scholarly journals ROS in AgingCaenorhabditis elegans: Damage or Signaling?

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Patricia Back ◽  
Bart P. Braeckman ◽  
Filip Matthijssens
Keyword(s):  
Oxidative Stress ◽  
Aging Process ◽  
Model Organism ◽  
Mechanistic Explanation ◽  
Redox Status ◽  
Oxygen Species ◽  
C Elegans ◽  
Development And Aging

Many insights into the mechanisms and signaling pathways underlying aging have resulted from research on the nematodeCaenorhabditis elegans. In this paper, we discuss the recent findings that emerged using this model organism concerning the role of reactive oxygen species (ROS) in the aging process. The accrual of oxidative stress and damage has been the predominant mechanistic explanation for the process of aging for many years, but reviewing the recent studies inC. eleganscalls this theory into question. Thus, it becomes more and more evident that ROS are not merely toxic byproducts of the oxidative metabolism. Rather it seems more likely that tightly controlled concentrations of ROS and fluctuations in redox potential are important mediators of signaling processes. We therefore discuss some theories that explain how redox signaling may be involved in aging and provide some examples of ROS functions and signaling inC. elegansmetabolism. To understand the role of ROS and the redox status in physiology, stress response, development, and aging, there is a rising need for accurate and reversiblein vivodetection. Therefore, we comment on some methods of ROS and redox detection with emphasis on the implementation of genetically encoded biosensors inC. elegans.

scholarly journals Paraoxonases Activities and Polymorphisms in Elderly and Old-Age Diseases: An Overview

Antioxidants ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 118 ◽  
Author(s):  
Débora Levy ◽  
Cadiele Oliana Reichert ◽  
Sérgio Paulo Bydlowski
Keyword(s):  
Oxidative Stress ◽  
Aging Process ◽  
Tissue Injury ◽  
Density Lipoprotein ◽  
The Elderly ◽  
Chromosome 7 ◽  
Oxygen Species ◽  
Structural Homology ◽  
Inflammatory Processes

Aging is defined as the accumulation of progressive organ dysfunction. There is much evidence linking the involvement of oxidative stress in the pathogenesis of aging. With increasing age, susceptibility to the development of diseases related to lipid peroxidation and tissue injury increases, due to chronic inflammatory processes, and production of reactive oxygen species (ROS) and free radicals. The paraoxonase (PON) gene family is composed of three members (PON1, PON2, PON3) that share considerable structural homology and are located adjacently on chromosome 7 in humans. The most studied member product is PON1, a protein associated with high-density lipoprotein with paraoxonase/esterase activity. Nevertheless, all the three proteins prevent oxidative stress. The major aim of this review is to highlight the importance of the role of PON enzymes in the aging process, and in the development of the main diseases present in the elderly: cardiovascular disease, diabetes mellitus, neurodegenerative diseases, and cancer.

scholarly journals Mulberry Anthocyanin Extract Ameliorates Oxidative Damage in HepG2 Cells and Prolongs the Lifespan of Caenorhabditis elegans through MAPK and Nrf2 Pathways

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Fujie Yan ◽  
Yushu Chen ◽  
Ramila Azat ◽  
Xiaodong Zheng
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Hepg2 Cells ◽  
Insulin Signalling ◽  
Glucose Consumption ◽  
Redox Status ◽  
C Elegans ◽  
Beneficial Effects

Mulberry anthocyanins possess many pharmacological effects including liver protection, anti-inflammation, and anticancer. The aim of this study was to evaluate whether mulberry anthocyanin extract (MAE) exerts beneficial effects against oxidative stress damage in HepG2 cells and Caenorhabditis elegans. In vitro, MAE prevented cytotoxicity, increased glucose consumption and uptake, and eliminated excessive intracellular free radicals in H2O2-induced cells. Moreover, MAE pretreatment maintained Nrf2, HO-1, and p38 MAPK stimulation and abolished upregulation of p-JNK, FOXO1, and PGC-1α that were involved in oxidative stress and insulin signalling modulation. In vivo, extended lifespan was observed in C. elegans damaged by paraquat in the presence of MAE, while these beneficial effects were disappeared in pmk-1 and daf-16 mutants. PMK-1 and SKN-1 were activated after exposure to paraquat and MAE suppressed PMK-1 activation but enhanced SKN-1 stimulation. Our findings suggested that MAE recovered redox status in HepG2 cells and C. elegans that suffered from oxidative stress, which might be by targeting MAPKs and Nrf2.

scholarly journals Drosophila SLC22 Orthologs Related to OATs, OCTs, and OCTNs Regulate Development and Responsiveness to Oxidative Stress

2020 ◽  
Vol 21 (6) ◽  
pp. 2002 ◽  
Author(s):  
Darcy C. Engelhart ◽  
Priti Azad ◽  
Suwayda Ali ◽  
Jeffry C. Granados ◽  
Gabriel G. Haddad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Drosophila Melanogaster ◽  
Organic Molecules ◽  
Fruit Fly ◽  
Evolutionary Analysis ◽  
Oxygen Species ◽  
Small Organic Molecules ◽  
Evolutionarily Conserved

The SLC22 family of transporters is widely expressed, evolutionarily conserved, and plays a major role in regulating homeostasis by transporting small organic molecules such as metabolites, signaling molecules, and antioxidants. Analysis of transporters in fruit flies provides a simple yet orthologous platform to study the endogenous function of drug transporters in vivo. Evolutionary analysis of Drosophila melanogaster putative SLC22 orthologs reveals that, while many of the 25 SLC22 fruit fly orthologs do not fall within previously established SLC22 subclades, at least four members appear orthologous to mammalian SLC22 members (SLC22A16:CG6356, SLC22A15:CG7458, CG7442 and SLC22A18:CG3168). We functionally evaluated the role of SLC22 transporters in Drosophila melanogaster by knocking down 14 of these genes. Three putative SLC22 ortholog knockdowns—CG3168, CG6356, and CG7442/SLC22A—did not undergo eclosion and were lethal at the pupa stage, indicating the developmental importance of these genes. Additionally, knocking down four SLC22 members increased resistance to oxidative stress via paraquat testing (CG4630: p < 0.05, CG6006: p < 0.05, CG6126: p < 0.01 and CG16727: p < 0.05). Consistent with recent evidence that SLC22 is central to a Remote Sensing and Signaling Network (RSSN) involved in signaling and metabolism, these phenotypes support a key role for SLC22 in handling reactive oxygen species.

scholarly journals FructationIn Vivo: Detrimental and Protective Effects of Fructose

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
H. M. Semchyshyn
Keyword(s):  
Oxidative Stress ◽  
Side Effects ◽  
Experimental Models ◽  
Oxygen Species ◽  
Protective Effects ◽  
Compelling Evidence ◽  
Animal Tissues

There is compelling evidence that long-term intake of excessive fructose can have deleterious side effects in different experimental models. However, the role of fructosein vivoremains controversial, since acute temporary application of fructose is found to protect yeast as well as animal tissues against exogenous oxidative stress. This review suggests the involvement of reactive carbonyl and oxygen species in both the cytotoxic and defensive effects of fructose. Potential mechanisms of the generation of reactive species by fructose in the nonenzymatic reactions, their implication in the detrimental and protective effects of fructose are discussed.

scholarly journals Caenorhabditis elegans: A Useful Model for Studying Metabolic Disorders in Which Oxidative Stress Is a Contributing Factor

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Elizabeth Moreno-Arriola ◽  
Noemí Cárdenas-Rodríguez ◽  
Elvia Coballase-Urrutia ◽  
José Pedraza-Chaverri ◽  
Liliana Carmona-Aparicio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Metabolic Disorders ◽  
Molecular Mechanisms ◽  
Second Messengers ◽  
Model Organism ◽  
Human Diseases ◽  
C Elegans ◽  
Molecular Bases

Caenorhabditis elegansis a powerful model organism that is invaluable for experimental research because it can be used to recapitulate most human diseases at either the metabolic or genomic levelin vivo. This organism contains many key components related to metabolic and oxidative stress networks that could conceivably allow us to increase and integrate information to understand the causes and mechanisms of complex diseases. Oxidative stress is an etiological factor that influences numerous human diseases, including diabetes.C. elegansdisplays remarkably similar molecular bases and cellular pathways to those of mammals. Defects in the insulin/insulin-like growth factor-1 signaling pathway or increased ROS levels induce the conserved phase II detoxification response via the SKN-1 pathway to fight against oxidative stress. However, it is noteworthy that, aside from the detrimental effects of ROS, they have been proposed as second messengers that trigger the mitohormetic response to attenuate the adverse effects of oxidative stress. Herein, we briefly describe the importance ofC. elegansas an experimental model system for studying metabolic disorders related to oxidative stress and the molecular mechanisms that underlie their pathophysiology.

Caenorhabditis elegans: A promising contrivance to study neurotoxicity and oxidative stress

2021 ◽  
Vol 16 (10) ◽  
pp. 198-206
Author(s):  
Kiran Singh ◽  
Shweta Yadav
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Genetic Manipulation ◽  
Model Organism ◽  
Mechanisms Of Toxicity ◽  
C Elegans ◽  
Toxicological Studies ◽  
And Oxidative Stress

Owing to ubiquitous distribution, high abundances and ecological relevance, Caenorhabditis elegans has strong potential interest as barometer of environment and human health. Ecotoxicological methods are used to evaluate the effect of various anthropogenic contaminants on the ecosystems that circumscribe both in-vivo and in-vitro toxicities to explore the pathways and mechanisms of toxicity and to set precise toxicity thresholds. The interest in C. elegans, as a model organism in toxicological studies, has increased over the past few decades. The enticement of C. elegans comes from the ease of metabolically active digestive, sensory, endocrine, neuromuscular, reproductive systems and genetic manipulation along with the ability to fluorescently label neuronal subtypes. The study reviews the competence of Caenorhabditis elegans as a potential model organism in various toxicity assays specifically neurotoxicity and oxidative stress.

scholarly journals Glutathione status in the blood of rats after reticulocytosis induced by phenylhydrazine and bleeding

2010 ◽  
Vol 62 (3) ◽  
pp. 589-594
Author(s):  
Snezana Markovic ◽  
Ana Obradovic ◽  
Jovana Zizic ◽  
Branka Ognjanovic ◽  
A.S. Stajn ◽  
...  
Keyword(s):  
Blood Cells ◽  
Redox Status ◽  
Oxygen Species ◽  
Oxidized Glutathione ◽  
Antioxidative Capacity ◽  
Glutathione System ◽  
Glutathione Status ◽  
In Vivo Effects

In this experiment, we compared the in vivo effects of phenylhydrazine (PHZ) and bleeding treatment on the redox status and glutathione antioxidative mechanism parameters in the plasma and red blood cells (RBC) of rats. Results showed a lower level of reactive oxygen species (ROS), a higher level of lipid peroxidation and the effective antioxidative role of the glutathione system in the blood of bleeding rats. PHZ-treatment induced higher concentrations of ROS and an accumulation of oxidized glutathione in the plasma, while the glutathione system showed a satisfactory antioxidative capacity in the RBC of rats. When comparing the two anemic groups, the PHZ-treated rats showed marked oxidative stress in the plasma. .

scholarly journals The Role of Ca2+ Signaling in Aging and Neurodegeneration: Insights from Caenorhabditis elegans Models

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 204 ◽  
Author(s):  
Javier Alvarez ◽  
Pilar Alvarez-Illera ◽  
Paloma García-Casas ◽  
Rosalba I. Fonteriz ◽  
Mayte Montero
Keyword(s):  
Caenorhabditis Elegans ◽  
Model Organism ◽  
Ample Evidence ◽  
C Elegans ◽  
Physiological Processes ◽  
Human Proteins ◽  
Β Amyloid ◽  
Key Events

Ca2+ is a ubiquitous second messenger that plays an essential role in physiological processes such as muscle contraction, neuronal secretion, and cell proliferation or differentiation. There is ample evidence that the dysregulation of Ca2+ signaling is one of the key events in the development of neurodegenerative processes, an idea called the “calcium hypothesis” of neurodegeneration. Caenorhabditis elegans (C. elegans) is a very good model for the study of aging and neurodegeneration. In fact, many of the signaling pathways involved in longevity were first discovered in this nematode, and many models of neurodegenerative diseases have also been developed therein, either through mutations in the worm genome or by expressing human proteins involved in neurodegeneration (β-amyloid, α-synuclein, polyglutamine, or others) in defined worm tissues. The worm is completely transparent throughout its whole life, which makes it possible to carry out Ca2+ dynamics studies in vivo at any time, by expressing Ca2+ fluorescent probes in defined worm tissues, and even in specific organelles such as mitochondria. This review will summarize the evidence obtained using this model organism to understand the role of Ca2+ signaling in aging and neurodegeneration.

Relevance of bioassay of biologically active substances (BAS) with geroprotective properties in the model of the nematode Caenorhabditis elegans in experiments in vivo

2021 ◽  
Vol 14 ◽  
Author(s):  
Lyubov S. Dyshlyuk ◽  
Anastasiya I. Dmitrieva ◽  
Margarita Yu. Drozdova ◽  
Irina S. Milentyeva ◽  
Alexander Yu. Prosekov
Keyword(s):  
Caenorhabditis Elegans ◽  
Plant Extracts ◽  
Aging Process ◽  
Model Organism ◽  
Biologically Active ◽  
Model Systems ◽  
C Elegans ◽  
Living Organisms ◽  
Active Substances

: Aging is a process global in nature. The age of living organisms contributes to the appearance of chronic diseases, which not only reduce the quality of life, but also significantly damage it. Modern medicines can successfully fight multiple diseases and prolong life. At the same time, medications have a large number of side effects. New research indicates that bioactive phytochemicals have great potential for treating even the most severe diseases and can become an alternative to medicines. Despite many studies in this area, the effects of many plant ingredients on living organisms are poorly understood. Analysis of the mechanisms through which herbal preparations influence the aging process helps to select the right active substances, determine the optimal doses to obtain the maximum positive effect. It is preferable to check the effectiveness of plant extracts and biologically active components with geroprotective properties in vivo. For these purposes, live model systems such as Rattus rattus, Mus musculus, Drosophila melanogaster, and Caenorhabditis elegans are used. These models help to comprehensively study the impact of the developed new drugs on the aging process. The model organism C. elegans is gaining increasing popularity in these studies because of its many advantages. This review article discusses the advantages of the nematode C. elegans as a model organism for studying the processes associated with aging. The influence of various BAS and plant extracts on the increase in the life span of the nematode, on the increase in its stress resistance and on other markers of aging is also considered. The review showed that the nematode C. elegans has a number of advantages over other organisms and is a promising model system for studying the geroprotective properties of BAS.

The role of oxidative stress in the toxicity of pyridoxal isonicotinoyl hydrazone (PIH) analogues

2002 ◽  
Vol 30 (4) ◽  
pp. 755-758 ◽  
Author(s):  
J. L. Buss ◽  
J. Neuzil ◽  
P. Ponka
Keyword(s):  
Oxidative Stress ◽  
K562 Cells ◽  
Redox Status ◽  
Jurkat Cells ◽  
Glutathione Depletion ◽  
Pyridoxal Isonicotinoyl Hydrazone ◽  
Fe Complexes

Pyridoxal isonicotinoyl hydrazone (PIH) analogues are effective iron chelators in vivo and in vitro, and may be of value for the treatment of secondary iron overload. The sensitivity of Jurkat cells to Fe-chelator complexes was enhanced several-fold by the depletion of the antioxidant glutathione, indicating the role of oxidative stress in their toxicity. K562 cells loaded with eicosapentaenoic acid, a fatty acid particularly susceptible to oxidation, were also more sensitive to the toxic effects of the Fe complexes, and toxicity was proportional to lipid peroxidation. Thus Fechelator complexes cause oxidative stress, which may be a major component of their toxicity. As was the case for their Fe complexes, the toxicity of PIH analogues was enhanced by glutathione depletion of Jurkat cells and eicosapentaenoic acidloading of K562 cells. Thus the toxicity of the chelators themselves is also enhanced by compromised cellular redox status. In addition, the toxicity of the chelators was diminished by culturing Jurkat cells under hypoxic conditions, which may limit the production of the reactive oxygen species that initiate oxidative stress. A significant part of the toxicity of the chelators may be due to intracellular formation of Fe-chelator complexes, which oxidatively destroy the cell.

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