Electrocorticography in rats has broad indications for use in biomedical research. This is due to the high translational potential from rodents to humans, established by comparative experimental electrocorticography under the action of a wide range of neurotropic substances. The paper presents the features and technique of manufacturing an electrocorticographic sensor, as well as the technique of its implantation in rats. The sensor was experimentally tested according to the validity of the received signal under the conditions of administration of neurotropic pharmacological probes: strychnine, corazole, sodium cyanide, tiletamine with zolazepam, xylazine, dexmedetomedin and diisopropylphenol. According to ethological and pathomorphological criteria, the tolerability of the structure in the skull by rats was assessed. It has been established that the design of the sensor and the technique of its implantation in rats are safe and effective for long-term monitoring in conditions of free movement. The correspondence of the received data to the expected ones and the high quality of the signal-to-noise ratio make it possible to consider the signal from the sensor as valid and diagnostically valuable. The design is well tolerated by rats and does not cause pronounced changes in the histomorphological picture of the brain in the area of electrode attachment to the cortex for 90 days after implantation.

Poisoning with acylating pulmonary toxicants results in toxic pulmonary edema (TPE), the approaches to treatment of which are limited. The lung injury similar to poisoning with acylating pulmonary toxicants can be simulation through body’s exposure to the fluoroplastic thermal degradation products containing perfluoroisobutylene. The study was aimed to compare toxic pulmonary edema manifestations in the laboratory animals poisoned with an acylating pulmonary toxicant (carbonyl chloride) and fluoroplastic thermal degradation products. Animals (male rats, n = 78) were divided into three groups: controls; Poisoning 1, where the animals were exposed to carbonyl chloride; Poisoning 2, where the animals were exposed to the fluoroplastic thermal degradation products. The animals’ lung/body ratio was determined and the partial pressure of arterial oxygen (PaO2) and carbon dioxide (PaCO2) was assesed 10 min, 1, 3, 6, 24, and 48 h after the exposure. Histological examination of lung tissue was performed 3 and 6 h after the exposure. The increase in the lung/body ratio, decrease in PaO2, and increase in PaCO2 relative to controls were revealed 3, 6, 24, and 48 h after the exposure to carbonyl chloride and fluoroplastic thermal degradation products. The signs of the interstitial toxic pulmonary edema phase were detected 3 h after the exposure to the studied toxicants, and the signs of alveolar phase were revealed after 6 h. Similar changes were identified in animals of the experimental groups. The findings have shown that the exposure to carbonyl chloride and the fluoroplastic thermal degradation products containing perfluoroisobutylene lead to similar changes in the early post-intoxication period.

Inhalation intake of acylating pulmonary toxicants (phosgene and perfluoroisobutylene) leads to the formation of toxic pulmonary edema; the pharmacological approaches to its treatment are inefficient. Respiratory therapy is successfully used to treat the pulmonary edema of nontoxic genesis. Data on the efficiency of respiratory support during toxic pulmonary edema are limited. The aim of this study was to experimentally test the efficiency of protective artificial ventilation with maintenance of positive end-expiratory pressure in the early period of intoxication with the products of thermal degradation of fluoroplast-4. In the experimental study, it was established that early implementation of protective artificial ventilation with maintenance of end-expiratory pressure is an efficient approach for the correction of toxic pulmonary edema in rabbits in the early period of intoxication with the products of thermal degradation of fluoroplast-4, which have a toxic pulmonary effect. Respiratory support can be a promising approach for the treatment of toxic pulmonary edema caused by intoxication with acylating pulmonary toxicants.

The paper summarizes the experience of the use of psychoactive compounds by the armies of foreign countries. The analyzed sources indicate the widespread use of psychostimulants, toxic substances and narcotic drugs. The latter often contributed to outbreaks of drug addiction among troops and civilians.

Фенотипический и функциональный анализ линии моноцитов THP-1 как модели воспаления 1 Федеральное государственное автономное образовательное учреждение высшего образования «Национальный исследовательский университет ИТМО» Министерства науки и высшего образования Российской Федерации, 197101, г.Санкт-Петербург, Российская Федерация 2 Федеральное государственное бюджетное учреждение «Научно-исследовательский институт гриппа имени А.А.Смородинцева» Министерства здравоохранения Российской Федерации

This paper continues the discussion of higher fungi toxins, here their toxic nitrogen-free organic compounds are considered. The challenges linked to their study and systematization are discussed. Modern concepts of toxic processes induced by toxic terphenyls, sesquiterpenes, triterpenes, trichothecenes, and oligoisoprenoids are analyzed. Some recently discovered cytotoxic compounds of a similar structure are presented. It is concluded that the systematic study of nitrogen-free toxins is in demand, and this area of research has still not been well investigated.

We studied the content of aquaporin-5 (AQP5) and epithelial sodium channel (ENaC) in rat lungs during the development of toxic pulmonary edema (TPE) caused by intoxication with phosgene and perfluoroisobutylene (1.5 LC50). The lung body weight index (LBI) was calculated and histological examination of the lung tissues was performed. Localization and expression of AQP5 and ENaC were determined by immunohistochemistry. Intoxication led to a significant (p<0.05) increase in LBI and histological changes typical of TPE 1 and 3 h after the exposure. In 1 and 3 h after phosgene intoxication, the AQP5 and ENaC content significantly (p<0.05) increased in comparison with the control. Similar changes in the AQP5 and ENaC content were observed 1 and 3 h after exposure to perfluoroisobutylene. It was hypothesized that AQP5 plays an important role in the formation of TPE caused by intoxication with acylating pulmonotoxicants. An increase in the content of ENaC can be considered as a compensatory reaction of the body aimed at clearance of the alveolar fluid.

В статье рассматривается проблема допустимости учета затрат, понесенных на осуществление компенсационного озеленения (восстановления зеленых насаждений в натуре) в счет выплаты восстановительной стоимости за их уничтожение. Автор приходит к выводу о необходимости распространения норм природоохранного законодательства на общественные отношения, связанные с охраной и воспроизводством зеленых насаждений, произрастающих на землях населенных пунктов. Кроме того, анализируется правовая природа осуществления компенсационного озеленения, выплаты восстановительной стоимости. В рамках статьи обращается внимание на существующие недостатки их квалификации в качестве форм возмещения вреда окружающей среде. Делаются основные выводы, даются рекомендации по изменению действующего законодательства.

Higher fungi represent a group of living organisms that remain poorly studied in terms of mycology and biochemistry. Among their secondary metabolites, toxic compounds are of particular interest, since they may be an etiological factor causing acute food intoxications, i.e., mycetismi. This review summarizes the information on the fungal species distributed in Russia and the toxicological properties of some of them as producers of simple nitrogen-containing compounds. The role of individual substances in toxidromes is discussed. The article considers a number of minor components that may have insignificant individual effects due to their low concentrations but may make a significant contribution to the modification of the toxic effect caused by a primary compound. A summary of data on new syndromes associated with toxins of higher fungi is presented. It was concluded that the combined effects of toxins can play an important role in intoxication with nitrogen-containing compounds.

Perfluoroisobutylene a is pulmonotoxic chemical generated during pyrolysis of perfluoro-nalkanes (polytetrafluoroethylene). The mechanisms of acute pulmonary toxicity induced by perfluoroisobutylene have not been studied yet. The analysis of tissues of brown frogs showed that the products of polytetrafluoroethylene pyrolysis induce typical inflammatory response in the lungs (fluid accumulation, erythrocyte stasis, desquamation of the epithelium, and capillary plethora in lung septa) and oropharyngeal cavity (degeneration of ciliated epithelium, hyperemia of underlying vessels with plasmatic imbibition of the connective tissue, and margination of segmented leukocytes and monocytes). The absence of surfactant is a specific feature of the blood—air barrier of the oropharyngeal cavity in frogs compared to the lungs. It can be hypothesized that toxic effects of perfluoroisobutylene are determined by its influence on epithelial (pneumocytes and cells of nonkeratinized stratified ciliated epithelium) and endothelial cells. Even though the effects of the agent on surfactant cannot be excluded, they do not determine the probability of development of inflammatory response.

Rats were exposed to fluoroplast-4 pyrolysis products (sample weight 2.6 g, pyrolysis temperature 440-750°C, pyrolysis duration 4 min) containing perfluoroisobutylene over 15 min. Lung tissue samples for histological and electron microscopic examination were isolated in 3 and 30 min after intoxication and processed routinely. Histological examination revealed no structural changes in the lungs. In ultrathin sections of rat lungs, some changes in the structure of type I pneumocytes were detected in 3 min after the exposure: detachment of cytoplasmic processes and the appearance of transcytosis pores. These changes attested to impaired cell—cell interactions and their adhesion to the basement membrane, where structural disorganization and edema of the collagen matrix were observed. In 30 min following exposure, the signs of damage to type I pneumocytes became more pronounced. The increase in the equivalents of transcellular and paracellular permeability in the alveolar lining profile was observed. No changes in the pulmonary capillary endotheliocytes were detected, which suggest that type I pneumocytes are the primary target of the toxic effect of perfluoroisobutylene. The vulnerability of a particular cell population, in view of specific metabolism of these cells, can be the key to deciphering of the mechanisms of the toxic effect of pyrolysis products of fluorinated polymer materials.

Purpose of research – To develop an experimental model of intoxication of laboratory animals by polyacrylonitrile pyrolysis products. Materials and methods. The study was performed on the rats. Pyrolysis of polyacrylonitrile fibers was carried out at temperature of 270–350 °C. The laboratory animals were exposed to static inhalation intoxication by pyrolysis products for 15 min. Vital signs were determined in animals before and 5 minutes after intoxication. Arterial blood oxygenation index and acid-base state parameters were evaluated at 10 min after exposure. Qualitative detection of cyanides in brain and myocardial samples obtained 15 minutes after intoxication was carried out by gas chromatography. Results and discussion. It was found that the weight of the material (containing 85 % polyacrylonitrile), which pyrolysis products lead to the death of 50 % of laboratory animals within 24 hours after exposure, was 0.81 ± 0.15 g. The animals showed signs of poisoning by substances interrupting the processes of cell bioenergy when exposed to pyrolysis products obtained under specified conditions. The evident bradycardia and bradypnea (p < 0,05), and significant decrease in rectal temperature was marked. The exposed animals did not differ (p > 0,05) from the rats of the control group by the parameters of oxygenation. The signs of decompensated metabolic acidosis were detected in blood. The cyanide peak was detected by gas chromatography with a retention time of 3.78 min in brain and heart muscle biopsies. The experimental model, in which inhalation exposure of pyrolysis products of polyacrylonitrile fibers led to severe intoxication of laboratory animals, was developed. The model can be used to search for means of etiotropic and pathogenetic therapy of poisoning by combustion products of nitrogen-containing polymeric materials.

Today, oncological diseases are an important social problem, as they occupy leading positions in the structure of mortality, lead to increased disability, reduced working capacity and quality of life of a significant part of the population worldwide. Among the methods used to treat malignant neoplasms, chemotherapy has been actively used in recent years. Its popularity is associated with the development and implementation of new chemotherapeutic drugs that can improve the prognosis, increase the duration and quality of life of patients. To date, more than 150 antitumor agents have been used in clinical practice, new therapeutic regimens have been tested, which allows expanding the possibilities and improving the results of treatment of cancer patients. However, the development of drug-induced liver damage in cancer patients on the background of chemotherapeutic treatment remains an extremely important problem of modern oncology. On the one hand, it is not always possible to cancel a chemotherapeutic drug because of the high risk of disease progression. On the other hand, continued therapy can lead to serious and irreversible damage to a number of body systems, including the liver. So, according to various authors, gastrointestinal toxicity is observed in more than 90% of cases against chemotherapy. A similar complication is associated with the ability of antitumor drugs to exert cytotoxic and cytostatic effects, but not only on malignant cells. It is known that antitumor drugs are active both in relation to malignant cells and in healthy cells, which is manifested by clinically significant side effects. In this connection, it is necessary to actively introduce methods of primary and secondary prevention of toxic liver damage in the practice of chemotherapeutic treatment in cancer patients.