remains unchanged in the medium containing 3 mmol/l of K+, but is inhibited at 8 mmol/l of potassium. Labelling of 17-hydroxylated corticosteroids, cortisol and cortisone grows at low K+ concentration and falls at the high concentration as a result of DHP-51 addition to the incubation medium. This relationship is disturbed only at high concentration of DHP-51. Incorporation of [3H]-leucine into proteins of adrenocorticocytes grows with K+ concentrations. DHP-51 causes insignificant changes in incorporation of [3H]-leucine into proteins at low potassium content, inhibiting incorporation in the medium at high K+ level. DHP-51 blocked Ca2+ transport into adrenocorticocytes, activated by raised level of potassium in the medium. The mechanism of DHP-51 action on regulation of steroidogenesis in adrenocorticocytes is discussed.

Adrenal Cortex↗
PubMedDate not supplied

[Activity of glutathione reductase in the adrenal glands and the liver of dogs after administration O,P-DDD, perthane and ACTH].

A study was made of the inhibitors of the adrenal gland function and ACTH on the activity of NADP-specific glutathionreductase in the adrenal glands and the liver of dogs. After a 10-day feeding to dogs of o,p'-dichlordiphenyldichlorethane (o,p'-DDD) and p,p'-diethyldiphenyl dichlorethane (p,p'-pertane) in a dose of 50 mg/kg there was observed a marked activation of glutathion reductase in the adrenal glands. Elevation of the activity of the enzyme was revealed as soon as 24 hours after the administration of o,p'-DDD. The inhibitors under study failed to influence the activity of the enzyme in the liver of dogs, this indicating a specific action of o,p'-DDD and pertane on the adrenal gland cortex. Stimulation of glucocorticoid biosynthesis under the effect of ACTH administered once in a dose of 25 Units/kg was not accompanied by the changes in the activity of glutathione reductase in the adrenal glands and the liver of dogs. Prolonged ACTH administration (4 Units/kg) caused a significant reduction of the enzyme activity calculated as per 1 mg of protein in the adrenal gland homogenate.

Adrenal Cortex↗
PubMedDate not supplied

[The participation of protein synthesis in the K+-dependent activation of hormonal biosynthesis in the adrenal cortex of guinea pigs].

An in vitro effect of cycloheximide (CHI), an inhibitor of protein synthesis, on the stimulation of steroidogenesis, caused by a rise of K+ concentration in a medium from 1 to 10 mM, was studied. A rise of a K+ level in the incubation of guinea-pig adrenocortical sections resulted in enhanced protein synthesis and activation of aldosterone and corticosterone synthesis from cholesterol. CHI addition completely suppressed these effects of K+. Comparison of incorporation of a cholesterol and corticosterone mark in aldosterone suggests that a rise of a K+ level within physiological limits enhanced hormone biosynthesis at the stage of splitting off a lateral cholesterol chain. The authors discuss a possible involvement of protein synthesis, stimulated by a high K+ concentration, in acceleration of final reactions of aldosterone biosynthesis.

Adrenal Cortex↗
PubMedDate not supplied

[The effect of ascorbate, NADPH and chloditan on lipid peroxidation in the adrenal glands of dogs and guinea pigs in vitro].

Lipid peroxidation was studied in dog and guinea pig adrenal cortex homogenates in vitro in presence of ascorbate, NADPH and I-(o-chlorophenyl)-I-(p-chlorophenyl)-2,2-dichloroethane (o,p'-DDD, chloditane) the substance exhibiting the specific impairing effect on human and dog adrenal gland cortex. The higher rate of spontaneous lipid peroxidation was detected in adrenal gland homogenates of guinea pig. NADPH inhibited accumulation of hydroperoxides in dog adrenal gland homogenates, while ascorbate-Fe2(+)-activated lipid peroxidation. Chloditane at concentrations 15.6 and 156 microM decreased the rate of spontaneous lipid peroxidation in dog adrenal gland homogenates and increased--in guinea pig preparations. Chloditane decreased distinctly the rate of lipid peroxidation in guinea pig adrenal gland homogenates, which was stimulated by ascorbate.

Adrenal Glands↗
PubMedDate not supplied

[Lipid peroxidation in the liver of dogs and guinea pigs receiving chloditan].

The contents and the rates of the formation of lipid peroxides in the liver homogenates were studied. Dogs and guinea pigs were fed with chloditan in doses of 50 and 150 mg/kg body weight, respectively, for 20 days. In the dogs chloditan caused atrophy of the adrenal glands. The drug accumulation in the adrenal glands of the guinea pigs did not produce damage of the glands. The feeding with chloditan failed to change the level of malondialdehyde in the livers of the dogs and decreased it in the livers of the guinea pigs. In vitro spontaneous and NADP N-dependent lipid peroxidation in the liver homogenates of the dogs treated with chloditan was slowed. The decrease of malondialdehyde content in the guinea pig liver and the slowing of lipid peroxidation rate in the dog liver homogenate can be explained by the change in the activity of the enzymes detoxicating xenobiotics and products of lipid peroxidation.

Animals↗
PubMedDate not supplied

[Changes in mitochondrial and microsomal electron transport as affected by o,p'-dichlorodiphenyldichloroethane].

The paper deals with the influence of 1-(o-chlorophenyl)-1-(p-chlorophenyl)-2.2-dichloroethane (o,p'-DDD, chloditane) on NADPH-dependent reduction of cytochrome c, ferricyanide, 2,6-dichlorophenolindophenol and neotetrazolium; 156 and 312 mumol o,p'-DDD was added to the dog adrenal mitochondrial and microsomal suspension. Ferricyanide reduction decreased and neotetrazolium reduction increased under the influence of o,p'-DDD. Reduction of cytochrome c was inhibited in microsomal fraction and activated in mitochondrial one. o,p'-DDD exerted no influence on 2,6-dichlorophenolindophenol reduction in the adrenal subcellular fractions. The possible mechanisms of o,p'-DDD action on the electron transport system were discussed.

Adrenal Glands↗
PubMedDate not supplied

[Insensitivity of purified glutathione reductase from adrenal cortex to o,p'-dichlorodiphenyldichloroethane].

The activity of partially purified glutathione reductase (EC 1.6.4.2) was studied as affected by 1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane (o,p'-DDD, chloditane). The glutathione reductase from human and dog adrenal cortex was purified by means of precipitation with (NH4)2SO4, by affinity chromatography, sephadex G25, DEAE-cellulose and CM-cellulose chromatography. A 56.6- and 41-fold purification was obtained for the enzyme from human and dog adrenal cortex, respectively. o,p'-DDD did not influence the activity of purified glutathione reductase in vitro. The rate of NADPH oxidation by adrenal cortex cytosol in the glutathione reductase reaction increased under the effect of o,p'-DDD.

Adrenal Cortex↗