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Introduction. Oxymethyluracil is an effective antihypoxant in a model of histotoxic hypoxia. Acetylcysteine combines the properties of a toxicotropic nonspecific and toxicokinetic antidote, promotes the synthesis of glutathione in the body. The aim of the research was a preliminary assessment of the antihypoxic properties of the complex compound of oxymethyluracil with acetylcysteine in the model of histotoxic hypoxia. Materials and methods. To study the antihypoxic properties, a model of acute histotoxic hypoxia was used. The studied compound was injected into the abdominal cavity of experimental mice three times with an interval of 30 minutes at 100 and 500 mg/kg of body weight, then after 30 minutes the toxicant was introduced. Comparators were oxymethyluracil and acetylcysteine. Results. The complex compound of oxymethyluracil with acetylcysteine in the model of acute histotoxic hypoxia statistically significantly was established to increase the lifespan of mice at a dose of 500 mg/kg of body weight. A dose of 100 mg/kg of the compound is practically ineffective. Limitations. The limitations of the study are related with antihypoxic properties of the new complex compound of oxymethyluracil with acetylcysteine previously studied in one model of hypoxia (histotoxic), because oxymethyluracil (as an antihypoxant) is most effective in this experimental model. For a final judgment on the antihypoxic properties of the studied compound, it is necessary to continue studies on other models of hypoxia. In addition, in order to identify possible synergism (potentiation) of the action of oxymethyluracil and acetylcysteine, it seems appropriate to conduct studies to evaluate the antihypoxic effect with their simultaneous administration (in the form of a simple mixture). Conclusion. A new complex compound of oxymethyluracil with acetylcysteine can be recommended for further wider (preclinical) research as a potential antihypoxant.

The aim of the study was to study the effect of hepatoprotective drugs on the expression of the Sod1 gene in rats with ethanol liver damage.Materials and methods. Male outbred white rats were used in the experiment. Five groups of animals were formed, 14 individuals each. Distilled water was administered to rats of the 1st group (control); Group 2 — ethanol at a dose of 5 g/kg of body weight; Group 3 — ethanol and heptor at a dose of 72 mg/kg; Group 4 — ethanol and mexidol at a dose of 50 mg/kg; Group 5 — ethanol and OMU at a dose of 50 mg/kg. The drugs were administered 1 hour before the introduction of ethanol. 24 and 72 hours after the introduction of ethanol (7 individuals), the animals were decapitated and the liver was removed. The expression level of the Sod1 gene was assessed using real-time reverse transcription PCR.Results. The fold change in Sod1 expression in rat liver after 24 h practically did not change in response to the introduction of ethanol to the animals. A tendency to a slight decrease was observed in relation to changes in the expression of Sod1 with the use of heptor and mexidol, while under the influence of OMU, the expression level increased moderately. After 72 h, the exposure to ethanol was accompanied by a slight decrease in the frequency of expression of the Sod1 gene. A similar trend was observed with respect to changes in Sod1 expression with the use of heptor, mexidol, and OMU.Conclusion. The results obtained indicate that the introduction of both ethanol and the prophylactic use of hepatoprotective drugs did not lead to significant changes in the level of Sod1 gene expression in rat liver. Additional studies are needed to identify the mechanisms of regulation of the antioxidant system, as well as the search for drugs that affect the transcriptional activity of genes.

Nowadays over the world absolute and relative number of aging population dramatically increases with life expectancy up and birth rate down. Aging and senescence assessment are assumed to reflect current changes, internal degeneration and various stressors respond ability (i.e. genetic, environmental and occupational factors) of human organism. Occupational experience time is leading risk factor and indicator for accelerated aging. Last years, many reports concerning aging rate dependence on physical and chemical occupational hazardous factors were published. Summarizing this exposures and their effects on aging reviews are almost absent despite many provided studies. Overview of main occupational neuropsychiatric, physical and chemical risk factors, that causes human aging acceleration presented here. Circadian rhythm disorders, allostatic load, heat stress, local vibration, chemical effects and suspended nanoparticles (fine dust) influences on aging and such signs as Alzheimer’s disease risk increase, telomere length decrease and epigenetic changes and possible interactions between them are also briefly presented. Agricultural, industrial workers, teachers and police officers aging acceleration is detected in results of analysis of biological age markers.

Control over use of genetically modified products is a vital task within a risk-oriented model for surveillance over food safety products all over the world including the Russian Federation. Our research goal was to examine domestically manufactured food products in order to determine whether they contained certain regulatory sequences typical for genetically modified organisms. We applied polymerase chain reaction with hybridization-fluorescent detection in real time mode to examine 77 food products samples; the task was to determine whether they contained DNA enhancer (E-35S) and promoter (P-35S) of S35 sequence belonging to cauliflower mosaic virus, terminator of nopaline synthase gene from Agrobacterium tumefaciens (T-NOS), 35S enhancer (E-FMV) and promoter (P-FMV) of Figwort mosaic virus, as well as vegetable DNA inducing soya DNA. When analyzing the extracted DNA, we didn’t detect transgenic elements in any samples; however, there were vegetable components reveled in them including 68.8% samples with soya DNA. We established that some sausages were falsified as they contained vegetable elements. In 15.6% cases data on a product structure turned out to be false because soya DNA was not listed on consumer package. Our research on determining soya DNA and transgenic elements in food products indicates that soya ingredients have been added into food products in spite of their absence in relevant documents as recipe components. All the obtained results taken into account, we assume it is necessary to improve control procedures for detecting genetically modified and vegetable components used as ingredients in food products as their falsification can make for changes not only in their consumer properties but also damage consumers’ health.