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Biomedical subjects

E M Khvatova

Publications and source records attributed to E M Khvatova.

At least 19 recordsLinked to original sources
PubMed1995

Effects of delta-sleep inducing peptide (DSIP) and some analogues on the activity of monoamine oxidase type A in rat brain under hypoxia stress.

Metabolic effects of delta-sleep inducing peptide (DSIP) under hypoxia stress were investigated in rats subjected to short-term hypoxic conditions (about 0.26 Bar). It was found that DSIP partially restricted stress-induced changes in activity of mitochondrial monoamine oxidase type A (MAO-A) and serotonin level in rat brain. A number of DSIP analogues was tested and among them there were some compounds with enhanced ability to counteract hypoxia induced changes in MAO-A activity and serotonin content in comparison with native neuropeptide.

Amino Acid Sequence↗
PubMed1976

[Experimental aortic stenosis, its subsequent correction and the activity of oxidative enzymes in the myocardium].

The activity of the respiratory enzymes of myocardial mitochondria--succinatedehydrogenase and cytochromixidase--was studied in experimentally induced aortic stenosis and after its elimination in 98 mongrel dogs. The observation period of stenosis was 1, 15, 30 and 60 days, and after its elimination--1, 7, 15 and 30 days. The activity of the enzymes in question was found to grow after the production of aortic stenosis. The highest level of their enzymatic activity was observed on the 15th day after the induction of stenosis. By the 30th and 60th day the enzymatic activity underwent some decrease, although it persisted on a level above the initial. The activity of succinatedehydrogenase fell sharper. After the elimination of the stenosis the activity of both enzymes decreased, and by the 7th day it was below the initial level. By the 15th day after the removal of the ligature from the aorta the activity of both enzymes corresponded to the initial values and did not change further till the end of the 1st month. The dynamics of the activity of succinatedehydrogenase and cytochromixidase after an experimentally induced aortic stenosis and its subsequent elimination seems to depend on the nature of the changes in the function of the heart muscle performed under such experimental pathology, and on the degree of coronary flow enhancement.

Animals↗
PubMedDate not supplied

[Macroergic phosphates in the brain under hypoxia].

Acute hypoxic hypoxia ("height" 7000 m) did not cause distinct alterations in content of adenyl and guanyl nucleotides from brain tissue. Negative alterations in the pool of macroergic phosphates occurred in a deficit of oxygen ("height" 8000 m). Short-term training with hypoxia prevented the alterations in nucleotide pool even if the extreme hypoxia was applied ("height" 9000 m). Pre-cooling of animals promoted the maintenance of nucleotide pool at the "height" of 8000 and 9000 m. Hypothermia did not protect against the distinct alterations in content of both adenyl and guanyl nucleotides under conditions of oxygen deficit ("height" 9500 m and 1100 m).

Acute Disease↗
PubMedDate not supplied

[The use of empirical correlations in adenine nucleotide systems for prediction of AMP level in the brain in hypoxia].

The empirical relationship between the changes of the AMP concentration and the AMP content under different kinds of hypoxia was showed. This relationship is determined by the function which is closely related to the totality parameters of the brain energy metabolism. This function may be used for the prognosis of the brain energy state under hypoxia.

Adenosine Monophosphate↗
PubMedDate not supplied

[Mitochondrial diseases--a new branch of the modern medicine].

The review highlights current aspects of a large group of diseases the main pathogenetic element of which is an inherited or acquired disturbance of gene expression of nuclear or mitochondrial genome encoding mitochondrial proteins. The recent data on mutant genetic loci specific to the most wide spread mitochondrial diseases are considered. The steps of pathogenesis, include the mutations of nuclear or mitochondrial genes, disturbances of mitochondrial protein synthesis, dissipation of proton membrane potential, opening of a permeability transition pore, releasing of procaspases, cytochrome c, and other proapoptotic molecules, and finally chromatin fragmentation and apoptotic cell death. We discuss the possible reasons of polysymptomatic character and different variants of mitochondrial disease manifestations on the basis of the phenomenon of mitochondrial DNA heteroplasmy and metabolic compensation of the genetic defects. Modern biochemical methods of a mitochondrial disease diagnostics: (PCR-amplification, polarographic research of mitochondrial respiration and oxidative phosphorylation, analysis and monitoring of metabolites in biological liquids) are characterized. The basic principles and perspectives of the treatment of mitochondrial diseases, (gene therapy, correction of metabolic disorders, application of antioxidants and neuropeptides) are described.

Antioxidants↗
PubMedDate not supplied

[Regulation of the activity of brain cytoplasmic creatine kinase by pyridine nucleotides].

Effect of oxidized and reduced forms of pyridine nucleotides on activity of creatine kinase BB was studied in rat brain. NAD did not affect the enzymatic activity at concentrations of 1.0-4.0 mM, while in presence of NADH activity of creatine kinase BB was gradually decreased as the coenzyme concentration increased. The plot of 1/V against 1/S at various NADH concentrations produced a series of lines intersecting at one point (-1/Km), thus indicating the noncompetitive type of brain cytoplasmic creatine kinase inhibition by reduced pyridine nucleotides. Apparent Ki value for NADH was about 1.5 mM which was lower than the known parameter for cytoplasmic creatine kinase isozymes from skeletal and heart muscles. Dependence of brain creatine kinase BB on the rate of pyridine nucleotide reduction suggested a possible mechanism for the enzyme regulation under hypoxic conditions.

Animals↗