BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700817
N. V. Belosludtseva, T. A. Uryupina, D. A. Khurtin, N. V. Khunderyakova, G. D. Mironova
{"title":"Comparative Study of Cardioprotective Properties of Uridine-5'-Monophosphate and Uridine in a Rat Model of Myocardial Damage Induced by Isoprenaline","authors":"N. V. Belosludtseva, T. A. Uryupina, D. A. Khurtin, N. V. Khunderyakova, G. D. Mironova","doi":"10.1134/S0006350924700817","DOIUrl":"10.1134/S0006350924700817","url":null,"abstract":"<div><p>The effects of uridine and its monophosphoryl derivative on the level of the main biochemical markers of myocardial damage in the blood and on the electrical activity of the heart were investigated in a rat model of cardiomyopathy induced by isoprenaline. It was shown that administration of isoprenaline (150 mg/kg, subcutaneously) caused an increase in the activity of serum enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT), leading to an elevated AST/ALT ratio (De Ritis ratio), and enhanced activity of lactate dehydrogenase in blood lymphocytes, which confirms the development of myocardial damage in experimental animals. ECG analysis revealed prolongation of the RR, P-R, QT, and QTc intervals and the QRS complex, indicating that the duration of both depolarization and repolarization phases increased relative to the duration of the cardiac cycle in rats with isoprenaline-induced myocardial damage. Preliminary administration of uridine and uridine-5'-monophosphate to experimental animals at a dose of 30 mg/kg equally effectively prevented an increase in the enzymatic activity of AST and the De Ritis ratio, led to a decrease in the duration of P-R, QRS, QT, and QTc intervals, and partially normalized the metabolic activity of rat blood lymphocytes. These findings suggest that uridine and uridine-5'-monophosphate have a similar protective effect on the contractile function of cardiomyocytes and can be considered as agents for metabolic therapy in the treatment of ischemic heart disease.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"729 - 737"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700763
M. E. Solovieva, Yu. V. Shatalin, V. S. Akatov
{"title":"Paraptosis and Other Types of Nonapoptotic Regulated Cell Death","authors":"M. E. Solovieva, Yu. V. Shatalin, V. S. Akatov","doi":"10.1134/S0006350924700763","DOIUrl":"10.1134/S0006350924700763","url":null,"abstract":"<div><p>This review is devoted to modern concepts of paraptosis as one of the types of regulated cell death, in comparison with other types of cell death. Paraptosis is a form of cell death caused by stress of the endoplasmic reticulum (ER), accompanied by the accumulation of damaged or incorrectly folded proteins in it, extensive nonautophagic vacuolation of the cisterns of the endoplasmic reticulum and, in some cases, mitochondria, with subsequent damage to the mitochondria and cytoskeleton and cell death. Knowledge about the molecular mechanisms of paraptosis is of interest for the treatment of cancer diseases resistant to apoptosis-inducing agents.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"674 - 691"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700726
A. S. Galashin, M. V. Konakov, V. V. Dynnik
{"title":"Evolution of Ideas about the Mechanisms of Neuronal Network Hyperactivation and Burst Firing in Epilepsy. Contribution of Potassium-Induced Activation of Potassium-Conducting Channels to Network Hyperactivation","authors":"A. S. Galashin, M. V. Konakov, V. V. Dynnik","doi":"10.1134/S0006350924700726","DOIUrl":"10.1134/S0006350924700726","url":null,"abstract":"<div><p>The existing concepts of the molecular mechanisms of pathological hyperexcitability and synchronization of neural networks in epileptogenesis, including potassium, GABA, membrane (cellular) and synaptic (network) models, are discussed. The focus of such models is the imbalance between excitation and inhibition involving numerous positive and negative feedback loops in neural networks. The paper considers modern concepts of (1) the reliability of dynamic systems with a large number of negative feedback loops and (2) the degeneracy, that is, the ability of heterogeneous elements (channels and currents) to replace each other, as the basis for the stable functioning of hyperexcitable networks in channelopathy and hyperexpression of various channels. The paper suggests a possible mechanism for the spontaneous occurrence of convulsive activity and accumulation of potassium in the intercellular space, based on the activation of a group of cationic channels (HCN, K<sub>ir</sub>2.x , hERG, Na<sub>v</sub>1.х, and BK<sub>Ca</sub>), which provides reliability and high sensitivity of epileptiform activity to external and internal factors due to degeneracy and formation of a group of connections of positive feedback loops.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"639 - 648"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700830
S. I. Glukhov, E. A. Kuznetsova
{"title":"The Molecular Mechanisms of the FLASH Effect in Radiobiology","authors":"S. I. Glukhov, E. A. Kuznetsova","doi":"10.1134/S0006350924700830","DOIUrl":"10.1134/S0006350924700830","url":null,"abstract":"<div><p>The use of ionizing radiation at an ultra-high dose rate (≥40 Gy/s), which is called FLASH irradiation, contributes to the preservation of healthy tissues with a level of tumor control comparable to that of irradiation at a standard dose rate. This review summarizes the current knowledge obtained in studies of irradiation of tumor and normal cell lines and animals, including tumor carriers, in conventional and FLASH modes. For comparison, data on FLASH irradiation with photons, electrons, and protons, as well as ions of helium and carbon, are also provided. The biophysical, molecular biological, and immunological aspects of FLASH exposure necessary for understanding radiation-induced processes in cells and tissues in order to improve tumor radiotherapy are discussed.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"749 - 767"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700842
A. E. Shemyakov, A. R. Dyukina, S. I. Zaichkina, A. V. Agapov, G. V. Mitsyn, K. N. Shipulin
{"title":"The Results of FLASH Irradiation of Mice In Vivo with High-Energy Protons","authors":"A. E. Shemyakov, A. R. Dyukina, S. I. Zaichkina, A. V. Agapov, G. V. Mitsyn, K. N. Shipulin","doi":"10.1134/S0006350924700842","DOIUrl":"10.1134/S0006350924700842","url":null,"abstract":"<div><p>The effect of high-energy (660 MeV) proton irradiation at the phasotron accelerator in FLASH mode (80 Gy/s) compared with the standard proton exposure power of 3.0 Gy/min was studied. When irradiated in two modes at doses of 1.0 and 1.5 Gy, the induction of cytogenetic damage in bone marrow cells and the state of lymphoid organs (thymus and spleen) were evaluated; survival under total in vivo irradiation of mice was analyzed at doses of 7.0 and 8.0 Gy. The growth rate of a model tumor under ex vivo irradiation was determined at doses of 40 and 60 Gy. It has been shown that irradiation of animals in the FLASH mode at a dose of 1.5 Gy protected the proliferative activity of the spleen and also led to a decrease in cytogenetic damage in bone marrow erythrocytes according to the micronucleus test compared with the standard irradiation mode at a dose of 1.5 Gy, that is, a milder effect of the FLASH mode dose was observed. However, irradiation of mice in FLASH mode at high doses (7.0 and 8.0 Gy) led to earlier death of animals compared to the standard irradiation regime. A tumor node formed with further growth only after FLASH irradiation of a suspension of Ehrlich ascites carcinoma at a dose of 40 Gy; in all other groups a tumor was not formed.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"768 - 774"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S000635092470074X
E. A. Kuznetsova, N. P. Sirota
{"title":"Rotenone, Rhodamine 123, and Janus Green Induce Damage to Nuclear DNA in Ascites Tumor Cells from Mice. Rotenone and Rhodamine in X-Ray Irradiated Cells Contribute to the Maintenance of Genome Integrity","authors":"E. A. Kuznetsova, N. P. Sirota","doi":"10.1134/S000635092470074X","DOIUrl":"10.1134/S000635092470074X","url":null,"abstract":"<div><p>The mitochondrial inhibitors rotenone and rhodamine 123 and the Janus Green B dye are being studied in order to develop pharmacological agents that cause mitochondrial dysfunction and apoptosis. Since mitochondrial dysfunction is associated with the production of reactive oxygen species, it seems relevant to compare the DNA damage induced by these substances to cells of ascitic Ehrlich carcinoma and murine lymphocytic leukemia P388 with exposure to a known inducer of reactive oxygen species, that is, ionizing (X-ray) radiation. The level of DNA damage was assessed using an alkaline version of the Comet assay. The level of DNA damage induced by rotenone was comparable to irradiation at a dose of 4 Gy in both cell types. Post-radiation incubation reduced the level of DNA damage, which indicates DNA repair. Treatment of Ehrlich’s ascitic carcinoma cells with rhodamine 123 followed by washing did not cause this increase; however, irradiation at a dose of 4 Gy in the presence of rhodamine 123 induced an increase in the level of DNA damage, which significantly decreased after 1 h incubation. It can be assumed that pretreatment of cells with rotenone and rhodamine 123, which impair the work of mitochondria, contributed to the preservation of the integrity of nuclear DNA in irradiated cells. Exposure to Janus Green B caused increased DNA damage and cell death. Based on the alkaline version of the Comet assay, damage induced by these compounds can be considered as single- and double-strand breaks and alkali-labile (apurine/apirimidine) sites in DNA.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"656 - 666"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700696
A. G. Pogorelov, L. G. Ipatova, A. I. Panait, A. A. Stankevich, A. K. Yunusova, V. N. Pogorelova
{"title":"Innovative Biophysical Approaches for Quercetin Extraction from Plant Cells","authors":"A. G. Pogorelov, L. G. Ipatova, A. I. Panait, A. A. Stankevich, A. K. Yunusova, V. N. Pogorelova","doi":"10.1134/S0006350924700696","DOIUrl":"10.1134/S0006350924700696","url":null,"abstract":"<div><p>A method of extraction of quercetin from a plant cell based on the combined action of ultrasound and a metastable fraction of an aqueous solution is proposed. This treatment leads to more efficient release of the cytoplasmic component due to etching and/or mechanical destruction of the plant cell envelope. The oxidized fraction of the solution has the most pronounced extractive properties; however, it acts on quercetin by oxidizing the chromophore part of the molecule. According to the criterion of pigment preservation, the best extraction medium is the reduced fraction of water. Analytical methods were used to analyze the extract samples: UV-Vis spectroscopy, gel electrophoresis of proteins, <sup>1</sup>H NMR spectroscopy, and QCM weighing, as well as scanning electron microscopy.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"609 - 616"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700702
T. Mamedov, A. Shvirst, M. V. Fedotova, G. N. Chuev
{"title":"Noncontact Atomic Force Microscopy for Studies of Biomolecules in Liquids","authors":"T. Mamedov, A. Shvirst, M. V. Fedotova, G. N. Chuev","doi":"10.1134/S0006350924700702","DOIUrl":"10.1134/S0006350924700702","url":null,"abstract":"<p><b>Abstract</b>—Noncontact atomic force microscopy, a type of scanning probe microscopy, has been actively used in the last 2 decades to study hydrated biomolecules. In particular, as the analysis of modern literature shows, it is very promising in the study of adsorbed biomacromolecules and biomacromolecular complexes at the interface or on the surface of membranes. This mini-review describes the basics of this method and its application to biomolecules; the requirements for the method and the possibilities of its extension due to additional processing of the experimental data obtained using theoretical analysis, molecular modeling and machine learning are discussed.</p>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"617 - 629"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700660
V. S. Shubina, Yu. V. Shatalin, A. L. Shatsauskas, A. S. Fisyuk
{"title":"The Kinetics of Oxidation of 3-Aminopyridin-2(1H)-ones by Hydrogen Peroxide in the Presence of Horseradish Peroxidase","authors":"V. S. Shubina, Yu. V. Shatalin, A. L. Shatsauskas, A. S. Fisyuk","doi":"10.1134/S0006350924700660","DOIUrl":"10.1134/S0006350924700660","url":null,"abstract":"<div><p>The aim of this study was to evaluate the kinetic parameters of the oxidation of some 3-aminopyridine-2(1H)-ones by hydrogen peroxide catalyzed by horseradish peroxidase and the affinity of horseradish peroxidase to these compounds. It has been shown that the oxidation of 3-aminopyridine-2(1H)-ones follows kinetics of the pseudo-first order. A hyperbolic decrease in the observed reaction rate constant (<i>k</i><sub>obs</sub>) was also found with an increase in the initial concentration of 3-aminopyridine-2(1H)-ones. The dependence of <i>k</i><sub>obs</sub> on the concentration of the enzyme was linear, suggesting competitive inhibition of oxidation by the reaction product. It was found that an increase in the polarity of the substituent in the fourth position leads to an increase in the rate of oxidation of pyridinones. <i>V</i><sub>max</sub>/<i>K</i><sub>m</sub> values were also higher for compounds carrying polar substituents in the fourth position. This kinetic parameter (<i>V</i><sub>max</sub>/<i>K</i><sub>m</sub>) reflects the substrate specificity of the enzyme. The data we obtained clarify the mechanisms of interaction between horseradish peroxidase and 3-aminopyridinones and suggest that 3-aminopyridinones can be used to develop sensitive methods for the detection of hydrogen peroxide and modification of immune enzyme analysis techniques.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"591 - 596"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiophysicsPub Date : 2025-02-26DOI: 10.1134/S0006350924700799
V. F. Kitchigina
{"title":"Theta Oscillations and the Comparator Function of the Hippocampus","authors":"V. F. Kitchigina","doi":"10.1134/S0006350924700799","DOIUrl":"10.1134/S0006350924700799","url":null,"abstract":"<div><p>Detecting environmental changes/novelty is of basic importance for adaptive behavior. By comparing the current context with the previous one, living organisms can make predictions and adjust their actions. The mechanisms and structures of the brain involved in the function of comparison have not yet been sufficiently elucidated. The available studies emphasize the special contribution of the hippocampus to the process of comparison; it is indicated that the identification of novelty is carried out by hippocampal neurons through the mechanisms of match/mismatch, or misalignment. Here, we provide information about existing hypotheses of how these mechanisms occur, which other brain structures are involved in detecting inconsistencies, how they are related to the hippocampus, and what processes contribute to this. In particular, it is assumed that it is not novelty in itself, but only novelty that contrasts with previously acquired experience that initiates the process of misalignment. The arguments that the theta rhythm plays a crucial role in the functioning of the hippocampus as a comparator are analyzed. Theta oscillations caused by the appearance of a new signal or a change in a situation mediate the mechanism of temporal coordination of structures involved in the comparison function. In comparison, the theta rhythm functions as an active filter: it participates in the selection and transmission of a new signal to the registration system in the hippocampus. An increase in theta oscillations and their coherence in the brain structures processing new information serves as a signal of misalignment, facilitating a change in behavior strategy. In addition to theta rhythm, gamma oscillations are also involved in comparison: during the generation of theta rhythm in the prefrontal cortex, the temporary coincidence of gamma oscillations in other areas of the brain with a certain phase of the theta cycle can perform the function of comparison during the memorization process. A deep understanding of the mechanisms of comparator function and its disorders can help in the treatment of pathologies such as schizophrenia, Alzheimer’s disease, and temporal lobe epilepsy.</p></div>","PeriodicalId":493,"journal":{"name":"Biophysics","volume":"69 4","pages":"706 - 719"},"PeriodicalIF":4.033,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143496687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}