[Visual function study of young children].
Explore the source record for details and available documents.
Adolescent↗
Biomedical subjects
N G Novoselova
Publications and source records attributed to N G Novoselova.
[Energy metabolism disorders in the myocardium due to alcoholic intoxication].
Energy metabolism was studied in rat myocardial mitochondria by estimation of respiratory enzymes activity and content of the Krebs cycle substrates under conditions of acute and chronic intoxication with ethyl alcohol. In the acute intoxication mitochondrial redox enzymes were inhibited (glutamate- and malate dehydrogenases, NADH cytochrome C oxidoreductase and cytochrome C oxidase), succinate- and lactate dehydrogenases were activated; at the same time, contents of pyruvate, succinate, and alpha-ketoglutarate were elevated and the content of oxalacetic acid was decreased. Prolonged administration of alcohol (within 2 months) caused an intensification of glycolysis and an increase in NADH cytochrome C oxidoreductase pathway with preferable oxidation of succinate and activation of cytochrome C oxidase; the phenomenon appears to be an adaptation to chronic "alcohol hypoxia". Discontinuation of alcohol administration led to deficiency of native substrates in myocardium (primarily, oxalacetic and succinic acids) due to decrease in NAD reduction via alcohol dehydrogenase reaction and to increase in oxidation of NAD-dependent endogenous substrates.
Alcoholic Intoxication↗
[Effect of ethyl alcohol on oxidation-reduction processes in the myocardium].
Evidence is given of disturbances of aerobic oxidative process in the myocardial mitochondria occurring in acute and chronic alcoholic intoxication. A single introduction of alcohol in a dose of 1 and 3 g/kg to rats and dogs produces "hypoxyform" changes in the myocardium, viz. a fall of PO2, a reduced activity of most NAD-independent enzymes, activation of succinate- and lactate-dehydrogenases in a moderate dissociation of oxidative phosphorylation reactions. The damaging effect of the alcohol persists for 24 hours after its one-time introduction. Following a 2-month long alcoholic intoxication there was seen a depressed respiratory activity of the mitochondria and of the study enzymes, except for cytochrome-C-oxidase. It is assumed that the cardiotoxic effect of alcohol is due to the damage of the energy-producing system of the mitochondria.
Alcoholic Intoxication↗