scholarly journals The role of mitochondria in the myocardium of senescent Meriones unguiculates

2017 ◽  
Vol 8 (4) ◽  
pp. 512-520
Author(s):  
Y. Potapenko ◽  
O. Dyomshina ◽  
G. Ushakova
Keyword(s):  
Oxidative Stress ◽  
Aspartate Aminotransferase ◽  
Large Scale ◽  
Cell Damage ◽  
Anaerobic Respiration ◽  
Metabolic Processes ◽  
Metabolic Disturbances ◽  
Irreversible Damage ◽  
Active Forms Of Oxygen

According to the mitochondrial theory of aging, changes in the functional state of mitochondria, which lead to excessive formation of active forms of oxygen, are the main factor in the development of age changes in organs and tissues of the whole organism. The assessment of the mitochondria state of the heart of senescent gerbils (Mongolian Gerbilia, Meriones unguiculates Milne-Edwards, 1867). It is proved that the aging of the heart is preceded by the appearance of dysfunction in mitochondria. The disturbance of metabolic processes in the myocardium of gerbils over the age of two years was established, which was accompanied by activation of oxidative stress by increasing the concentration of TBK-active compounds. An increase in the concentration of cytochrome C in cytosol has been shown due to the destructive effects of oxidized products on the outer membrane of mitochondria and enhancement of its permeability. The violation of bioenergetic processes, increase of the anaerobic respiration and the accumulation of lactate and unoxidative metabolites, which increases oxidative stress and cell damage, are determined. We established that for gerbils the critical age for senescence is 24 months. Major metabolic changes in the heart occur mostly at this age. This is marked by activation of prooxidants formation, proteolytic processes (decrease in total protein concentration) and inhibition of aminotransferase activity in cytosol. The switching of metabolic processes in the mitochondria of the heart with the participation of aminotransferases has been registered: increased activity of the mitochondrial isoenzyme alanine aminotransferase and reciprocal reduction of aspartate aminotransferase. After two years of age in the experimental gerbils the intensification of adaptive processes was established: activation of catalase, γ-glutamyltransferase, relative restoration of the activity of alanine and aspartate aminotransferase, thus maintaining the processes of the vital activity of the whole organism, but at a new metabolic level. With age, irreversible damage to cardiomyocytes occurs, which gradually lose the ability to convert lactate, resulting in its increase, and the processes of its utilization are inhibited. The results confirm the key role of mitochondria in the process of aging of the myocardium. However, when gerbils reach the 36 months of age the metabolic disturbances in the myocardium reach their peak, resulting in large-scale cell damage. 

MicroRNAs in Noise-Induced Hearing Loss and their Regulation by Oxidative Stress and Inflammation

2020 ◽  
Vol 21 (12) ◽  
pp. 1216-1224
Author(s):  
Fatemeh Forouzanfar ◽  
Samira Asgharzade
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Hair Cell ◽  
Noise Exposure ◽  
Cell Damage ◽  
Sensory Cells ◽  
Noise Induced Hearing Loss ◽  
Irreversible Damage ◽  
Open Access Journals

Noise exposure (NE) has been recognized as one of the causes of sensorineural hearing loss (SNHL), which can bring about irreversible damage to sensory hair cells in the cochlea, through the launch of oxidative stress pathways and inflammation. Accordingly, determining the molecular mechanism involved in regulating hair cell apoptosis via NE is essential to prevent hair cell damage. However, the role of microRNAs (miRNAs) in the degeneration of sensory cells of the cochlea during NE has not been so far uncovered. Thus, the main purpose of this study was to demonstrate the regulatory role of miRNAs in the oxidative stress pathway and inflammation induced by NE. In this respect, articles related to noise-induced hearing loss (NIHL), oxidative stress, inflammation, and miRNA from various databases of Directory of Open Access Journals (DOAJ), Google Scholar, PubMed; Library, Information Science & Technology Abstracts (LISTA), and Web of Science were searched and retrieved. The findings revealed that several studies had suggested that up-regulation of miR-1229-5p, miR-451a, 185-5p, 186 and down-regulation of miRNA-96/182/183 and miR-30b were involved in oxidative stress and inflammation which could be used as biomarkers for NIHL. There was also a close relationship between NIHL and miRNAs, but further research is required to prove a causal association between miRNA alterations and NE, and also to determine miRNAs as biomarkers indicating responses to NE.

scholarly journals SIRT3: A New Regulator of Cardiovascular Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Sun ◽  
Caixia Liu ◽  
Qiuhui Chen ◽  
Ning Liu ◽  
Youyou Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Mitochondrial Function ◽  
Causes Of Death ◽  
Cell Damage ◽  
Heart Diseases ◽  
Tca Cycle ◽  
Metabolic Disturbances ◽  
Glucose And Lipid Metabolism

Cardiovascular diseases (CVDs) are the leading causes of death worldwide, and defects in mitochondrial function contribute largely to the occurrence of CVDs. Recent studies suggest that sirtuin 3 (SIRT3), the mitochondrial NAD+-dependent deacetylase, may regulate mitochondrial function and biosynthetic pathways such as glucose and fatty acid metabolism and the tricarboxylic acid (TCA) cycle, oxidative stress, and apoptosis by reversible protein lysine deacetylation. SIRT3 regulates glucose and lipid metabolism and maintains myocardial ATP levels, which protects the heart from metabolic disturbances. SIRT3 can also protect cardiomyocytes from oxidative stress-mediated cell damage and block the development of cardiac hypertrophy. Recent reports show that SIRT3 is involved in the protection of several heart diseases. This review discusses the progress in SIRT3-related research and the role of SIRT3 in the prevention and treatment of CVDs.

scholarly journals Staphylococcus aureus Infection Induced Oxidative Imbalance in Neutrophils: Possible Protective Role of Nanoconjugated Vancomycin

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Subhankari Prasad Chakraborty ◽  
Panchanan Pramanik ◽  
Somenath Roy
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Cell Damage ◽  
Treated Group ◽  
Protective Role ◽  
Control Group ◽  
Similar Dose ◽  
Cellular Components

Staphylococcus aureus infection causes oxidative stress in neutrophils. The immune cells use reactive oxygen species (ROS) for carrying out their normal functions while an excess amount of ROS can attack cellular components that lead to cell damage. The present study was aimed to test the protective role of nanoconjugated vancomycin against vancomycin-sensitive Staphylococcus aureus (VSSA) and vancomycin-resistant Staphylococcus aureus (VRSA) infection induced oxidative stress in neutrophils. VSSA- and VRSA-infection were developed in Swiss mice by intraperitoneal injection of 5×106 CFU/mL bacterial solutions. Nanoconjugated vancomycin was treated to VSSA- and VRSA-infected mice at its effective dose for 10 days. Vancomycin was treated to VSSA and VRSA infected mice at similar dose, respectively, for 10 days. The result reveals that in vivo VSSA and VRSA infection significantly increases the level of lipid peroxidation, protein oxidation, oxidized glutathione level, and nitrite generation and decreases the level of reduced glutathione, antioxidant enzyme status, and glutathione-dependent enzymes as compared to control group; which were increased or decreased significantly near to normal in nanoconjugated vancomycin-treated group. These finding suggests the potential use and beneficial protective role of nanoconjugated vancomycin against VSSA and VRSA infection induced oxidative imbalance in neutrophils.

scholarly journals Role of Forkhead Transcription Factors in Diabetes-Induced Oxidative Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Bhaskar Ponugoti ◽  
Guangyu Dong ◽  
Dana T. Graves
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Cellular Response ◽  
Cell Damage ◽  
Cell Types ◽  
Biological Processes ◽  
Oxygen Species ◽  
Forkhead Transcription Factors ◽  
Foxo Transcription Factors

Diabetes is a chronic metabolic disorder, characterized by hyperglycemia resulting from insulin deficiency and/or insulin resistance. Recent evidence suggests that high levels of reactive oxygen species (ROS) and subsequent oxidative stress are key contributors in the development of diabetic complications. The FOXO family of forkhead transcription factors including FOXO1, FOXO3, FOXO4, and FOXO6 play important roles in the regulation of many cellular and biological processes and are critical regulators of cellular oxidative stress response pathways. FOXO1 transcription factors can affect a number of different tissues including liver, retina, bone, and cell types ranging from hepatocytes to microvascular endothelial cells and pericytes to osteoblasts. They are induced by oxidative stress and contribute to ROS-induced cell damage and apoptosis. In this paper, we discuss the role of FOXO transcription factors in mediating oxidative stress-induced cellular response.

scholarly journals The Role of Nrf2 in Hearing Loss

2021 ◽  
Vol 12 ◽  
Author(s):  
Dafei Li ◽  
Haiyan Zhao ◽  
Zhong-Kai Cui ◽  
Guangyong Tian
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Cell Damage ◽  
Hearing Protection ◽  
Related Factor ◽  
Nuclear Factor ◽  
The World ◽  
Hair Cell Damage ◽  
Heavy Burden

Hearing loss is a major unresolved problem in the world, which has brought a heavy burden to society, economy, and families. Hair cell damage and loss mediated by oxidative stress are considered to be important causes of hearing loss. The nuclear factor erythroid 2–related factor 2 (Nrf2) is a major regulator of antioxidant capacity and is involved in the occurrence and development of a series of toxic and chronic diseases associated with oxidative stress. In recent years, studies on the correlation between hearing loss and Nrf2 target have continuously broadened our knowledge, and Nrf2 has become a new strategic target for the development and reuse of hearing protection drugs. This review summarized the correlation of Nrf2 in various types of hearing loss, and the role of drugs in hearing protection through Nrf2 from the literature.

scholarly journals The Role of Thioredoxin/Peroxiredoxin in the β-Cell Defense Against Oxidative Damage

2021 ◽  
Vol 12 ◽  
Author(s):  
Jennifer S. Stancill ◽  
John A. Corbett
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Cell Function ◽  
Cell Damage ◽  
Thioredoxin Reductase ◽  
Β Cells ◽  
Β Cell ◽  
Cell Defense ◽  
Β Cell Function

Oxidative stress is hypothesized to play a role in pancreatic β-cell damage, potentially contributing to β-cell dysfunction and death in both type 1 and type 2 diabetes. Oxidative stress arises when naturally occurring reactive oxygen species (ROS) are produced at levels that overwhelm the antioxidant capacity of the cell. ROS, including superoxide and hydrogen peroxide, are primarily produced by electron leak during mitochondrial oxidative metabolism. Additionally, peroxynitrite, an oxidant generated by the reaction of superoxide and nitric oxide, may also cause β-cell damage during autoimmune destruction of these cells. β-cells are thought to be susceptible to oxidative damage based on reports that they express low levels of antioxidant enzymes compared to other tissues. Furthermore, markers of oxidative damage are observed in islets from diabetic rodent models and human patients. However, recent studies have demonstrated high expression of various isoforms of peroxiredoxins, thioredoxin, and thioredoxin reductase in β-cells and have provided experimental evidence supporting a role for these enzymes in promoting β-cell function and survival in response to a variety of oxidative stressors. This mini-review will focus on the mechanism by which thioredoxins and peroxiredoxins detoxify ROS and on the protective roles of these enzymes in β-cells. Additionally, we speculate about the role of this antioxidant system in promoting insulin secretion.

Prenatal stress and its role in children's pathology: historical aspects and the current status of the question (review of literature)

2020 ◽  
Vol 24 (3) ◽  
pp. 28-41
Author(s):  
A. A. Vyalkova ◽  
B. A. Frolov ◽  
E. V. Savelyeva ◽  
S. A. Chesnokova
Keyword(s):  
Oxidative Stress ◽  
Kidney Diseases ◽  
Scientific Evidence ◽  
Current Status ◽  
Stress Reactions ◽  
Metabolic Disturbances ◽  
Negative Effects ◽  
Adaptation Mechanism ◽  
Increased Risk

The article presents an analysis of fundamental data on the problem of stress and its role in the development of stressful diseases. Scientific evidence on the role of stress in childhood pathology indicates the extreme pathogenetic significance of stress. It is proved that stress has three interconnected faces: stress as a link in the adaptation mechanism, stress as a link in the pathogenesis of diseases and adaptation to stressful situations as a natural prevention of stressful diseases. The scientific substantiation of the main evolutionarily determined role of stress as an adaptation link indicates the possibility of acquiring some degree of resistance to stressful situations. Prevention of reducing the excess of stress reactions and reducing the possibility of its transformation into a link in the pathogenesis of diseases limits the complex of mechanisms designated as a stress-limiting system. Important information is the development and coordination of the stress response, which is provided by a complex set of mechanisms of neuroendocrine regulation, united by the concept of “stress-implementing system”. The most common forms of stress are fetal hypoxia, metabolic disturbances, and toxic effects leading to uncontrolled oxidative stress at the cellular and tissue levels with the development of pregnancy complications, intrauterine growth retardation syndrome (IUGR), persistent changes and pathological conditions. As the fetus grows, the flow of oxygen and nutrients from the mother through the placenta increases, which is accompanied by an increased risk of the formation of pathologies of the brain, heart, liver and kidneys with the development of a multi-organ pathology in the subsequent life. It has been proven that oxidative stress combined with stress of malnutrition in the prenatal period increases the risk of endocrinopathies, kidney diseases, and a number of other chronic diseases in the adult state. In practical terms, the negative effects of stress are of particular interest. Early detection of psychosocial and sympathomimetic factors causing stress is the basis for the prevention of childhood pathology.

scholarly journals New Insights in the Pathogenesis of HPV Infection and the Associated Carcinogenic Processes: The Role of Chronic Inflammation and Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Simona Roxana Georgescu ◽  
Cristina Iulia Mitran ◽  
Madalina Irina Mitran ◽  
Constantin Caruntu ◽  
Maria Isabela Sarbu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Cell Damage ◽  
Redox Homeostasis ◽  
Harmful Effect ◽  
Hpv Infection ◽  
Host Cells ◽  
E6 And E7 ◽  
And Oxidative Stress

Human papillomavirus (HPV) is a small double-stranded DNA virus with tropism for epithelial cells. To this date, over 150 genotypes are known and are classified into two major groups, low-risk and high-risk strains, depending on the ability of the virus to induce malignant transformation. The host’s immunity plays a central role in the course of the infection; therefore, it may not be clinically manifest or may produce various benign or malignant lesions. The pathogenic mechanisms are complex and incompletely elucidated. Recent research suggests the role of chronic inflammation and oxidative stress (OS) in the pathogenesis of HPV infection and the associated carcinogenic processes. Chronic inflammation induces OS, which in turn promotes the perpetuation of the inflammatory process resulting in the release of numerous molecules which cause cell damage. Reactive oxygen species exert a harmful effect on proteins, lipids, and nucleic acids. Viral oncogenes E5, E6, and E7 are involved in the development of chronic inflammation through various mechanisms. In addition, HPV may interfere with redox homeostasis of host cells, inducing OS which may be involved in the persistence of the infection and play a certain role in viral integration and promotion of carcinogenesis. Knowledge regarding the interplay between chronic inflammation and OS in the pathogenesis of HPV infection and HPV-induced carcinogenesis has important consequences on the development of new therapeutic strategies.

scholarly journals Carotenoids as a Protection Mechanism against Oxidative Stress in Haloferax mediterranei

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1060
Author(s):  
Micaela Giani ◽  
Rosa María Martínez-Espinosa
Keyword(s):  
Oxidative Stress ◽  
Large Scale ◽  
Antioxidant Properties ◽  
Natural Ecosystem ◽  
Haloferax Mediterranei ◽  
Protection Mechanism ◽  
Different Types ◽  
Potential Applications ◽  
Extremophilic Microorganisms

Haloarchaea are extremophilic microorganisms that in their natural ecosystem encounter several sources of oxidative stress. They have developed different strategies to cope with these harsh environmental conditions, among which bacterioruberin production is a very notable strategy. Bacterioruberin (BR) is a C50 carotenoid synthesized in response to different types of stress. Previous works demonstrated that it shows interesting antioxidant properties with potential applications in biotechnology. In this study, Haloferax mediterranei strain R-4 was exposed to different concentrations of the oxidant compound H2O2 to evaluate the effect on carotenoid production focusing the attention on the synthesis of bacterioruberin. Hfx. mediterranei was able to grow in the presence of H2O2 from 1 mM to 25 mM. Cells produced between 16% and 78% (w/v) more carotenoids under the induced oxidative stress compared to control cultures. HPLC-MS analysis detected BR as the major identified carotenoid and confirmed the gradual increase of BR content as higher concentrations of hydrogen peroxide were added to the medium. These results shed some light on the biological role of bacterioruberin in haloarchaea, provide interesting information about the increase of the cellular pigmentation under oxidative stress conditions and will allow the optimization of the production of this pigment at large scale using these microbes as biofactories.

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