scholarly journals Impact of EcSOD Perturbations in Cancer Progression

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1219
Author(s):  
Brianne R. O’Leary ◽  
Rory S. Carroll ◽  
Garett J. Steers ◽  
Jennifer Hrabe ◽  
Frederick E. Domann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Responses ◽  
Cancer Progression ◽  
Superoxide Anion ◽  
Cellular Proliferation ◽  
Redox Balance ◽  
Extracellular Superoxide Dismutase ◽  
Oxygen Species ◽  
Altered Metabolism ◽  
Extracellular Environment

Reactive oxygen species (ROS) are a normal byproduct of cellular metabolism and are required components in cell signaling and immune responses. However, an imbalance of ROS can lead to oxidative stress in various pathological states. Increases in oxidative stress are one of the hallmarks in cancer cells, which display an altered metabolism when compared to corresponding normal cells. Extracellular superoxide dismutase (EcSOD) is an antioxidant enzyme that catalyzes the dismutation of superoxide anion (O2−) in the extracellular environment. By doing so, this enzyme provides the cell with a defense against oxidative damage by contributing to redox balance. Interestingly, EcSOD expression has been found to be decreased in a variety of cancers, and this loss of expression may contribute to the development and progression of malignancies. In addition, recent compounds can increase EcSOD activity and expression, which has the potential for altering this redox signaling and cellular proliferation. This review will explore the role that EcSOD expression plays in cancer in order to better understand its potential as a tool for the detection, predicted outcomes and potential treatment of malignancies.

scholarly journals Reactive Oxygen Species: A Key Constituent in Cancer Survival

2018 ◽  
Vol 13 ◽  
pp. 117727191875539 ◽  
Author(s):  
Seema Kumari ◽  
Anil Kumar Badana ◽  
Murali Mohan G ◽  
Shailender G ◽  
RamaRao Malla
Keyword(s):  
Reactive Oxygen Species ◽  
Cancer Progression ◽  
Cancer Survival ◽  
Reactive Oxygen ◽  
Redox Balance ◽  
High Morbidity ◽  
Oxygen Species ◽  
Oncogenic Signaling ◽  
Cancer Cell Death ◽  
New Strategy

Background: Cancer is one of the major heterogeneous disease with high morbidity and mortality with poor prognosis. Elevated levels of reactive oxygen species (ROS), alteration in redox balance, and deregulated redox signaling are common hallmarks of cancer progression and resistance to treatment. Mitochondria contribute mainly in the generation of ROS during oxidative phosphorylation. Elevated levels of ROS have been detected in cancers cells due to high metabolic activity, cellular signaling, peroxisomal activity, mitochondrial dysfunction, activation of oncogene, and increased enzymatic activity of oxidases, cyclooxygenases, lipoxygenases, and thymidine phosphorylases. Cells maintain intracellular homeostasis by developing an immense antioxidant system including catalase, superoxide dismutase, and glutathione peroxidase. Besides these enzymes exist an important antioxidant glutathione and transcription factor Nrf2 which contribute in balancing oxidative stress. Reactive oxygen species–mediated signaling pathways activate pro-oncogenic signaling which eases in cancer progression, angiogenesis, and survival. Concomitantly, to maintain ROS homeostasis and evade cancer cell death, an increased level of antioxidant capacity is associated with cancer cells. Conclusions: This review focuses the role of ROS in cancer survival pathways and importance of targeting the ROS signal involved in cancer development, which is a new strategy in cancer treatment.

scholarly journals Microenvironmental Reactive Oxygen Species in Colorectal Cancer: Involved Processes and Therapeutic Opportunities

Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5037
Author(s):  
Maria Alba Sorolla ◽  
Ivan Hidalgo ◽  
Anabel Sorolla ◽  
Robert Montal ◽  
Ona Pallisé ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Reactive Oxygen Species ◽  
Cancer Progression ◽  
Cellular Proliferation ◽  
Therapeutic Potential ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mesenchymal Transition ◽  
Screening Programs ◽  
Systemic Treatments

Colorectal cancer (CRC) is the fourth most common cause of cancer deaths worldwide. Although screening programs have reduced mortality rates, there is a need for research focused on finding the main factors that lead primary CRC to progress and metastasize. During tumor progression, malignant cells modify their habitat, corrupting or transforming cells of different origins and creating the tumor microenvironment (TME). Cells forming the TME like macrophages, neutrophils, and fibroblasts generate reactive oxygen species (ROS) that modify the cancer niche. The effects of ROS in cancer are very diverse: they promote cellular proliferation, epithelial-to-mesenchymal transition (EMT), evasion of cell death programs, migration, and angiogenesis. Due to the multifaceted role of ROS in cancer cell survival and function, ROS-modulating agents such as antioxidants or pro-oxidants could have therapeutic potential in cancer prevention and/or as a complement to systemic treatments. In this review, we will examine the main ROS producer cells and their effects on cancer progression and metastasis. Furthermore, we will enumerate the latest clinical trials where pro-oxidants and antioxidants have therapeutic uses in CRC.

scholarly journals Endometriosis and Oxidative Stress. Do Reactive Oxygen Species Always Lead to Damages of Gametes and Embryos?

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Török A ◽  
◽  
Máté G ◽  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cellular Proliferation ◽  
Uterine Cavity ◽  
Reactive Oxygen ◽  
Clinical Results ◽  
Oxygen Species ◽  
Negative Effects ◽  
Tubal Infertility ◽  
And Oxidative Stress

Reactive Oxygen Species (ROS) play a crucial role in the pathogenesis of many reproductive disorders, such as endometriosis on the one hand, but on the other hand they participate in different cellular proliferation processes, too. Endometriosis is an apoptotic endometrial, menstrual cells and lysed erythrocytes-induced inflammatory disease outside the uterine cavity, which activates macrophages leading to ROS production and oxidative stress. However, based on the available literature, the reproductive outcomes are still contradictory. In this study, the demographic, embryological and clinical results of 252 patients suffering from tubal infertility (control), ASRM I-II and III-IV endometriosis were analyzed. Endometriosis was associated with decreased anti-Müllerian hormone level and increased gonadotropin doses during stimulation (p<0.0001). In ASRM III-IV, reduced embryological parameters were observed, which resulted in 13.73% and 15.21% decrements in the implantation rates, 19.96% and 23.89% in the clinical pregnancy rates of patients suffering from ASRM III-IV endometriosis in comparison with control or ASRM I-II, respectively. In addition, miscarriage rates were 19.04%, 29.03% and 38.46% in control, ASRM I-II and ASRM III-IV, respectively. In our study, the supposed altered oxido-reduction environment of gametes and embryos obviously exerted negative effects on the embryological and clinical parameters, but these effects could not be observed in case of mild endometriosis with low level of stress.

scholarly journals Redox Potential of Antioxidants in Cancer Progression and Prevention

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1156
Author(s):  
Sajan George ◽  
Heidi Abrahamse
Keyword(s):  
Oxidative Stress ◽  
Cancer Progression ◽  
Natural Antioxidants ◽  
Redox Balance ◽  
Redox Status ◽  
Enzyme Activation ◽  
Metabolic Reprogramming ◽  
Cellular Functions ◽  
Cellular Redox ◽  
The Right

The benevolent and detrimental effects of antioxidants are much debated in clinical trials and cancer research. Several antioxidant enzymes and molecules are overexpressed in oxidative stress conditions that can damage cellular proteins, lipids, and DNA. Natural antioxidants remove excess free radical intermediates by reducing hydrogen donors or quenching singlet oxygen and delaying oxidative reactions in actively growing cancer cells. These reducing agents have the potential to hinder cancer progression only when administered at the right proportions along with chemo-/radiotherapies. Antioxidants and enzymes affect signal transduction and energy metabolism pathways for the maintenance of cellular redox status. A decline in antioxidant capacity arising from genetic mutations may increase the mitochondrial flux of free radicals resulting in misfiring of cellular signalling pathways. Often, a metabolic reprogramming arising from these mutations in metabolic enzymes leads to the overproduction of so called ’oncometabolites’ in a state of ‘pseudohypoxia’. This can inactivate several of the intracellular molecules involved in epigenetic and redox regulations, thereby increasing oxidative stress giving rise to growth advantages for cancerous cells. Undeniably, these are cell-type and Reactive Oxygen Species (ROS) specific, which is manifested as changes in the enzyme activation, differences in gene expression, cellular functions as well as cell death mechanisms. Photodynamic therapy (PDT) using light-activated photosensitizing molecules that can regulate cellular redox balance in accordance with the changes in endogenous ROS production is a solution for many of these challenges in cancer therapy.

Applications of nanomaterials for scavenging reactive oxygen species in the treatment of central nervous system diseases

2020 ◽  
Vol 8 (38) ◽  
pp. 8748-8767
Author(s):  
Zhen An ◽  
Jincong Yan ◽  
Ye Zhang ◽  
Renjun Pei
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Central Nervous System ◽  
Nervous System ◽  
Redox Balance ◽  
Oxygen Species ◽  
Nervous System Diseases ◽  
Central Nervous System Diseases ◽  
Ros Scavenging ◽  
Function Recovery

Nanomaterials with excellent ROS-scavenging ability and biodistribution are considered as promising candidates in alleviating oxidative stress and restoring redox balance in CNS diseases, further facilitating the function recovery of the CNS.

scholarly journals Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

2021 ◽  
Author(s):  
Marta Justyna Kozieł ◽  
Karolina Kowalska ◽  
Agnieszka Wanda Piastowska-Ciesielska
Keyword(s):  
Oxidative Stress ◽  
Redox Balance ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Animal Cells ◽  
Nrf2 Signaling Pathway ◽  
Responsive Element ◽  
Almost All ◽  
In Cells

AbstractNuclear factor erythroid 2-like 2 (Nrf2) is a transcription factor participating in response to cellular oxidative stress to maintain the redox balance. Generation of reactive oxygen species (ROS) and, in consequence, oxidative stress, are physiological as well as pathological processes which take place in almost all types of cells. Nrf2, in response to oxidative stress, activates expression and production of antioxidant enzymes to remove free radicals. However, the role of Nrf2 seems to be more sophisticated and its increased expression observed in cancer cells allows to draw a conclusion that its role is tissue—and condition—dependent. Interestingly, Nrf2 might also play a crucial role in response to environmental factors like mycotoxins. Thus, the aim of the study is to review the role of Nrf2 in cells exposed to most common mycotoxins to check if the Nrf2 signaling pathway serves as the main response element to mycotoxin-induced oxidative stress in human and animal cells and if it can be a target of detoxifying agents.

scholarly journals Oxidative Stress-Inducing Anticancer Therapies: Taking a Closer Look at Their Immunomodulating Effects

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1188
Author(s):  
Jinthe Van Loenhout ◽  
Marc Peeters ◽  
Annemie Bogaerts ◽  
Evelien Smits ◽  
Christophe Deben
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Treatment Strategies ◽  
Redox Balance ◽  
Cellular Responses ◽  
Anticancer Therapy ◽  
Treatment Modalities ◽  
Oxygen Species ◽  
Novel Target ◽  
High Level

Cancer cells are characterized by higher levels of reactive oxygen species (ROS) compared to normal cells as a result of an imbalance between oxidants and antioxidants. However, cancer cells maintain their redox balance due to their high antioxidant capacity. Recently, a high level of oxidative stress is considered a novel target for anticancer therapy. This can be induced by increasing exogenous ROS and/or inhibiting the endogenous protective antioxidant system. Additionally, the immune system has been shown to be a significant ally in the fight against cancer. Since ROS levels are important to modulate the antitumor immune response, it is essential to consider the effects of oxidative stress-inducing treatments on this response. In this review, we provide an overview of the mechanistic cellular responses of cancer cells towards exogenous and endogenous ROS-inducing treatments, as well as the indirect and direct antitumoral immune effects, which can be both immunostimulatory and/or immunosuppressive. For future perspectives, there is a clear need for comprehensive investigations of different oxidative stress-inducing treatment strategies and their specific immunomodulating effects, since the effects cannot be generalized over different treatment modalities. It is essential to elucidate all these underlying immune effects to make oxidative stress-inducing treatments effective anticancer therapy.

scholarly journals Resistance of Postharvest Biocontrol Yeasts to Oxidative Stress: A Possible New Mechanism of Action

2003 ◽  
Vol 93 (5) ◽  
pp. 564-572 ◽  
Author(s):  
Raffaello Castoria ◽  
Leonardo Caputo ◽  
Filippo De Curtis ◽  
Vincenzo De Cicco
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Rhodotorula Glutinis ◽  
Antagonistic Activity ◽  
Model System ◽  
Penicillium Expansum ◽  
Cryptococcus Laurentii ◽  
Oxygen Species ◽  
Combined Application

We detected the generation of the reactive oxygen species (ROS) superoxide anion ( O·- 2) and hydrogen peroxide (H2O2) in apple wounds 2 immediately after wounding, and assessed the relationships between (i) timely colonization of apple wounds by biocontrol yeasts, (ii) resistance of these microorganisms to oxidative stress caused by ROS, and (iii) their antagonism against postharvest wound pathogens. We analyzed a model system consisting of two yeasts with higher (Cryptococcus laurentii LS-28) or lower (Rhodotorula glutinis LS-11) antagonistic activity against the postharvest pathogens Botrytis cinerea and Penicillium expansum. LS-28 exhibited faster and greater colonization of wounds than LS-11. In contrast to LS-28, the number of LS-11 cells dropped 1 and 2 h after application, and then increased only later. In vitro, LS-28 was more resistant to ROS-generated oxidative stress. The combined application of biocontrol yeasts and ROS-deactivating enzymes in apple wounds prevented the decrease in number of LS-11 cells mentioned above, and enhanced colonization and antagonistic activity of both biocontrol yeasts against B. cinerea and P. expansum. Polar lipids of LS-11 contained the more unsaturated and oxidizable α-linolenic acid, which was absent in LS-28. Resistance to oxidative stress could be a key mechanism of biocontrol yeasts antagonism against postharvest wound pathogens.

scholarly journals Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody production

2007 ◽  
Vol 402 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Yoshihito Iuchi ◽  
Futoshi Okada ◽  
Kunishige Onuma ◽  
Tadashi Onoda ◽  
Hironobu Asao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox Balance ◽  
Oxidative Modification ◽  
Autoimmune Response ◽  
Oxygen Species ◽  
Autoantibody Production ◽  
Oxidative Modification Of Proteins ◽  
High Level ◽  
Continuous Destruction

Reactive oxygen species are involved in the aging process and diseases. Despite the important role of Cu/Zn SOD (superoxide dismutase) encoded by SOD1, SOD1−/− mice appear to grow normally under conventional breeding conditions. In the present paper we report on a novel finding showing a distinct connection between oxidative stress in erythrocytes and the production of autoantibodies against erythrocytes in SOD1−/− mice. Evidence is presented to show that SOD1 is primarily required for maintaining erythrocyte lifespan by suppressing oxidative stress. A SOD1 deficiency led to an increased erythrocyte vulnerability by the oxidative modification of proteins and lipids, resulting in anaemia and compensatory activation of erythropoiesis. The continuous destruction of oxidized erythrocytes appears to induce the formation of autoantibodies against certain erythrocyte components, e.g. carbonic anhydrase II, and the immune complex is deposited in the glomeruli. The administration of an antioxidant, N-acetylcysteine, suppressed erythrocyte oxidation, ameliorated the anaemia, and inhibited the production of autoantibodies. These data imply that a high level of oxidative stress in erythrocytes increases the production of autoantibodies, possibly leading to an autoimmune response, and that the intake of antioxidants would prevent certain autoimmune responses by maintaining an appropriate redox balance in erythrocytes.

scholarly journals Oxidative Stress Level in the Testes of Mice and Rats during Nickel Intoxication

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Eugenia Murawska-Ciałowicz ◽  
Wojciech Bal ◽  
Lidia Januszewska ◽  
Marcin Zawadzki ◽  
Joanna Rychel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Stress Level ◽  
Reduced Glutathione ◽  
Redox Balance ◽  
Oxygen Species ◽  
Antioxidative Defense ◽  
Carcinogenic Effect ◽  
Oxidative Stress Level

The genotioxic and carcinogenic effect of nickel probably results from its capacity to produce reactive oxygen species (ROS) and disturb the redox balance. The aim of the study was to find out if rats lacking spermatic protamine 2 are less susceptible to Ni(II) than mice. Consequently, the levels of malondialdehyde + 4 hydroxynonenal (MDA+4HDA) − markers of lipid peroxidation, as well as the level of reduced glutathione (GSH) were measured within the rat and mouse testes. Our results showed that the levels of lipid peroxidation markers were elevated in testicular homogenates of intoxicated mice without any changes in rats. GSH level was lower in the group of intoxicated mice comparing to the control without statistically significant changes in rats’ homogenates. Moreover, the level of GSH in the testes of intoxicated mice was lower than in rats. On the basis of our results, it appears that Ni(II) can initiate oxidative stress in the testes of mice but not of rats and can reduce GSH level. Consequently, the antioxidative defense of the testes is reduced. Ni(II) that causes oxidative stress in the testes may also contribute to infertility.

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