scholarly journals A new method to localise and quantify oxidative stress in live juvenile mussels

Biology Open ◽  
2021 ◽  
Author(s):  
Natalí J. Delorme ◽  
Alfonso J. Schmidt ◽  
Leonardo N. Zamora ◽  
David J. Burritt ◽  
Norman L. C. Ragg
Keyword(s):  
Oxidative Stress ◽  
Economic Performance ◽  
Model Organism ◽  
New Method ◽  
Life Stages ◽  
Integrated Method ◽  
Perna Canaliculus ◽  
Subsequent Application ◽  
Practical Field

Stress and survival of juvenile New Zealand green-lipped mussel, Perna canaliculus, is a poorly-understood bottleneck in the ecological and economic performance of a significant aquaculture crop. This species was therefore selected as a model organism for the development of a new method to quantify oxidative stress in whole individuals. An in vivo ROS-activated stain (CellROX™) was administered to anaesthetised, translucent juveniles that were subsequently formaldehyde-fixed and visualised using confocal microscopy. Subsequent application of image analysis to quantifying ROS-positive tissue areas was successfully used to detect stress differences in juvenile mussels exposed to varying levels of emersion. This integrated method can be used to localise and quantify ROS production in individual translucent bivalve life stages (larval and juvenile), while relative stability following fixation greatly expands potential practical field applications.

scholarly journals Synthesis, Characterization of Pyrano-[2,3-c]-Pyrazoles Derivatives and Determination of Their Antioxidant Activities

2021 ◽  
Vol 15 (3) ◽  
pp. 175-194
Author(s):  
Boutaina Addoum ◽  
◽  
Bouchra El khalfi ◽  
Mohamed Idiken ◽  
Souraya Sakoui ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Performance ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Model Organism ◽  
Biologically Active ◽  
Strong Activity ◽  
Nitrative Stress

Background: Antioxidants are developed to assist the immune system and overcome oxidative stress, the aggression of cellular constituents due to imbalance between reactive oxygen species and the inner antioxidant system. The main objective of this study was to search for new and potent antioxidants to protect humans against diseases associated with oxidative stress. Methods: In this study, three pyrano-[2,3-c]-pyrazole derivatives were synthesized via Multicomponent Reaction (MCR) approach and were characterized, using a melting point, High-Performance Liquid Chromatography (HPLC), and spectroscopic analyses (IR; 1H-NMR; 13C-NMR). All of the generated compounds were screened for their antioxidant properties in vivo, using ciliate “Tetrahymena” as a model organism exposed to oxidative and nitrative stress. They were then studied in vitro by using 1,1-diphenyl-2-picrylhydrazyl (DPPH) assays. Results: The results demonstrated that the three compounds (5a, b, c) are biologically active and possess potent antioxidant activities, especially the 5a and 5b derivatives. On the other hand, the in vitro bioassays revealed that the 5a derivative possessed a significant antioxidant activity much greater than ascorbic acid. Accordingly, the in silico data are consistent with the experimental data. Conclusion: These findings confirmed the potent antioxidant property of the synthesized compounds, providing us with new inspiration and challenges to design a library of pharmaceutical compounds with strong activity and low toxicity in the future.

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 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.

σB Plays a Limited Role in the Ability of Listeria monocytogenes Strain F2365 To Survive Oxidative and Acid Stress and in Its Virulence Characteristics

2013 ◽  
Vol 76 (12) ◽  
pp. 2079-2086 ◽  
Author(s):  
H. F. OLIVER ◽  
R. H. ORSI ◽  
M. WIEDMANN ◽  
K. J. BOOR
Keyword(s):  
Oxidative Stress ◽  
Listeria Monocytogenes ◽  
Acid Stress ◽  
Model Organism ◽  
Soft Cheese ◽  
Response To Stress ◽  
Serotype 4B ◽  
And Oxidative Stress

Listeria monocytogenes strain F2365 was the first strain representative of serotype 4b (lineage I) to be sequenced in 2004, suggesting it could become the model organism for this serotype, which is associated with most human outbreaks of listeriosis worldwide to date. F2365 itself is an outbreak strain that was involved in the listeriosis outbreak associated with Mexican-style soft cheese in California in 1985. In this study, we show through phenotypic and transcriptomic analysis that L. monocytogenes strain F2365 has reduced ability to respond to acid and oxidative stress. F2365 has neither the σB-dependent ability to survive acid or oxidative stress nor the σB-dependent ability to infect Caco-2 epithelial cells in vitro or guinea pigs in vivo. More studies are needed to determine whether the atypical σB-independent response to stress observed in F2365 is strain specific, serotype specific, or even lineage specific.

scholarly journals Polygonum multiflorum Extract Exerts Antioxidative Effects and Increases Life Span and Stress Resistance in the Model Organism Caenorhabditis elegans via DAF-16 and SIR-2.1

Plants ◽  
2018 ◽  
Vol 7 (3) ◽  
pp. 60 ◽  
Author(s):  
Christina Saier ◽  
Christian Büchter ◽  
Karoline Koch ◽  
Wim Wätjen
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Life Span ◽  
Stress Resistance ◽  
Model Organism ◽  
Aging Effects ◽  
Polygonum Multiflorum ◽  
Oxidative Stress Resistance ◽  
Antioxidative Effects

Extracts of the Chinese plant Polygonum multiflorum (PME) are used for medicinal purposes as well as food supplement due to anti-aging effects. Despite of the common use of these food supplements, experimental data on physiological effects of PME and its underlying molecular mechanisms in vivo are limited. We used the model organism Caenorhabditis elegans to analyze anti-aging-effects of PME in vivo (life span, lipofuscin accumulation, oxidative stress resistance, thermal stress resistance) as well as the molecular signaling pathways involved. The effects of PME were examined in wildtype animals and mutants defective in the sirtuin-homologue SIR-2.1 (VC199) and the FOXO-homologue DAF-16 (CF1038). PME possesses antioxidative effects in vivo and increases oxidative stress resistance of the nematodes. While the accumulation of lipofuscin is only slightly decreased, PME causes a significant elongation (18.6%) of mean life span. DAF-16 is essential for the reduction of thermally induced ROS accumulation, while the resistance against paraquat-induced oxidative stress is dependent on SIR-2.1. For the extension of the life span, both DAF-16 and SIR-2.1 are needed. We demonstrate that PME exerts protective effects in C. elegans via modulation of distinct intracellular pathways.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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