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Biomedical subjects

M V Bilenko

Publications and source records attributed to M V Bilenko.

At least 19 recordsLinked to original sources
PubMed2003

Tumor necrosis factor-alpha in low doses preactivates and activates macrophages by increasing their ability to produce reactive oxygen species and oxidize low-density lipoproteins: protective effect of antioxidants.

Tumor necrosis factor-alpha in low doses activated rat peritoneal macrophages and intensified production of reactive oxygen species (zymosan-depended chemiluminescence). Single or 2-fold incubation with tumor necrosis factor-a activated and preactivated human blood macrophages and promoted oxidative modification of low-density lipoproteins (increased their mobility in agarose gel). Antioxidants (potassium phenosan, probucol, and desferal) suppressed oxidative modification of low-density lipoproteins induced by nonactivated, preactivated, and activated macrophages. Our results show that antioxidants hold much promise for the prevention and therapy of atherosclerosis.

Animals↗
PubMed2003

Effect of antioxidant probucol on cell-mediated LDL oxidation in vitro and in vivo.

We studied the effect of phenol antioxidant probucol on free radical oxidation of LDL isolated from blood plasma of healthy donors. Oxidation was induced by co-incubation of LDL with cultured peripheral blood monocyte-macrophages and human umbilical vein endothelial cells under conditions of ischemia-reperfusion. In addition, the effect of probucol therapy on oxidability of plasma LDL in CHD patients was examined. Probucol (0.1-10 microM) efficiently protected LDL from free radical oxidation in vitro and in vivo.

Anticholesteremic Agents↗
PubMed1992

[The evaluation of the possibility of using prodigiozan for isolating extracts that stimulate proliferative processes in the resected liver].

The experiments were performed on 126 white male rats. The inclusion of 3H-thymidine in nuclear DNA of the liver was studied on h 24 and 48 after 70% resection of the liver versus prodigiosan injection or combination of prodigiosan with 70% resection of the liver. Liver extracts stimulating proliferation (ESP) obtained under the above schedules were studied on the model of 30% liver resection. It is shown that prodigiosan (0.25 mg/kg) injected to intact rats and rats with 70% resected liver initiated ESP production promoting the inclusion of 3H-thymidine in nuclear DNA of the liver after 30% resection of the liver.

Animals↗
PubMed1992

[Changes in EEG and higher nervous activity of rats during cerebral anti-ischemic protection by acelysin].

The water-soluble aspirin (acelysin) has been used as an anti-ischaemic protector when injected in the dose of 150 mg/kg 30 min before ischaemia. The EEG has been registered during the whole period of experiment and the total EEG power index has been calculated. The higher nervous activity has been evaluated during analysis of rat's abilities for elaboration of conditional reflex of an active escape reaction in Y-labyrinth. The results have demonstrated the complete rehabilitation and restoration of brain functional activity 8 days after endurance of brain ischaemia under protection of acelisin.

Animals↗
PubMed1992

[Anti-ischemic protection of the brain using water-soluble form of aspirin-acelisin].

The domestic water-soluble aspirin (acelisin) has been used as an anti-ischemic brain protector. The total brain ischemia has been implemented in accordance with an original technique for 17 to 35 min. The doses of acelisin from 25 to 250 mg/kg have been tested during experiments. The infusion of solutions has been carried out before ischemia, 15 min before reperfusion and just after the beginning of reperfusion. The functional status and survival of rats have been evaluated during a week. The best result has been reached with 150 mg/kg acelisin injected 30 min before ischaemia. A positive effect was reported when acelisin was used in early postischaemic period.

Animals↗
PubMed1991

[Anti-ischemic action of a 1-hydroxy-2,2,6,6-tetramethylpiperidine derivative from a series of nitroxyl bioantioxidants].

The experiments have been performed on 216 Wistar rats to examine anti-ischaemic action of the 1-hydroxy-2,2,6,6-tetramethyl-piperidine derivative (I), whose antioxidant properties were, earlier shown for model systems. Introduction of I (10(-4) M) into the perfusion medium and the subsequent storage (37 degrees C) of isolated liver was shown to decrease the accumulation of lipid peroxidation products (MDA). Compound I administrated (5 x 10(-6)-10(-5) M) in perfuse medium of isolated (Langendorff method) and ischemized (30 min, 37 degrees C) heart improves contractile function (Pmax) and decreases end-diastolic pressure at postischaemic period. In vivo injection of I increases (12 mg/kg, i.p.) the number of rats survival after sublethal time (2.5 h) of liver total ischaemia, increase (35 mg/kg, i.p.) the number of rats survival and improves parameters of heart function after ischaemic shock (6 h ischaemia and reperfusion of limbs). The analog of I, corresponding amine, possessing no antioxidant properties also fails to exhibit any anti-ischaemic effect.

Animals↗
PubMed1990

[Is xanthine oxidase a universal source of superoxide radicals in ischemic and reperfusion lesions?].

While studying xanthine-xanthine oxidase system it was found, that a considerable accumulation of xanthine and uric acid occurred whereas xanthine dehydrogenase did not transfer in xanthine oxidase during 2 hours of total rat liver ischemia. These data make it possible to reject the generally accepted hypothesis of xanthine oxidase key role in free radical mechanism of ischemia damage.

Animals↗
PubMed1990

[Membranes of subcellular organelles as the source of superoxide radicals in liver ischemia].

O2-generation rate (Vo2-) in microsomal, mitochondrial and nuclei liver membranes was measured by ESR method, by accumulation of stable nitroxide radicals. These Vo2- values were compared with Cu, ZnSOD and MnSOD activities after 2 hours ischemia and 24 hours reoxygenation. O2- radicals generated by electron transfer chains are concluded to damage mainly during the ischemia, but not the reoxygenation.

Animals↗
PubMed1989

[Disorders of cardiac contractile function in ischemic shock; the protective effect of antioxidants and liposomes made from egg phospholipids].

Experiments were made on Wistar rats with 6h tourniqueting of the hind limbs to study animal survival rate, myocardial contractile function and protective action of antioxidants and egg phospholipid liposomes during ischemic shock. It has been shown that reperfusion of the limbs leads to a high animal lethality, make lower myocardial contractile function and coronary flow of the hearts isolated from rats following a 6h reperfusion of the limbs. Well-known antioxidant butylated hydroxytoluene and a new antioxidant tetramethylpiperidine derivative bring animal lethality down and improve coronary flow and contractile function of the isolated heart. Phospholipid liposomes increase survival rate moderately but have no any effect on the heart contractile function. It has been deduced that lipid peroxidation takes part in the disturbance of heart contractile function and genesis of the death within ischemic shock.

Animals↗
PubMed1989

[Negative inotropic and vasoconstrictor effects of oxidized phospholipids].

Effects of oxidized yolk phospholipids (PL) on the coronary perfusion rate (CPR) and myocardial contractility were studied in the experiments with the isolated or isolated and 30-minute ischemia-induced heart of the rat or isolated myocardial strip of the frog. The oxidized PL were demonstrated to possess a more pronounced and steady negative inotropic effect than unoxidized PL, which was due to their direct dose-dependent damaging action on myocardial contractility. The oxidized PL also made the unrestored CPR worse in the early postischemic period, the concomitant administration of aspirin producing no effects and that of the antioxidant ionol making ischemic myocardial contractility better. The findings suggest that the circulating oxidized PL may contribute to the impairment of coronary tone and contractility of the intact or ischemic myocardium and the induction of endogenous processes of lipid peroxidation plays a role in showing these effects.

Animals↗
PubMed1988

[The state of lipid peroxidation and enzymes of calcium transport system in sarcoplasmic reticulum of ischemic myocardium].

In 30 experiments on mongrel dog hearts it was shown that 30 min of total ischemia (37 degrees C) followed by accumulation of MDA in the SR membranes and decrease of their Ca2+-uptake, but had no effect on activity Ca2+-ATPase. After 60-120 min ischemia marked a decrease of Ca2+-uptake and activity Ca2+-ATPase took place, MDA content remained at the increased level. The results show that lipid peroxidation take part in the increase of the permeability of SR membranes for Ca2+ and inhibiting of Ca2+-ATPase.

Animals↗