Neurotransmitters are found not only in animals, but also in other living organisms, including plants. They are found in other living organisms, including plants. However, the data on the functions of these compounds in the plant world are far from being comprehensive. In particular, the issue concerning their impact on plant cell death still awaits further research.  In the present work, the effects of neurotransmitters on programmed cell death and the formation of reactive oxygen species (ROS) in plants were tested. Programmed cell death was estimated from the destruction of cell nuclei, and ROS was determined using 2',7'-dichlorofluorescein. Dopamine, norepinephrine, serotonin, histamine, acetylcholine and its synthetic analog acetylthiocholine were used. The catecholamines dopamine and norepinephrine at concentrations of 0.01–1 mM suppressed the destruction of guard cell nuclei in the epidermis of pea leaves, which was caused by KCN. Serotonin and acetylcholine at a concentration of 1–3 mM, on the contrary, increased the destruction of nuclei that was induced by KCN. Histamine and acetylthiocholine had no effect on KCN-dependent destruction of nuclei at concentrations of 0.01–3 mM. Acetylthiocholine at a concentration of 3 mM, in contrast to natural neurotransmitters, caused the destruction of guard cell nuclei in the absence of KCN. Dopamine, norepinephrine, and serotonin reduced the formation of ROS in the epidermis of pea leaves, which was induced by menadione. Histamine, acetylcholine and acetylthiocholine did not have a similar effect. The results demonstrate that dopamine, norepinephrine and serotonin have antioxidant properties in plants. In addition, dopamine and norepinephrine can prevent cell death.

Histone proteins are key epigenetic factors, which play an important role in chromatin dynamics and gene activity regulation. They are divided into two broad classes: canonical histones and their variants. Canonical histones are expressed mainly during the S-phase of the cell cycle, as they are involved in DNA packaging during cell division. Histone variants are histone genes that are expressed and regulate chromatin dynamics throughout the cell cycle. Due to the functional and species diversity, various families of histone variants are distinguished. Some proteins may differ slightly from canonical histones, while others, on the contrary, may have many important structural and functional features that affect nucleosome stability and chromatin dynamics. In order to assess the variability of the H2A histone family and their role in nucleosome structure, we performed a bioinformatic analysis of the amino acid sequences of the H2A histone family. The clustering performed by the UPGMA method made it possible to reveal two main subfamilies of H2A proteins: short H2A and other H2A variants demonstrating highly conserved amino acid sequences. We also constructed and analyzed multiple alignments for various H2A histone subfamilies. It is important to note that the proteins of the short H2A subfamily are not only the least conserved within the H2A family, but also have features that significantly affect the structural properties of the nucleosome. In addition, we performed a phylogenetic analysis of short H2A, which resulted in the identification and characterization of individual clades on the phylogenetic tree for the variants H2A.B, H2A.P, H2A.Q, H2A.L.

Neutrophils release decondensed nuclear chromatin or Neutrophil Extracellular Traps (NETs) in response to a great number of physiological stimuli to protect the host from pathogens. However, NETs have recently been shown to play an important role in the pathogenesis of autoimmune, inflammatory, and malignant diseases. Therefore, understanding the molecular mechanisms underlying NETs formation, usually leading to the neutrophil death (NETosis), is extremely important to control the aberrant release of chromatin. Mitogen-activated protein kinases (MAP-kinases) are involved in various cellular functions such as oxidative burst, chemotaxis, degranulation, adhesion, and apoptosis, but their role in NETosis is not well understood. Three families of MAP-kinases, p38, ERK1/2, and JNK, have been described in human neutrophils, and we investigated the contribution of p38, ERK1/2, and protein kinase B Akt1/2 in oxidative burst and NETosis using inhibitory analysis. We have shown that MAP-kinase p38 as well as protein kinase B Akt1/2 are activated upon stimulation of oxidative burst and NETosis with calcium ionophore ionomycin. However, these kinases are not involved in the oxidative burst induced by diacylglycerol mimetic phorbol 12-myristate 13-acetate (PMA) but are involved in PMA-induced NETosis.

Animal husbandry is a rapidly developing branch of agriculture, increasing the volume of production annually, and keratin-containing waste (feathers, bristles) make up the majority of all waste from this industry. The development of methods of environmentally friendly processing of such waste to obtain valuable resources (amino acids and oligopeptides) is an important mission of modern science, including biotechnology. One of the ways to dispose of animal husbandry waste that meets modern trends in the development of a green economy is the use of microorganisms and their enzymes. The possibility of obtaining keratinolytic enzymes of Aspergillus clavatus VKPM F-1593 under deep conditions with various sources of nitrogen and carbon, including with the growth of the producer on animal waste, was studied. The highest target activity (96.1 E) was achieved using mixed carbon and nitrogen sources: inorganic – sodium nitrate, easily digestible organic – fish meal hydrolysate and hard–to-reach organic – ground chicken feather. Varying the content of various substrates in the composition of fermentation media allowed not only to regulate the level of proteolytic activity, but also to reach the peak of producer activity on different days of cultivation. The specific keratinase activity of A. clavatus VKPM F-1593 (pI 9.3) to various protein substrates with the activity of a commercial proteinase K. Both enzymes showed a similar level of activity regarding most of the substrates used. However, protease A. clavatus VKPM F-1593 has a greater overall proteolytic activity, which confirms the prospects of this culture for biodegradation of animal waste.

Cardiac tissue contains adrenergic receptors (AR) not only of the beta type, but also of the alpha type (α-AR). Both types of ARs play significant role in regulation of cardiomyocytes electrophysiology in different parts of the heart, including the atrioventricular node (AVN). An augmentation of α₁-AR mediated component of adrenergic signaling results in impaired conduction of excitation in the heart and onset of various rhythm disturbances including AVN-associated arrhythmias. The activation of α₁-AR facilitates anionic transmembrane transport causing electrophysiological changes in myocytes. Current study is aimed to the investigation of the effects of anion/chloride blockade on α₁-AR-mediated proarrhythmic alteration of AVN functioning. Functional characteristics of AVN including AVN conduction time, AVN refractoriness and the AVN conduction alterations were examined via recording of surface electrograms in Langendorff-perfused isolated rat heart (Wistar, 250 ± 30 g). Phenylephrine was used as α₁-AR agonist. Probenecid demonstrating anion/chloride transmembrane conductance blocking activity was used to modify Phe-induced α₁-AR-mediated effects in AVN. The activation of α₁-AR by Phe results in a significant increase in the duration of AV intervals (N = 10, p < 0.001) and effective refractory period (ERP) in the AVN (by 9.8% ± 1.2%, n = 10, p < 0.001). Also, Phe induces AV-blocks of conduction and oscillations in atrioventricular delay (N = 10) at the stimulation rates close to ERP. Probenecid significantly reduces the magnitude of AVD oscillations during non-stationary conduction in the AV node. In addition, probenecid attenuates ERP prolongation caused by Phe (107 ± 4 ms, N = 6) and 114.2 ± 5.35 ms (N = 10) in presence of only Phe and Phe with probenecid, respectively, returning its values toward typical for normal conditions. In conclusion, probenecid maintains physiological mode of AVN conduction when α₁-AR are stimulated. This also suggests that chloride ion channels and anion carriers may contribute to the α₁-AR-mediated AVN arrhythmias.

Titanium dioxide or aminopropylsilanol nanoparticles were shown to be effective vehicles for delivering oligodeoxyribonucleotides and deoxyribozymes to cells to affect target nucleic acids. In this paper, the proposed principle of the delivery has been implemented in relation to oligoribonucleotides (ORN), components of short interfering RNAs (siRNAs). It has been shown that the obtained ORN-containing nanocomplexes (Si~NH₂▪ORN) based on aminopropylsilanol nanoparticles penetrate eukaryotic cells. These nanocomplexes have been investigated as agents for suppressing the replication of influenza A virus (IAV) in the cellular system. It has been shown that the ORN strands targeted to (+)RNA and (–)RNA of the IAV 5th segment reduces the titer of the virus by 99.7% and 98.4%, respectively. Thus, oligoribonucleotides in the Si~NH₂▪ORN nanocomplexes effectively inhibit the replication of the influenza A virus.

We studied the effect of stevia leaf extract, saccharinate and cyclamate in various dosages on the glycogen content of blood leukocytes in mice, as a necessary substrate for the realization of phagocytosis. An increase of glycogen content was found in all experimental groups which obtained sweeteners at a dosage of 10 mg/g of body weight. The effect of sweeteners on the differential leukocyte counts was found only for mice treated with stevia leaf extract at a dosage of 10 mg/g of body weight. They demonstrated increase of neutrophil-to-lymphocyte ratio. New data expand our understanding of the metabolism of sugar substitutes in the organism and their effect on physiological systems, in particular the hematopoietic and immune systems.

The search and testing of drugs with senolytic activity is one of the new directions in gerontology. The number of “senescent” cells that increases with age contributes to the development of age-related diseases and chronic non-infectious inflammation. Removing “senescent” cells or suppressing their influence on surrounding tissues seems a logical step to improve the quality of life and, possibly, prolong lifespan. However, drugs that have senolytic and senomorphic activity in model systems cause the development of a number of side effects in clinical trials. In this review, we consider the main advances in the field of senotherapy, the prospects for the use of senotherapy drugs, and the limitations that researchers and clinicians may encounter.