scholarly journals The Good, the Bad, and the Ugly of ROS: New Insights on Aging and Aging-Related Diseases from Eukaryotic and Prokaryotic Model Organisms

2018 ◽  
Vol 2018 ◽  
pp. 1-23 ◽  
Author(s):  
Ana L. Santos ◽  
Sanchari Sinha ◽  
Ariel B. Lindner
Keyword(s):  
Cellular Damage ◽  
Model Organisms ◽  
Oxygen Species ◽  
Cellular Physiology ◽  
Age Related ◽  
Normal Metabolism ◽  
Health And Disease ◽  
Genetic Interventions ◽  
Mitochondrial Networks

Aging is associated with the accumulation of cellular damage over the course of a lifetime. This process is promoted in large part by reactive oxygen species (ROS) generated via cellular metabolic and respiratory pathways. Pharmacological, nonpharmacological, and genetic interventions have been used to target cellular and mitochondrial networks in an effort to decipher aging and age-related disorders. While ROS historically have been viewed as a detrimental byproduct of normal metabolism and associated with several pathologies, recent research has revealed a more complex and beneficial role of ROS in regulating metabolism, development, and lifespan. In this review, we summarize the recent advances in ROS research, focusing on both the beneficial and harmful roles of ROS, many of which are conserved across species from bacteria to humans, in various aspects of cellular physiology. These studies provide a new context for our understanding of the parts ROS play in health and disease. Moreover, we highlight the utility of bacterial models to elucidate the molecular pathways by which ROS mediate aging and aging-related diseases.

scholarly journals Age-Related Macular Degeneration: Role of Oxidative Stress and Blood Vessels

2021 ◽  
Vol 22 (3) ◽  
pp. 1296
Author(s):  
Yue Ruan ◽  
Subao Jiang ◽  
Adrian Gericke
Keyword(s):  
Oxidative Stress ◽  
Macular Degeneration ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Therapeutic Strategies ◽  
Vision Impairment ◽  
Age Related Macular Degeneration ◽  
Oxygen Species ◽  
Age Related

Age-related macular degeneration (AMD) is a common irreversible ocular disease characterized by vision impairment among older people. Many risk factors are related to AMD and interact with each other in its pathogenesis. Notably, oxidative stress and choroidal vascular dysfunction were suggested to be critically involved in AMD pathogenesis. In this review, we give an overview on the factors contributing to the pathophysiology of this multifactorial disease and discuss the role of reactive oxygen species and vascular function in more detail. Moreover, we give an overview on therapeutic strategies for patients suffering from AMD.

scholarly journals The Role of MicroRNAs in Diabetes-Related Oxidative Stress

2019 ◽  
Vol 20 (21) ◽  
pp. 5423 ◽  
Author(s):  
Mirza Muhammad Fahd Qadir ◽  
Dagmar Klein ◽  
Silvia Álvarez-Cubela ◽  
Juan Domínguez-Bendala ◽  
Ricardo Luis Pastori
Keyword(s):  
Oxidative Stress ◽  
Target Gene ◽  
Cellular Stress ◽  
Cellular Damage ◽  
Oxygen Species ◽  
Non Coding Rnas ◽  
And Oxidative Stress

Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous ROS production and disease such as Type 1 (T1D) and Type 2 (T2D) diabetes, as well as their complications, has been well established. However, there is a lack of understanding about genome-driven responses to ROS-mediated cellular stress. Over the last decade, multiple studies have suggested a link between oxidative stress and microRNAs (miRNAs). The miRNAs are small non-coding RNAs that mostly suppress expression of the target gene by interaction with its 3’untranslated region (3′UTR). In this paper, we review the recent progress in the field, focusing on the association between miRNAs and oxidative stress during the progression of diabetes.

scholarly journals The Redox System inC. elegans, a Phylogenetic Approach

2012 ◽  
Vol 2012 ◽  
pp. 1-20 ◽  
Author(s):  
Andrew D. Johnston ◽  
Paul R. Ebert
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Cellular Damage ◽  
Future Research ◽  
Homologous Proteins ◽  
Redox Biology ◽  
Redox Signalling ◽  
C Elegans ◽  
Age Related

Oxidative stress is a toxic state caused by an imbalance between the production and elimination of reactive oxygen species (ROS). ROS cause oxidative damage to cellular components such as proteins, lipids, and nucleic acids. While the role of ROS in cellular damage is frequently all that is noted, ROS are also important in redox signalling. The “Redox Hypothesis" has been proposed to emphasize a dual role of ROS. This hypothesis suggests that the primary effect of changes to the redox state is modified cellular signalling rather than simply oxidative damage. In extreme cases, alteration of redox signalling can contribute to the toxicity of ROS, as well as to ageing and age-related diseases. The nematode speciesCaenorhabditis elegansprovides an excellent model for the study of oxidative stress and redox signalling in animals. We use protein sequences from central redox systems inHomo sapiens,Drosophila melanogaster, andSaccharomyces cerevisiaeto query Genbank for homologous proteins inC. elegans. We then use maximum likelihood phylogenetic analysis to compare protein families betweenC. elegansand the other organisms to facilitate future research into the genetics of redox biology.

scholarly journals Mitochondria and Aging—The Role of Exercise as a Countermeasure

Biology ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 40 ◽  
Author(s):  
Mats I Nilsson ◽  
Mark A Tarnopolsky
Keyword(s):  
Reactive Oxygen Species Generation ◽  
Biological Aging ◽  
Primary Role ◽  
Oxygen Species ◽  
Vicious Cycle ◽  
Life And Death ◽  
Cell Functions ◽  
Age Related ◽  
Damage Protein

Mitochondria orchestrate the life and death of most eukaryotic cells by virtue of their ability to supply adenosine triphosphate from aerobic respiration for growth, development, and maintenance of the ‘physiologic reserve’. Although their double-membrane structure and primary role as ‘powerhouses of the cell’ have essentially remained the same for ~2 billion years, they have evolved to regulate other cell functions that contribute to the aging process, such as reactive oxygen species generation, inflammation, senescence, and apoptosis. Biological aging is characterized by buildup of intracellular debris (e.g., oxidative damage, protein aggregates, and lipofuscin), which fuels a ‘vicious cycle’ of cell/DNA danger response activation (CDR and DDR, respectively), chronic inflammation (‘inflammaging’), and progressive cell deterioration. Therapeutic options that coordinately mitigate age-related declines in mitochondria and organelles involved in quality control, repair, and recycling are therefore highly desirable. Rejuvenation by exercise is a non-pharmacological approach that targets all the major hallmarks of aging and extends both health- and lifespan in modern humans.

scholarly journals The Role of Oxidative Stress and Inflammation in Cardiovascular Aging

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Junzhen Wu ◽  
Shijin Xia ◽  
Bill Kalionis ◽  
Wenbin Wan ◽  
Tao Sun
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Low Grade ◽  
Oxygen Species ◽  
Age Related ◽  
Vascular Elasticity ◽  
Low Grade Inflammation

Age is an independent risk factor of cardiovascular disease, even in the absence of other traditional factors. Emerging evidence in experimental animal and human models has emphasized a central role for two main mechanisms of age-related cardiovascular disease: oxidative stress and inflammation. Excess reactive oxygen species (ROS) and superoxide generated by oxidative stress and low-grade inflammation accompanying aging recapitulate age-related cardiovascular dysfunction, that is, left ventricular hypertrophy, fibrosis, and diastolic dysfunction in the heart as well as endothelial dysfunction, reduced vascular elasticity, and increased vascular stiffness. We describe the signaling involved in these two main mechanisms that include the factors NF-κB, JunD, p66Shc, and Nrf2. Potential therapeutic strategies to improve the cardiovascular function with aging are discussed, with a focus on calorie restriction, SIRT1, and resveratrol.

scholarly journals The Role of NrF2 in the Regulation of Periodontal Health and Disease

2017 ◽  
Vol 96 (9) ◽  
pp. 975-983 ◽  
Author(s):  
A.V. Chiu ◽  
M. Al Saigh ◽  
C.A. McCulloch ◽  
M. Glogauer
Keyword(s):  
Cell Types ◽  
Related Factor ◽  
Oxygen Species ◽  
Tissue Destruction ◽  
Concept Of Disease ◽  
Periodontal Health ◽  
Disease Tolerance ◽  
Host Protection ◽  
Health And Disease

Immune-related disease tolerance is an important defense strategy that facilitates the maintenance of health in organs and tissues that are commonly colonized by bacteria. Immune tolerance to dysbiotic, tooth-borne biofilms is a poorly understood yet clinically relevant concept in the immunopathological mechanisms that are involved in the pathogenesis of periodontitis, particularly those related to neutrophil and macrophage responses. In periodontal health, neutrophils and macrophages respond to the formation of pathogenic bacterial biofilms by the production of bactericidal reactive oxygen species (ROS). However, when released in excess, ROS cause tissue damage and exacerbate inflammation. To counter these destructive responses, many cell types, including neutrophils and macrophages, launch a dedicated antioxidant system that limits the cell and tissue-damaging effects of ROS. The expression of antioxidants is primarily regulated by genetic response elements in their promoters. Here we consider the roles of nuclear factor erythroid 2-related factor (NrF2), a transcription factor, and other key regulators of antioxidants. The concept of disease tolerance, neutrophil and macrophage-generated oxidative stress, and their relationship to the pathogenesis of periodontitis is reviewed. We focus on the regulation of NrF2 and recent evidence suggesting that NrF2 plays a central role in host protection against tissue destruction in periodontitis.

scholarly journals The Potential of High-Anthocyanin Purple Rice as a Functional Ingredient in Human Health

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 833
Author(s):  
Supapohn Yamuangmorn ◽  
Chanakan Prom-u-Thai
Keyword(s):  
Human Health ◽  
Physiological Role ◽  
Cellular Damage ◽  
Anthocyanin Synthesis ◽  
Antioxidant Compounds ◽  
Anthocyanin Content ◽  
Oxygen Species ◽  
Whole Plant ◽  
Light Quantity

Purple rice is recognized as a source of natural anthocyanin compounds among health-conscious consumers who employ rice as their staple food. Anthocyanin is one of the major antioxidant compounds that protect against the reactive oxygen species (ROS) that cause cellular damage in plants and animals, including humans. The physiological role of anthocyanin in plants is not fully understood, but the benefits to human health are apparent against both chronic and non-chronic diseases. This review focuses on anthocyanin synthesis and accumulation in the whole plant of purple rice, from cultivation to the processed end products. The anthocyanin content in purple rice varies due to many factors, including genotype, cultivation, and management as well as post-harvest processing. The cultivation method strongly influences anthocyanin content in rice plants; water conditions, light quantity and quality, and available nutrients in the soil are important factors, while the low stability of anthocyanins means that they can be dramatically degraded under high-temperature conditions. The application of purple rice anthocyanins has been developed in both functional food and other purposes. To maximize the benefits of purple rice to human health, understanding the factors influencing anthocyanin synthesis and accumulation during the entire process from cultivation to product development can be a path for success.

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