In vitro effects of gentamicin, ampicillin, and cefobid on energy supply and antioxidant protection systems of venous blood erythrocytes in newborns.

We studied the effects of antibiotics of different classes on reserve capacities of the energy supply and antioxidant protection systems in newborns. Erythrocyte catalase activity was high in children with perinatal asphyxia. Penicillin antibiotics, aminoglycosides, and cephalosporins decreased enzyme activity of the glutathione-associated antioxidant system. Ampicillin most significantly inhibited ATP synthesis in erythrocytes under conditions of hypoxia. Gentamicin was least potent in this respect. Impairment of ATP synthesis in erythrocytes was associated with inhibition of antioxidant enzymes catalase and glutathione reductase. Ampicillin increased glutathione peroxidase activity in response to addition of H2O2. None of the antibiotics modulated activity of cytosolic superoxide dismutase in blood erythrocytes from healthy newborns and newborns with perinatal asphyxia.

Effect of monotherapy and combination therapy with richlocaine on tissue hypoxia and activity of keratinocyte detoxifying systems in ischemic skin flap.

Treatment with richlocaine alone and, especially, in combination with antihypoxant energostim decreased the total content of hydroxyproline in the ischemic skin flap on day 3 after excision. Combination therapy with richlocaine and energostim normalized the redox potential in the energy supply system, improved antioxidant protection, and promoted the recovery of a balance between various components in the antioxidant system. These changes were not accompanied enhanced production of malonic dialdehyde. Our results suggest that combination therapy with richlocaine and energostim maintains the adaptive reserves of detoxifying systems in keratinocytes and prevents endotoxemia. Richlocaine primarily stimulates glycolytic synthesis of ATP, activates nonmitochondrial antioxidant enzymes, and increases RNase activity in lysosomes.

[Effect of energostim on myocardial damage during coronary artery occlusion]. / Vliianie énergostima na porazhenie miokarda pri okkliuzii koronarnoi arterii.

In contrast to traditional therapy (beta-adrenoblocker and nitrates), energostim improves the systolic and diastolic functions of myocardium during 120-min occlusion of the left descending coronary artery. The energostim-induced improvement in the central hemodynamics is correlated with an adaptive increase in activity of the antioxidant system enzymes in response to the ischemic production of reactive oxygen species, which is evidence of the mobilization of reserves of the enzymatic link in the antioxidant defense system of cardiomyocytes. Analogous pattern is observed in the blood. In the control group of traditional therapy, a decrease in the superoxide dismutase (SOD) activity and the redox potential (NAD/NADH) in myocardium are correlated with a decrease in the maximum rate of pressure increase in the left ventricle (R 6.4, p < 0.01) observed 2 h after the coronary occlusion. In the energostim treated group, there is a correlation between the SOD activity and the content of cytochrome C in mitochondria (R 6.1, p < 0.01): a change in the level of cytochrome C during 2-h acute ischemia is correlated with the decrease in redox potential (NAD/NADH) and in the ratio of glutathione peroxidase to Mn-dependent SOD (r 0.64, p < 0.01). Thus, disturbances in the antioxidant defense system of both myocardium and blood plasma of the patients with acute myocardium infarction are correlated with inability of the energy supply system to utilize oxygen in the process of glycolysis and oxidative phosphorylation in mitochondria. Stable adaptive increase in activity of the antioxidant defense system enzymes and a decrease in the content of cytochrome C in the blood plasma are probably the independent indications of beneficial prognosis and high efficacy of the proposed treatment of the ischemic damage of myocardium.

[Regulation of RNA synthesis in the rat heart in L-thyroxine toxicosis and hypothyroidism; the role of RNA-polymerases and the template activity of chromatin]. / Reguliatsiia sinteza RNK v serdtse krysy pri L-tiroksinovom toksikoze i gipotireoze; rol' RNK-polimeraz i matrichnoi aktivnosti khromatina.

It is shown that L-thyroxin applied to rats has induced in them development of pronounced cardiac hypertrophy accompanied by an increase in the total amount of nucleic acids in the myocardium (per organ) and enhancement of the RNA synthesis rate. It is confirmed by a considerable rise of the intensity of the labelled uridine incorporation into RNA without alteration of the specific radioactivity in a pool of free nucleotides and by the growth of the RNA-polymerase I activity. When L-thyroxin toxicosis lasts for four weeks and heart weight has not already increased the content of nucleic acids remains high, the rate of the label incorporation into RNA lowering down to the normal level. The activity of RNA-polymerase I is almost twice as low as that under thyrotoxicosis lasting for a week. In this case the matrix activity of chromatin tested by exogenous RNA-polymerase III of the rat gets lower. Under mercasolyl-induced hypothyrosis the heart weight decreases as well as the amount of nucleic acids, RNA synthesis intensity (by 40%) and RNA-polymerase I activity in it. The data obtained testify to the versatile effect of the thyroid hormones on RNA biosynthesis in the cardiac muscle and on the activity of both the RNA-polymerases and chromatin matrix.