Participation of Free-Radical Processes in Structural and Metabolic Disturbances in the Lung Tissues Caused by Exposure to Coal-Rock Dust and their Adaptogenic Correction.

Adaptive correction of structural and metabolic disturbances in the lungs caused by longterm exposure to coal-rock dust were studied in experiments on rats. It was shown that the complex antioxidant preparation containing dihydroquercetin compensated disturbances in the redox balance in the lung tissue, prevented the formation of dust granulomas, and reduced the severity of degenerative changes in the bronchopulmonary system.

Correction of Abnormalities Provoked by Long-Term Alcoholization with Hypoxic-Hyperoxic Training.

Free radical oxidation in the liver and skeletal muscles as well as stress behavior were examined in rats subjected to a gradual long-term alcoholization with elevated ethanol content from 10 to 40% followed by correction of alcohol-induced disturbances with hypoxic-hyperoxic training. The elevated plus-maze test revealed increased anxiety and appearance of risky behavior in alcoholized rats in the absence of changes in motor and orientation activity. In the liver and skeletal muscles of alcoholized rats, free radical oxidation processes were decompensated despite activation of antioxidant enzymes. Adaptation to intermittent hypoxia-hyperoxia during last two weeks of alcoholization exerted a protective effect against ethanol-induced oxidative stress: reduced anxious and risk behavior, normalized tissue tolerance of free radical oxidation processes, and restored the level of protective proteins.

Addition of Hyperoxic Component to Adaptation to Hypoxia Prevents Impairments Induced by Low Doses of Toxicants (Free Radical Oxidation and Proteins of HSP Family).

We studied the possibility of preventing disturbances caused by administration of low doses of toxicants by adaptation to interval hypoxia and hyperoxia. The preventive protective effect of adaptation to hypoxia-hyperoxia manifested in suppression of free radical oxidation, decrease in the levels of HIF-1α and inducible HOx-1, and improvement of tolerance to physical exercises.

[MAXIMUM SINGLE DOSE OF COLLOIDAL SILVER NEGATIVELY AFFECTS ERYTHROPOIESIS IN VITRO].

Erythroblastic islets (EI) of rat bone marrow were cultured for 24 h in the presence of silver nanoparticles (1.07 · 10(-4) mg/ml; 1.07 · 10(-3) mg/ml; and 1.07 · 10(-2) mg/mL). The colloidal silver at 1.07 · 10(-3) mg/ml concentration inhibited the formation of new Elby disrupting contacts of bone marrow macrophages with CFU-E (erythropoiesis de novo) by 65.3% (p < 0.05). Colloidal silver nanoparticles suppressed the reconstruction of erythropoiesis and inhibited the formation of new EI by disrupting contacts of CFU-E and central macrophages with matured erythroidal "crown" (erythropoiesis de repeto). The colloidal silver concentration of 1.07 · 10(-3) mg/ml in the culture medium also reduced the number of self-reconstructing EI by 67.5% (p <0.05), whereas 1.07 · 10(-2) mg/ml colloidal silver reduced this value by 93.7% (p < 0.05). Silver nanoparticles retarded maturation of erythroid cells at the stage of oxiphylic normoblast denucleation: 1.07 · 10(-3) mg/ml colloidal silver increased the number of mature El by 53% (p < 0.05). The retardation of erythropoiesis by colloidal silver in concentration equivalent to the maximum single dose is related to the effect of silver nanoparticles rather than glycerol present in the colloidal suspension.

Effects of fullerenol C60(OH)24 on erythropoiesis in vitro.

The effects of fullerenol C60(OH)24 in doses of 0.1-100 µg/ml on erythropoiesis were studied in the culture of erythroblastic islets of the bone marrow. Fullerenol in concentrations of 10 and 100 µg/ml had negative effects on the development of erythroid tissue: it inhibits proliferation of erythroid cells, delays erythroblast maturation, decelerates recruitment of erythroid CFU to differentiation, and suppresses repeated involvement of macrophages in erythroblastic islets.

Induction of HSPs and antioxidant defense enzymes during activation of free radical oxidation at the early stage of hypokinesia.

We studied the stress component of the early stage of hypokinesia during hindlimb unloading. The intensity of free radical processes was evaluated and the content of protective proteins (antioxidant defense enzymes and proteins of the HSP family) was measured in the heart and liver. Three-hour hypokinesia increased the content of constitutive protective proteins, including hemoxygenase-2 and antioxidant defense enzymes, in the heart. Hypokinesia for 72 h was accompanied by more potent activation of antioxidant defense enzymes and increase in the content of inducible hemoxygenase-1, which leads to partial compensation of activated free radical oxidation. In the liver, hypokinesia of different duration suppressed the protective systems: the synthesis of inducible and constitutive hemoxygenases and antioxidant defense enzymes decreased, while the sensitivity of liver membrane structures to reactive oxygen species increased. We revealed a tissue-specific response to hypokinesia: pronounced damaging effect predominated in the liver and partial compensation of elevated production of reactive oxygen species was observed in the heart due to activation of protective systems.

Adaptation to periodic hypoxia and hyperoxia improves resistance of membrane structures in heart, liver, and brain.

A novel principle of short-term periodic adaptive training by varying the oxygen level from hypo- to hyperoxia is substantiated both theoretically and experimentally. Short-term adaptation to hypoxia-normoxia produced a membrane-protective effect in the heart and cerebral cortex, but increased the sensitivity to free radical oxidation and decreased the level of components of the antioxidant defense system in the liver. Hypo-hyperoxia adaptation produced a membrane-stabilizing effect in the heart, brain, and liver, which was more pronounced compared to the effect of hypoxia-normoxia training. In contrast to hypoxia-normoxia adaptation, in case of hypo-hyperoxia training the adaptive defense developed as early as 15 days after the start of training.

Effect of long-term hypokinesia on monoamine system and antioxidant status of the brain.

Long-term hypokinesia (30 days) was accompanied by activation of the serotoninergic and dopaminergic systems. Exhaustion of the antioxidant system was observed on days 10-30 of immobilization.

August rats are more resistant to arrhythmogenic effect of myocardial ischemia and reperfusion than Wistar rats.

As differentiated from Wistar rats, myocardial ischemia and reperfusion produce no ventricular fibrillation in August rats. Pretreatment with nitric oxide synthase inhibitor Nw-nitro-L-arginine increased mortality rate in August rats with acute myocardial infarction from 20 to 40%. Under these conditions mortality rate in Wistar rats increased from 50 to 71%. Interstrain differences in the resistance of these animals to the arrhythmogenic effect of ischemia are probably associated with higher activity of the nitric oxide system in August rats compared to Wistar rats.