scholarly journals Natural Compounds as Modulators of NADPH Oxidases

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Tullia Maraldi
Keyword(s):  
Mammalian Cells ◽  
Redox State ◽  
Regulation Of Gene Expression ◽  
Natural Compounds ◽  
Oxygen Species ◽  
Nadph Oxidases ◽  
Natural Extracts ◽  
Current State ◽  
Wide Range

Reactive oxygen species (ROS) are cellular signals generated ubiquitously by all mammalian cells, but their relative unbalance triggers also diseases through intracellular damage to DNA, RNA, proteins, and lipids. NADPH oxidases (NOX) are the only known enzyme family with the sole function to produce ROS. The NOX physiological functions concern host defence, cellular signaling, regulation of gene expression, and cell differentiation. On the other hand, increased NOX activity contributes to a wide range of pathological processes, including cardiovascular diseases, neurodegeneration, organ failure, and cancer. Therefore targeting these enzymatic ROS sources by natural compounds, without affecting the physiological redox state, may be an important tool. This review summarizes the current state of knowledge of the role of NOX enzymes in physiology and pathology and provides an overview of the currently available NADPH oxidase inhibitors derived from natural extracts such as polyphenols.

scholarly journals The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology

2007 ◽  
Vol 87 (1) ◽  
pp. 245-313 ◽  
Author(s):  
Karen Bedard ◽  
Karl-Heinz Krause
Keyword(s):  
Nadph Oxidase ◽  
Regulation Of Gene Expression ◽  
Nadph Oxidases ◽  
Phagocyte Nadph Oxidase ◽  
Current State ◽  
Wide Range ◽  
The Family ◽  
Activation Mechanisms ◽  
Long Time ◽  
Nox Family

For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2/gp91phox), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX actvity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.

scholarly journals Role of microRNAs in Lung Carcinogenesis Induced by Asbestos

2021 ◽  
Vol 11 (2) ◽  
pp. 97
Author(s):  
Rakhmetkazhy Bersimbaev ◽  
Olga Bulgakova ◽  
Akmaral Aripova ◽  
Assiya Kussainova ◽  
Oralbek Ilderbayev
Keyword(s):  
Lung Cancer ◽  
Expression Profile ◽  
Regulation Of Gene Expression ◽  
International Agency ◽  
Oxygen Species ◽  
Lung Carcinogenesis ◽  
Mrna Targets ◽  
The World ◽  
Post Transcriptional Regulation

MicroRNAs are a class of small noncoding endogenous RNAs 19–25 nucleotides long, which play an important role in the post-transcriptional regulation of gene expression by targeting mRNA targets with subsequent repression of translation. MicroRNAs are involved in the pathogenesis of numerous diseases, including cancer. Lung cancer is the leading cause of cancer death in the world. Lung cancer is usually associated with tobacco smoking. However, about 25% of lung cancer cases occur in people who have never smoked. According to the International Agency for Research on Cancer, asbestos has been classified as one of the cancerogenic factors for lung cancer. The mechanism of malignant transformation under the influence of asbestos is associated with the genotoxic effect of reactive oxygen species, which initiate the processes of DNA damage in the cell. However, epigenetic mechanisms such as changes in the microRNA expression profile may also be implicated in the pathogenesis of asbestos-induced lung cancer. Numerous studies have shown that microRNAs can serve as a biomarker of the effects of various adverse environmental factors on the human body. This review examines the role of microRNAs, the expression profile of which changes upon exposure to asbestos, in key processes of carcinogenesis, such as proliferation, cell survival, metastasis, neo-angiogenesis, and immune response avoidance.

Mutagenicity of PFOA in Mammalian Cells: Role of Mitochondria-Dependent Reactive Oxygen Species

2011 ◽  
Vol 45 (4) ◽  
pp. 1638-1644 ◽  
Author(s):  
Guoping Zhao ◽  
Jun Wang ◽  
Xiaofei Wang ◽  
Shaopeng Chen ◽  
Ye Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mammalian Cells ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals The signalling role of ROS in the regulation of seed germination and dormancy

2019 ◽  
Vol 476 (20) ◽  
pp. 3019-3032 ◽  
Author(s):  
Christophe Bailly
Keyword(s):  
Seed Germination ◽  
Oxygen Species ◽  
Direct Oxidation ◽  
Cellular Events ◽  
Seed Physiology ◽  
Spatiotemporal Regulation ◽  
Wide Range ◽  
Living Organisms ◽  
Hormone Signalling

Abstract Reactive oxygen species (ROS) are versatile compounds which can have toxic or signalling effects in a wide range living organisms, including seeds. They have been reported to play a pivotal role in the regulation of seed germination and dormancy but their mechanisms of action are still far from being fully understood. In this review, we sum-up the major findings that have been carried out this last decade in this field of research and which altogether shed a new light on the signalling roles of ROS in seed physiology. ROS participate in dormancy release during seed dry storage through the direct oxidation of a subset of biomolecules. During seed imbibition, the controlled generation of ROS is involved in the perception and transduction of environmental conditions that control germination. When these conditions are permissive for germination, ROS levels are maintained at a level which triggers cellular events associated with germination, such as hormone signalling. Here we propose that the spatiotemporal regulation of ROS production acts in concert with hormone signalling to regulate the cellular events involved in cell expansion associated with germination.

scholarly journals Melatonin reduces oxidative damage in mouse granulosa cells via restraining JNK-dependent autophagy

Reproduction ◽  
2018 ◽  
Vol 155 (3) ◽  
pp. 307-319 ◽  
Author(s):  
Yan Cao ◽  
Ming Shen ◽  
Yi Jiang ◽  
Shao-chen Sun ◽  
Honglin Liu
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Mammalian Cells ◽  
Therapeutic Strategies ◽  
Oxygen Species ◽  
Protective Effects ◽  
Follicular Atresia ◽  
Direct Role ◽  
Jnk Pathway

Oxidative stress-induced granulosa cell (GCs) injury is believed to be a common trigger for follicular atresia. Emerging evidence indicates that excessive autophagy occurs in mammalian cells with oxidative damage. N-acetyl-5-methoxytrypamine (melatonin) has been shown to prevent GCs from oxidative injury, although the exact mechanism remains to be elucidated. Here, we first demonstrated that the suppression of autophagy through the JNK/BCL-2/BECN1 signaling is engaged in melatonin-mediated GCs protection against oxidative damage. Melatonin inhibited the loss of GCs viability, formation of GFP-MAP1LC3B puncta, accumulation of MAP1LC3B-II blots, degradation of SQSTM1 and the expression of BECN1, which was correlated with impaired activation of JNK during oxidative stress. On the other hand, blocking of autophagy and/or JNK also reduced the level of H2O2-induced GCs death, but failed to further restore GCs viability in the presence of melatonin. Particularly, the suppression of autophagy provided no additional protective effects when GCs were pretreated with JNK inhibitor and/or melatonin. Importantly, we found that the enhanced interaction between BCL-2 and BECN1 might be a responsive mechanism for autophagy suppression via the melatonin/JNK pathway. Moreover, blocking the downstream antioxidant system of melatonin using specific inhibitors further confirmed a direct role of melatonin/JNK/autophagy axis in preserving GCs survival without scavenging reactive oxygen species (ROS). Taken together, our findings uncover a novel function of melatonin in preventing GCs from oxidative damage by targeting JNK-mediated autophagy, which might contribute to develop therapeutic strategies for patients with ovulation failure-related disorders.

scholarly journals NADPH Oxidases: Insights into Selected Functions and Mechanisms of Action in Cancer and Stem Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Magdalena Skonieczna ◽  
Tomasz Hejmo ◽  
Aleksandra Poterala-Hejmo ◽  
Artur Cieslar-Pobuda ◽  
Rafal J. Buldak
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Tissue Regeneration ◽  
Mechanisms Of Action ◽  
Cell Physiology ◽  
Oxygen Species ◽  
Nadph Oxidases ◽  
Wide Range ◽  
Selected Functions ◽  
Complex Activities

NADPH oxidases (NOX) are reactive oxygen species- (ROS-) generating enzymes regulating numerous redox-dependent signaling pathways. NOX are important regulators of cell differentiation, growth, and proliferation and of mechanisms, important for a wide range of processes from embryonic development, through tissue regeneration to the development and spread of cancer. In this review, we discuss the roles of NOX and NOX-derived ROS in the functioning of stem cells and cancer stem cells and in selected aspects of cancer cell physiology. Understanding the functions and complex activities of NOX is important for the application of stem cells in tissue engineering, regenerative medicine, and development of new therapies toward invasive forms of cancers.

scholarly journals Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging

2012 ◽  
Vol 2012 ◽  
pp. 1-17 ◽  
Author(s):  
Saverio Marchi ◽  
Carlotta Giorgi ◽  
Jan M. Suski ◽  
Chiara Agnoletto ◽  
Angela Bononi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Redox State ◽  
Balance Of Power ◽  
Molecular Pathways ◽  
Oxygen Species ◽  
Intrinsic Apoptotic Pathway ◽  
Apoptotic Pathway ◽  
Induce Cell Death

Reactive oxygen species (ROS) are highly reactive molecules, mainly generated inside mitochondria that can oxidize DNA, proteins, and lipids. At physiological levels, ROS function as “redox messengers” in intracellular signalling and regulation, whereas excess ROS induce cell death by promoting the intrinsic apoptotic pathway. Recent work has pointed to a further role of ROS in activation of autophagy and their importance in the regulation of aging. This review will focus on mitochondria as producers and targets of ROS and will summarize different proteins that modulate the redox state of the cell. Moreover, the involvement of ROS and mitochondria in different molecular pathways controlling lifespan will be reported, pointing out the role of ROS as a “balance of power,” directing the cell towards life or death.

scholarly journals PRECONDITIONS OF ADMINISTRATIVE RESPONSIBILITY: DOCTRINAL ISSUES

2021 ◽  
Vol 1 ◽  
pp. 102-111
Author(s):  
Oleksandr Gerasymenko
Keyword(s):  
Law Enforcement ◽  
Public Relations ◽  
Practical Significance ◽  
Clear Understanding ◽  
Current State ◽  
Wide Range ◽  
Scientific Approach ◽  
Rule Making ◽  
Administrative Responsibility

A thorough analysis of liability for administrative offence is not possible without clear understanding of its preconditions. The problem of preconditions for administrative responsibility is directly related to administrative delictization of offenses, effectiveness of the fight against delict, prominent state policy in the field of law enforcement and law order. In this aspect, the role of the preconditions for administrative responsibility is a lot more important because they formulate proper foundations for achieving its general objectives. Thus, they determine the effectiveness of administrative responsibility at sectoral and general social levels. The importance of the definition is due to the urgent needs of rule-making and law enforcement practice, the effectiveness of which directly depends on how reasonable and appropriate each administrative delict norm is. Unfortunately, despite all its scientific and practical significance, the issue of preconditions for administrative liability has not been resolved yet. Therefore, there is a need to form unified, consistent scientific approach to understanding the grounds for administrative liability. To this end, the article provides a critical analysis of the basic doctrinal concepts of the preconditions of administrative responsibility. A wide range of social, economic, technical and other factors that determine the effectiveness of administrative responsibility, its current state, its dynamics and prospects for its development have been studied. Discovered the role of these factors in creating a favorable socio-economic and information-technical environment for the implementation of the main tasks of administrative responsibility, in particular: offences prevention, reliable protection of public relations and education of citizens in the spirit of law. The author concluded the scientific and practical expediency of the systematic study of the preconditions for establishing administrative responsibility (preconditions for administrative delictization) and the preconditions for the effectiveness of administrative responsibility.

scholarly journals Transcriptome-wide assessment of the m6A methylome of intestinal porcine epithelial cells treated with deoxynivalenol

2020 ◽  
Author(s):  
Zhengchang Wu ◽  
Chao Xu ◽  
Haifei Wang ◽  
Song Gao ◽  
Shenglong Wu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammalian Cells ◽  
Tumor Necrosis ◽  
Cytotoxic Compound ◽  
Wide Range ◽  
Food And Feed ◽  
Functional Relevance ◽  
And Control ◽  
Necrosis Factor

Abstract Background: Deoxynivalenol (DON) is a cytotoxic compound found in various food and feed products. N6-Methyladenosine (m6A) is a highly abundant epitranscriptomic marker that modifies a wide range of mRNA molecules in mammalian cells. However, the role of the m6A methylome in DON-induced damage remains poorly understood.Results: In this study, we assessed the transcriptome-wide m6A profile of intestinal porcine epithelial cells (IPEC-J2) treated with 1000 ng/mL DON by m6A sequencing and RNA sequencing. Overall, 5406 new m6A peaks appeared with the disappearance of 2615 peaks in DON-treated IPEC-J2 cells. Genes that were uniquely m6A-modified following DON treatment were found to be associated with the tumor necrosis factor (TNF) signaling pathway. On comparing DON-treated and control cells, we identified 733 differentially expressed mRNAs bearing hyper- or hypomethylated m6A peaks. Further experimental data suggested that METTL3-dependent m6A methylation might also play a role in DON-induced inflammatory response, and CSF2 marker is key functional relevance in the context of DON-induced toxicity. Conclusions: This is the first study to perform a transcriptome-wide assessment of the m6A methylome of IPEC-J2 cells treated with DON. We believe that our findings should be useful for identifying mechanisms whereby m6A modifications influence the outcomes of DON exposure.

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