scholarly journals The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword?

2021 ◽  
Vol 9 ◽  
Author(s):  
Hongli Li ◽  
Celien Lismont ◽  
Iulia Revenco ◽  
Mohamed A. F. Hussein ◽  
Cláudio F. Costa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Molecular Mechanisms ◽  
Protective Role ◽  
Local Concentration ◽  
Comprehensive Overview ◽  
Selective Autophagy ◽  
Bidirectional Relationship ◽  
Health And Disease ◽  
To Receive

Peroxisomes harbor numerous enzymes that can produce or degrade hydrogen peroxide (H2O2). Depending on its local concentration and environment, this oxidant can function as a redox signaling molecule or cause stochastic oxidative damage. Currently, it is well-accepted that dysfunctional peroxisomes are selectively removed by the autophagy-lysosome pathway. This process, known as “pexophagy,” may serve a protective role in curbing peroxisome-derived oxidative stress. Peroxisomes also have the intrinsic ability to mediate and modulate H2O2-driven processes, including (selective) autophagy. However, the molecular mechanisms underlying these phenomena are multifaceted and have only recently begun to receive the attention they deserve. This review provides a comprehensive overview of what is known about the bidirectional relationship between peroxisomal H2O2 metabolism and (selective) autophagy. After introducing the general concepts of (selective) autophagy, we critically examine the emerging roles of H2O2 as one of the key modulators of the lysosome-dependent catabolic program. In addition, we explore possible relationships among peroxisome functioning, cellular H2O2 levels, and autophagic signaling in health and disease. Finally, we highlight the most important challenges that need to be tackled to understand how alterations in peroxisomal H2O2 metabolism contribute to autophagy-related disorders.

scholarly journals Improved Effect of a Mitochondria-Targeted Antioxidant on Hydrogen Peroxide-Induced Oxidative Stress in Human Retinal Pigment Epithelium Cells

2020 ◽  
Author(s):  
MYUNG HEE KIM ◽  
Dae Hyun Kim ◽  
Su Geun Yang ◽  
Dae Yu Kim
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Transcription Factors ◽  
Mitochondrial Dysfunction ◽  
Retinal Pigment ◽  
Protective Role ◽  
Age Related Macular Degeneration ◽  
Ros Generation ◽  
Rpe Cells ◽  
Age Related

Abstract Background: Oxidative damage in retinal pigmented epithelium (RPE) cells contributes to the development of age-related macular degeneration, which is among the leading causes of visual loss in elderly people. In the present study, we evaluated the protective role of TPP-Niacin against the hydrogen peroxide (H2O2)-induced oxidative stress to RPE cells. Methods: The cellular viability, lactate dehydrogenase, reactive oxygen species (ROS), and mitochondrial function were determined in the retinal ARPE-19 cells under the treatment with H2O2 or pre-treatment with TPP-Niacin. The expression level of mitochondrial related genes and some transcription factors were assessed using real-time polymerase chain reaction (RT-PCR). Results: TPP-Niacin significantly improved cell viability reduction, reduced ROS generation and increased the antioxidant enzymes in H2O2-treated ARPE-19 cells. Mitochondrial dysfunction from H2O2-induced oxidative stress was also significantly diminished by the TPP-Niacin treatment, reduced generation of ROS, an ameliorated reduction of mitochondrial membrane potential (MMP) and an upregulated mitochondrial associated gene. In addition, TPP-Niacin markedly enhanced the expression of transcription factors (PGC-1α and NRF2) and antioxidant associated genes (especially, HO-1 and NQO-1). Conclusion: We proved the protective effect of TPP-Niacin against H2O2-induced oxidative stress in RPE cells. TPP-Niacin is believed to have played a protective role against mitochondrial dysfunction by up-regulating antioxidant-related genes such as PGC-1α, NRF2, HO-1 and NQO-1 in RPE cells.

Crosstalk between adipose and lymphatics in health and disease

Endocrinology ◽  
2021 ◽  
Author(s):  
Gregory P Westcott ◽  
Evan D Rosen
Keyword(s):  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Lymphatic Function ◽  
Lipid Trafficking ◽  
Resident Cell ◽  
Bidirectional Relationship ◽  
Lymphatic Vasculature ◽  
Health And Disease ◽  
Scientific Attention ◽  
The Relationship

Abstract Adipose tissue, once thought to be an inert receptacle for energy storage, is now recognized as a complex tissue with multiple resident cell populations which actively collaborate in response to diverse local and systemic metabolic, thermal, and inflammatory signals. A key participant in adipose tissue homeostasis that has only recently captured broad scientific attention is the lymphatic vasculature. The lymphatic system’s role in lipid trafficking and mediating inflammation makes it a natural partner in the regulation of adipose tissue, and evidence supporting a bidirectional relationship between lymphatics and adipose tissue has accumulated in recent years. Obesity is now understood to impair lymphatic function, while altered lymphatic function results in aberrant adipose tissue deposition, though the molecular mechanisms governing these phenomena have yet to be fully elucidated. We will review our current understanding of the relationship between adipose tissue and the lymphatic system here, focusing on known mechanisms of lymphatic-adipose cross-talk.

Cytoglobin Up-regulated by Hydrogen Peroxide Plays a Protective Role in Oxidative Stress

2007 ◽  
Vol 32 (8) ◽  
pp. 1375-1380 ◽  
Author(s):  
Dan Li ◽  
Xiao Qian Chen ◽  
Wu-Jian Li ◽  
Yu-Hui Yang ◽  
Jian-Zhi Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protective Role

scholarly journals p62/SQSTM1-droplet serves as a platform for autophagosome formation and anti-oxidative stress response

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shun Kageyama ◽  
Sigurdur Runar Gudmundsson ◽  
Yu-Shin Sou ◽  
Yoshinobu Ichimura ◽  
Naoki Tamura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Oxidative Stress Response ◽  
Liquid Droplets ◽  
Autophagosome Formation ◽  
Selective Autophagy ◽  
Selective Degradation ◽  
Physiological Relevance ◽  
Related Proteins

AbstractAutophagy contributes to the selective degradation of liquid droplets, including the P-Granule, Ape1-complex and p62/SQSTM1-body, although the molecular mechanisms and physiological relevance of selective degradation remain unclear. In this report, we describe the properties of endogenous p62-bodies, the effect of autophagosome biogenesis on these bodies, and the in vivo significance of their turnover. p62-bodies are low-liquidity gels containing ubiquitin and core autophagy-related proteins. Multiple autophagosomes form on the p62-gels, and the interaction of autophagosome-localizing Atg8-proteins with p62 directs autophagosome formation toward the p62-gel. Keap1 also reversibly translocates to the p62-gels in a p62-binding dependent fashion to activate the transcription factor Nrf2. Mice deficient for Atg8-interaction-dependent selective autophagy show that impaired turnover of p62-gels leads to Nrf2 hyperactivation in vivo. These results indicate that p62-gels are not simple substrates for autophagy but serve as platforms for both autophagosome formation and anti-oxidative stress.

scholarly journals Peroxisomal Hydrogen Peroxide Metabolism and Signaling in Health and Disease

2019 ◽  
Vol 20 (15) ◽  
pp. 3673 ◽  
Author(s):  
Lismont ◽  
Revenco ◽  
Fransen
Keyword(s):  
Hydrogen Peroxide ◽  
Molecular Mechanisms ◽  
Signaling Network ◽  
H2o2 Production ◽  
Peroxisomal Enzyme ◽  
Pathological Conditions ◽  
Health And Disease ◽  
Precise Role ◽  
Insight Into

Hydrogen peroxide (H2O2), a non-radical reactive oxygen species generated during many (patho)physiological conditions, is currently universally recognized as an important mediator of redox-regulated processes. Depending on its spatiotemporal accumulation profile, this molecule may act as a signaling messenger or cause oxidative damage. The focus of this review is to comprehensively evaluate the evidence that peroxisomes, organelles best known for their role in cellular lipid metabolism, also serve as hubs in the H2O2 signaling network. We first briefly introduce the basic concepts of how H2O2 can drive cellular signaling events. Next, we outline the peroxisomal enzyme systems involved in H2O2 metabolism in mammals and reflect on how this oxidant can permeate across the organellar membrane. In addition, we provide an up-to-date overview of molecular targets and biological processes that can be affected by changes in peroxisomal H2O2 metabolism. Where possible, emphasis is placed on the molecular mechanisms and factors involved. From the data presented, it is clear that there are still numerous gaps in our knowledge. Therefore, gaining more insight into how peroxisomes are integrated in the cellular H2O2 signaling network is of key importance to unravel the precise role of peroxisomal H2O2 production and scavenging in normal and pathological conditions.

Protective role of nitric oxide during hydrogen peroxide-induced oxidative stress in tobacco plants

2007 ◽  
Vol 54 (6) ◽  
pp. 755-762 ◽  
Author(s):  
L. V. Dubovskaya ◽  
E. V. Kolesneva ◽  
D. M. Knyazev ◽  
I. D. Volotovskii
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Protective Role ◽  
Tobacco Plants

scholarly journals Role of Nrf2 in Disease: Novel Molecular Mechanisms and Therapeutic Approaches – Pulmonary Disease/Asthma

2021 ◽  
Vol 12 ◽  
Author(s):  
Camille Audousset ◽  
Toby McGovern ◽  
James G. Martin
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Disease ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Antioxidant Response ◽  
Protective Role ◽  
Experimental Models ◽  
Chronic Obstructive ◽  
Related Factor ◽  
Obstructive Pulmonary Disease

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a major transcription factor involved in redox homeostasis and in the response induced by oxidative injury. Nrf2 is present in an inactive state in the cytoplasm of cells. Its activation by internal or external stimuli, such as infections or pollution, leads to the transcription of more than 500 elements through its binding to the antioxidant response element. The lungs are particularly susceptible to factors that generate oxidative stress such as infections, allergens and hyperoxia. Nrf2 has a crucial protective role against these ROS. Oxidative stress and subsequent activation of Nrf2 have been demonstrated in many human respiratory diseases affecting the airways, including asthma and chronic obstructive pulmonary disease (COPD), or the pulmonary parenchyma such as acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Several compounds, both naturally occurring and synthetic, have been identified as Nrf2 inducers and enhance the activation of Nrf2 and expression of Nrf2-dependent genes. These inducers have proven particularly effective at reducing the severity of the oxidative stress-driven lung injury in various animal models. In humans, these compounds offer promise as potential therapeutic strategies for the management of respiratory pathologies associated with oxidative stress but there is thus far little evidence of efficacy through human trials. The purpose of this review is to summarize the involvement of Nrf2 and its inducers in ARDS, COPD, asthma and lung fibrosis in both human and in experimental models.

scholarly journals Biochemical Hallmarks of Oxidative Stress-Induced Overactivation of Xenopus Eggs

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Alexander A. Tokmakov ◽  
Misaki Awamura ◽  
Ken-Ichi Sato
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protein Content ◽  
Molecular Mechanisms ◽  
Low Frequency ◽  
Cytoplasmic Protein ◽  
Lipofuscin Accumulation ◽  
Progressive Development ◽  
Biochemical Analyses ◽  
Dose Dependent

Egg overactivation occurs with a low frequency in the populations of naturally ovulated frog eggs. At present, its natural inducers, molecular mechanisms, and intracellular events remain unknown. Using microscopic and biochemical analyses, we demonstrate here that high levels of hydrogen peroxide-induced oxidative stress can cause time- and dose-dependent overactivation of Xenopus eggs. Lipofuscin accumulation, decrease of soluble cytoplasmic protein content, and depletion of intracellular ATP were found to take place in the overactivated eggs. Progressive development of these processes suggests that egg overactivation unfolds in a sequential and ordered fashion.

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