Aim: To investigate changes in oxidative stress indicators in rats under conditions of long-term ethanol exposure.
Materials and Methods: We studied the effect of prolonged exposure to ethanol on the activity of free radical processes in the gonads of rats of both sexes. Experimental animals were divided into 2 groups: Group I (control group) rats, which were injected with distilled water orally for 28 days; II group – which for 28 days were injected intragastrically with a 30% ethanol solution at the rate of 2ml/100g of body weight once a day.
Results: The conducted experimental studies showed that the level of free radicals increases in animals that were injected with ethanol for 28 days, as indicated by an increase in the ROS index by 1.6 times in males and 1.7 times in females. Lipid peroxidation processes are also activated, as evidenced by an increase in the level of initial products of the lipoperoxidation chain – HPL by 54.6%, intermediate products – TBP by 57.9% and final products – SHO – by 80.3% in males and by 68.2%, respectively , 80.9% and 84.6% in females. Along with this, the activity of oxidative modification of proteins in the organs of the reproductive system of the experimental group of animals also increased. In particular, the level of OMР370 in the testes of male rats increased by 89.1%, and OMР430 increased by 56.4% from the level of animals that were not given ethanol. In the ovaries of female rats, the level of OMР370 increased by 112.%, and OMР430 increased by 60.7% from the level of animals without simulating ethanol intoxication. Therefore, we were able to establish significant changes and disturbances in the processes of free radical oxidation in the organs of the reproductive system of animals under the toxic effect of ethanol, which can negatively affect the reproductive function and quality of offspring in animals that were simulated ethanol intoxication.
Conclusions: In animals of both sexes, under the conditions of chronic ethanol exposure, there is an increase in free radical oxidation indicators, namely ROS, lipid peroxidation, oxidative modification of proteins, and the growth indicators in females are more significant than in males. This indicates a negative effect of chronic ethanol intoxication on the state of the membrane structures of germ cells, with DNA damage, which can lead to a violation of the function of the genital organs.
UDC 612.822:616.831-092.18
This review presents an analysis and synthesis of the world literature, forming an up-to-date vision of the func- tional system of utilisation of end metabolites from the central nervous system, discussing impaired brain clearance in some neurodegenerative nosologies, as well as in strokes and traumatic brain injury. The central nervous system, lacking a classically conventional lymphatic system, requires alternative systems to clear the brain of potentially toxic cellular metabolic products. Over the past decade, world scientific sources have highlighted a new system of views, or the concept of the so-called glymphatic system, which makes it possible to drain the brain from extracel- lular harmful substances dissolved in the interstitium. Water channels such as aquaporin-4 (AQP4) are an important system component associated with neuropathologies such as Alzheimer's. The clearance of amyloid β (Aβ) and tau (tau) proteins associated with Alzheimer's disease, for example, is reduced due to the impaired function of the glym- phatic system in the absence of AQP. The detected changes in AQP4 expression associated with certain pathologies make it possible to predict that this water channel could be a potentially interesting pharmacological target. Recent studies in this context have also shown that biomarkers of traumatic brain injury are eliminated from the brain through the glymphatic system. The degree of suppression of glymphatic function under these conditions may affect the likely prognosis after traumatic brain injury. The obtained results predict the clinical value of pharmacological manipulations of the glymphatic system after acute traumatic brain injury. It has also been shown that with ageing, the processes of glymphatic drainage in the CNS decrease, which can contribute to the accumulation of misfolded and hyperphosphorylated proteins and thus make the brain susceptible to the development of neurodegenerative pathology. According to the experimental evidence presented in modern scientific sources, the concept of "acute or chronic glymphatic insufficiency" should be distinguished, and the issue of finding criteria for their correct as- sessment should be updated. It is known that the number of vasteosomes or starchy bodies can be considered a marker of chronic glymphatic insufficiency. According to the researchers, this knowledge will facilitate the study of glymphatic insufficiency and allow us to understand which moderating variables will critically impact the function- ing or failure of this system. Moreover, the fact that they are markers of chronic glymphatic insufficiency gives them promising clinical significance.
Global demand for crude oil has grown signi- ficantly over the past two decades. However, conventional light crude oil production is declining, and more and more deposits of heavy and waxy oil, including high waxy ones, are being developed, creating new technological challenges at every level of the process, from production to trans- portation and refining. Among the various problems, the main one is wax deposition. Since the costs of maintenance, repair, and achieving the required low-temperature properties of commercial oil products are very high, solving this problem becomes critical. The paper discusses the existing problems of production, transportation, and refining of waxy crude oil and analyzes the methods of their solution.
УДК: 612.822:616.831-092.18
This review aims to summarize the world's scientific sources that highlight the current vision of the role of the brain glymphatic system in the utilisation of end metabolites from the central nervous system. It has been reported that protein clots or aggregates that are produced in brain cells and, importantly, failure of their elimination can cause cognitive problems in neurodegenerative diseases. In particular, Alzheimer's and Parkinson's dis- ease, as well as the other neurodegenerative diseases, the aging process can be reproduced in experimental models by overproducing these conglomerates.Current investigations are focused as well on clarifying changes in brain glymphatic drainage in the condition of traumatic brain injury. Modern research has shown that acute brain injury, including traumatic brain injury, subarachnoid hemorrhage, or stroke, dramatically alters glymphatic function. It is evident that aging is a critical risk factor for neurodegenerative diseases. It has also been experimentally proven that glymphatic activity decreases with aging. Accordingly, this can lead to the accumulation of misfolded and hyperphosphorylated proteins, and thus the brain becomes vulnerable to the development of neurodegenerative pathology. Comprehensive analysis of the causes and mechanisms of glymphatic system dysfunction will help to predict and develop methods for diagnosing and treating serious neurodegenerative diseases and traumatic brain injuries.
УДК 612.433.65
У представленому огляді викладено структуровані дані, наявні у сучасній літературі щодо соматотропного гормону, молекулярні механізми активації внутрішньоклітинних шляхів за його участі та передачі сигналу, а також фізіологічні наслідки сигналінгу соматотропного гормону. Незважаючи на інтенсивні дослідження впродовж останнього десятиліття, молекулярні механізми сигналінгу, пов’язаного з гормоном росту, залишаються не до кінця зрозумілими. Згідно з сучасними уявленнями, гормон росту активує сигнальний шлях Янус-кінази 2 - JAK2 та спряжених STAT-білків - сигнальних траyсдукторів та активаторів транскрипції, і нещодавні дослідження представили нове розуміння механізму активації JAK2 шляхом зв’язування гормону росту з його рецептором. Активація JAK2 необхідна для опосередкованої гормоном росту активації STAT1, STAT3 та STAT5, а негативна регуляція сигналізації JAK2 – STAT включає важливий етап у контролі цього сигнального шляху. Попри достатню кіль- кість сучасних даних, представлених у літературі, для адекватного розуміння механізму активації Янус-кінази 2 необхідна більш детальна структур- на інформація, що стосується JAK та комплексу JAK - цитокінових-рецепторів. На наш погляд, пред- ставлені сучасні дані сприятимуть поглибленню розуміння фундаментальних основ фізіології, біо- хімії, ендокринології, тощо студентами–медиками різних спеціальностей, а також фахівцями теоретичної та прикладної медицини.