scholarly journals Oxidative Stress, Prooxidants, and Antioxidants: The Interplay

2014 ◽  
Vol 2014 ◽  
pp. 1-19 ◽  
Author(s):  
Anu Rahal ◽  
Amit Kumar ◽  
Vivek Singh ◽  
Brijesh Yadav ◽  
Ruchi Tiwari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Medical Personnel ◽  
The Body ◽  
Bioactive Molecules ◽  
Low Levels ◽  
Species Production ◽  
Increased Susceptibility

Oxidative stress is a normal phenomenon in the body. Under normal conditions, the physiologically important intracellular levels of reactive oxygen species (ROS) are maintained at low levels by various enzyme systems participating in thein vivoredox homeostasis. Therefore, oxidative stress can also be viewed as an imbalance between the prooxidants and antioxidants in the body. For the last two decades, oxidative stress has been one of the most burning topics among the biological researchers all over the world. Several reasons can be assigned to justify its importance: knowledge about reactive oxygen and nitrogen species production and metabolism; identification of biomarkers for oxidative damage; evidence relating manifestation of chronic and some acute health problems to oxidative stress; identification of various dietary antioxidants present in plant foods as bioactive molecules; and so on. This review discusses the importance of oxidative stress in the body growth and development as well as proteomic and genomic evidences of its relationship with disease development, incidence of malignancies and autoimmune disorders, increased susceptibility to bacterial, viral, and parasitic diseases, and an interplay with prooxidants and antioxidants for maintaining a sound health, which would be helpful in enhancing the knowledge of any biochemist, pathophysiologist, or medical personnel regarding this important issue.

scholarly journals Cellular oxidative stress stimulated by microcystin: review

2021 ◽  
Vol 10 (11) ◽  
pp. e422101119765
Author(s):  
Iara Bezerra de Oliveira ◽  
Hanndson Araújo Silva
Keyword(s):  
Oxidative Stress ◽  
The Body ◽  
Bioactive Molecules ◽  
Cyanobacterial Blooms ◽  
Protein Phosphatase 1 ◽  
Cell Integrity ◽  
Inclusion Criteria ◽  
Radical Generation

Introduction: Cyanobacteria are organisms capable of producing a high number of bioactive molecules, known as cyanotoxins. Among the cyanotoxins, microcystins stand out, compounds with hepatotoxic potential. Studies claim that the most common and most toxic isoform among microcystins is microcystin-LR. One of the most frequently detected properties of microcystins is their ability to generate cellular oxidative stress. Thus, the present study is a bibliographic research about the biochemical mechanism of free radical generation caused by Microcystin LR. Methodology: for the preparation of this review, a survey was carried out in the national and international literature. The inclusion criteria for the construction of this work were original and review articles that addressed the ability of microcystin LR to generate oxidative damage. Results: Once they enter the body, microcystins accumulate in the liver, so that toxicity is associated with specific inhibition of protein phosphatase 1 and 2A (PP1 and PP2A), leading to disruption of cell integrity. Studies prove that MCs produce oxidative stress in vitro and in vivo and that they can act as tumor promoters. Conclusion: there is a possible relationship between cellular oxidative stress caused by microcystin. Thus, cyanobacterial blooms represent a threat to the health of several animals, including man, however, further studies on the topic addressed are needed.

MYB134-RNAi poplar plants show reduced tannin synthesis in leaves but not roots, and increased susceptibility to oxidative stress

2020 ◽  
Vol 71 (20) ◽  
pp. 6601-6611
Author(s):  
Geraldine Gourlay ◽  
Dawei Ma ◽  
Axel Schmidt ◽  
C Peter Constabel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Condensed Tannin ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Rna Seq ◽  
Wild Type ◽  
And Control ◽  
Increased Susceptibility

Abstract The importance of the poplar MYB134 gene in controlling condensed tannin (CT) biosynthesis was tested by suppressing its expression using RNA interference (RNAi). MYB134-RNAi plants grew normally but showed reduced accumulation of stress-induced CTs in leaves. RNA-seq analysis indicated that flavonoid- and CT-related genes, as well as additional CT regulators, were strongly and specifically down-regulated by MYB134 suppression. This confirmed that the primary MYB134 target is the leaf flavonoid and CT pathway. Root CT accumulation was not impacted by MYB suppression, suggesting that additional CT regulators are active in roots and emphasizing the complexity of the regulation of CTs in poplar. To test the effect of CT down-regulation on oxidative stress resistance, leaves of MYB134-RNAi and control plants were exposed to the reactive oxygen species generator methyl viologen. MYB134-RNAi leaves sustained significantly more photosystem II damage, as seen in reduced chlorophyll fluorescence, compared with wild-type leaves. MYB134-RNAi leaves also contained more hydrogen peroxide, a reactive oxygen species, compared with the wild type. Our data thus corroborate the hypothesis that CT can act as an antioxidant in vivo and protect against oxidative stress. Overall, MYB134 was shown to be a central player in the regulation of CT synthesis in leaves.

Targeting PPARalpha in Alzheimer's Disease

2018 ◽  
Vol 15 (4) ◽  
pp. 345-354 ◽  
Author(s):  
Barbara D'Orio ◽  
Anna Fracassi ◽  
Maria Paola Cerù ◽  
Sandra Moreno
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Antioxidant Response ◽  
Peroxisome Proliferator ◽  
Prevailing Paradigm

Background: The molecular mechanisms underlying Alzheimer's disease (AD) are yet to be fully elucidated. The so-called “amyloid cascade hypothesis” has long been the prevailing paradigm for causation of disease, and is today being revisited in relation to other pathogenic pathways, such as oxidative stress, neuroinflammation and energy dysmetabolism. The peroxisome proliferator-activated receptors (PPARs) are expressed in the central nervous system (CNS) and regulate many physiological processes, such as energy metabolism, neurotransmission, redox homeostasis, autophagy and cell cycle. Among the three isotypes (α, β/δ, γ), PPARγ role is the most extensively studied, while information on α and β/δ are still scanty. However, recent in vitro and in vivo evidence point to PPARα as a promising therapeutic target in AD. Conclusion: This review provides an update on this topic, focussing on the effects of natural or synthetic agonists in modulating pathogenetic mechanisms at AD onset and during its progression. Ligandactivated PPARα inihibits amyloidogenic pathway, Tau hyperphosphorylation and neuroinflammation. Concomitantly, the receptor elicits an enzymatic antioxidant response to oxidative stress, ameliorates glucose and lipid dysmetabolism, and stimulates autophagy.

scholarly journals How to express the antioxidant properties of substances properly?

2021 ◽  
Author(s):  
Małgorzata Olszowy-Tomczyk
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Literature Review ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
The Body ◽  
Universal Method ◽  
Oxygen Species ◽  
Good Tool

AbstractOxidative stress, associated with an imbalance between the oxidants (reactive oxygen species) and the antioxidants in the body, contributes to the development of many diseases. The body’s fight against reactive oxygen species is supported by antioxidants. Nowadays, there are too many analytical methods, but there is no one universal technique for assessing antioxidant properties. Moreover, the applied different ways of expressing the results lead to their incompatibility and unreasonable interpretation. The paper is a literature review concerning the most frequent ways of antioxidant activities expression and for an easy and universal method of the obtained results discussion. This paper is an attempt to point out their disadvantages and advantages. The manuscript can support the searching interpretation of the obtained results which will be a good tool for the development of a number of fields, especially medicine what can help in the future detection and treatment of many serious diseases. Graphic abstract

scholarly journals Vesicular Formation of Trans-Ferulic Acid: an Efficient Approach to Improve the Radical Scavenging and Antimicrobial Properties

2021 ◽  
Author(s):  
Anahita Rezaeiroshan ◽  
Majid Saeedi ◽  
Katayoun Morteza-Semnani ◽  
Jafar Akbari ◽  
Akbar Hedayatizadeh-Omran ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Reactive Oxygen Species ◽  
Ferulic Acid ◽  
Reactive Oxygen Species Production ◽  
Radical Scavenging ◽  
Reactive Oxygen ◽  
Entrapment Efficiency ◽  
The Body ◽  
Oxygen Species ◽  
Species Production

Abstract Purposes Reactive oxygen species production is harmful to human’s health. The presence of antioxidants in the body may help to diminish reactive oxygen species. Trans-ferulic acid is a good antioxidant, but its low water solubility excludes its utilization. The study aims to explore whether a vesicular drug delivery could be a way to overcome the poor absorption of trans-ferulic acid hence improving its antimicrobial efficiency and antioxidant effect. Methods Niosomal vesicles containing the drug were prepared by film hydration method. The obtained vesicles were investigated in terms of morphology, size, entrapment efficiency, release behavior, cellular cytotoxicity, antioxidant, cellular protection study, and antimicrobial evaluations. Results The optimized niosomal formulation had a particle size of 158.7 nm and entrapment efficiency of 21.64%. The results showed that the optimized formulation containing 25 μM of trans-ferulic acid could enhance the viability of human foreskin fibroblast HFF cell line against reactive oxygen species production. The minimum effective dose of the plain drug and the niosomal formulation against Staphylococcus aurous (ATCC 29213) was 750 µg/mL and 375 µg/mL, respectively, and for Escherichia coli (ATCC 25922), it was 750 µg/mL and 187/5 µg/mL, respectively. The formulation could also improve the minimum bactericidal concentration of the drug in Staphylococcus aurous, Escherichia coli, and Acinobacter baumannii (ATCC 19606). Conclusion These results revealed an improvement in both antibacterial and antioxidant effects of the drug in the niosomal formulation.

scholarly journals Pleiotropic Effects of Biguanides on Mitochondrial Reactive Oxygen Species Production

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Alena Pecinova ◽  
Zdenek Drahota ◽  
Jana Kovalcikova ◽  
Nikola Kovarova ◽  
Petr Pecina ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Respiratory Chain ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Epidemiological Studies ◽  
The Body ◽  
Oxygen Species ◽  
Brown Adipose ◽  
First Choice ◽  
Species Production

Metformin is widely prescribed as a first-choice antihyperglycemic drug for treatment of type 2 diabetes mellitus, and recent epidemiological studies showed its utility also in cancer therapy. Although it is in use since the 1970s, its molecular target, either for antihyperglycemic or antineoplastic action, remains elusive. However, the body of the research on metformin effect oscillates around mitochondrial metabolism, including the function of oxidative phosphorylation (OXPHOS) apparatus. In this study, we focused on direct inhibitory mechanism of biguanides (metformin and phenformin) on OXPHOS complexes and its functional impact, using the model of isolated brown adipose tissue mitochondria. We demonstrate that biguanides nonspecifically target the activities of all respiratory chain dehydrogenases (mitochondrial NADH, succinate, and glycerophosphate dehydrogenases), but only at very high concentrations (10−2–10−1 M) that highly exceed cellular concentrations observed during the treatment. In addition, these concentrations of biguanides also trigger burst of reactive oxygen species production which, in combination with pleiotropic OXPHOS inhibition, can be toxic for the organism. We conclude that the beneficial effect of biguanides should probably be associated with subtler mechanism, different from the generalized inhibition of the respiratory chain.

scholarly journals Dengue Virus Targets Nrf2 for NS2B3-Mediated Degradation Leading to Enhanced Oxidative Stress and Viral Replication

2020 ◽  
Vol 94 (24) ◽  
Author(s):  
Matteo Ferrari ◽  
Alessandra Zevini ◽  
Enrico Palermo ◽  
Michela Muscolini ◽  
Magdalini Alexandridi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Dengue Virus ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Hemorrhagic Fever ◽  
Denv Infection ◽  
Progressive Increase ◽  
Severe Dengue ◽  
Oxygen Species

ABSTRACT Dengue virus (DENV) is a mosquito-borne virus that infects upward of 300 million people annually and has the potential to cause fatal hemorrhagic fever and shock. While the parameters contributing to dengue immunopathogenesis remain unclear, the collapse of redox homeostasis and the damage induced by oxidative stress have been correlated with the development of inflammation and progression toward the more severe forms of disease. In the present study, we demonstrate that the accumulation of reactive oxygen species (ROS) late after DENV infection (>24 hpi) resulted from a disruption in the balance between oxidative stress and the nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent antioxidant response. The DENV NS2B3 protease complex strategically targeted Nrf2 for degradation in a proteolysis-independent manner; NS2B3 licensed Nrf2 for lysosomal degradation. Impairment of the Nrf2 regulator by the NS2B3 complex inhibited the antioxidant gene network and contributed to the progressive increase in ROS levels, along with increased virus replication and inflammatory or apoptotic gene expression. By 24 hpi, when increased levels of ROS and antiviral proteins were observed, it appeared that the proviral effect of ROS overcame the antiviral effects of the interferon (IFN) response. Overall, these studies demonstrate that DENV infection disrupts the regulatory interplay between DENV-induced stress responses, Nrf2 antioxidant signaling, and the host antiviral immune response, thus exacerbating oxidative stress and inflammation in DENV infection. IMPORTANCE Dengue virus (DENV) is a mosquito-borne pathogen that threatens 2.5 billion people in more than 100 countries annually. Dengue infection induces a spectrum of clinical symptoms, ranging from classical dengue fever to severe dengue hemorrhagic fever or dengue shock syndrome; however, the complexities of DENV immunopathogenesis remain controversial. Previous studies have reported the importance of the transcription factor Nrf2 in the control of redox homeostasis and antiviral/inflammatory or death responses to DENV. Importantly, the production of reactive oxygen species and the subsequent stress response have been linked to the development of inflammation and progression toward the more severe forms of the disease. Here, we demonstrate that DENV uses the NS2B3 protease complex to strategically target Nrf2 for degradation, leading to a progressive increase in oxidative stress, inflammation, and cell death in infected cells. This study underlines the pivotal role of the Nrf2 regulatory network in the context of DENV infection.

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