scholarly journals Oxidized dimeric Scapharca inaequivalvis. Co-driven perturbation of the redox equilibrium.

1991 ◽  
Vol 266 (27) ◽  
pp. 17898-17903
Author(s):  
A. Boffi ◽  
C. Bonaventura ◽  
J. Bonaventura ◽  
R. Cashon ◽  
E. Chiancone
Keyword(s):  
Redox Equilibrium

scholarly journals Contribution of Adipose Tissue Oxidative Stress to Obesity-Associated Diabetes Risk and Ethnic Differences: Focus on Women of African Ancestry

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 622
Author(s):  
Pamela A. Nono Nankam ◽  
Télesphore B. Nguelefack ◽  
Julia H. Goedecke ◽  
Matthias Blüher
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Metabolic Diseases ◽  
African Ancestry ◽  
Fat Distribution ◽  
African Women ◽  
European Ancestry ◽  
Whole Body ◽  
Redox Equilibrium ◽  
Systemic Oxidative Stress

Adipose tissue (AT) storage capacity is central in the maintenance of whole-body homeostasis, especially in obesity states. However, sustained nutrients overflow may dysregulate this function resulting in adipocytes hypertrophy, AT hypoxia, inflammation and oxidative stress. Systemic inflammation may also contribute to the disruption of AT redox equilibrium. AT and systemic oxidative stress have been involved in the development of obesity-associated insulin resistance (IR) and type 2 diabetes (T2D) through several mechanisms. Interestingly, fat accumulation, body fat distribution and the degree of how adiposity translates into cardio-metabolic diseases differ between ethnicities. Populations of African ancestry have a higher prevalence of obesity and higher T2D risk than populations of European ancestry, mainly driven by higher rates among African women. Considering the reported ethnic-specific differences in AT distribution and function and higher levels of systemic oxidative stress markers, oxidative stress is a potential contributor to the higher susceptibility for metabolic diseases in African women. This review summarizes existing evidence supporting this hypothesis while acknowledging a lack of data on AT oxidative stress in relation to IR in Africans, and the potential influence of other ethnicity-related modulators (e.g., genetic-environment interplay, socioeconomic factors) for consideration in future studies with different ethnicities.

Assembly of high-valent oxomanganese clusters in aqueous solution. Redox equilibrium of water-stable Mn3O44+ and Mn2O23+ complexes. [Erratum to document cited in CA113(18):161042g]

1992 ◽  
Vol 114 (14) ◽  
pp. 5907-5907
Author(s):  
Joseph E. Sarneski ◽  
H. Holden Thorp ◽  
Gary W. Brudvig ◽  
Robert H. Crabtree ◽  
Gayle K. Schulte
Keyword(s):  
Aqueous Solution ◽  
Redox Equilibrium ◽  
High Valent

scholarly journals Modulating the Redox Equilibrium of Silver Using Electron Beams

2017 ◽  
Vol 23 (S1) ◽  
pp. 1682-1683
Author(s):  
Huaping Sheng ◽  
Jianguo Wen ◽  
Lifen Wang ◽  
Dean J. Miller ◽  
He Zheng ◽  
...  
Keyword(s):  
Electron Beams ◽  
Redox Equilibrium

scholarly journals Elucidating the Neuroprotective Role of PPARs in Parkinson’s Disease: A Neoteric and Prospective Target

2021 ◽  
Vol 22 (18) ◽  
pp. 10161
Author(s):  
Tapan Behl ◽  
Piyush Madaan ◽  
Aayush Sehgal ◽  
Sukhbir Singh ◽  
Neelam Sharma ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Neurodegenerative Diseases ◽  
Hormone Receptors ◽  
Nerve Cells ◽  
Substantia Nigra Pars Compacta ◽  
Redox Equilibrium ◽  
Ppar Agonists

One of the utmost frequently emerging neurodegenerative diseases, Parkinson’s disease (PD) must be comprehended through the forfeit of dopamine (DA)-generating nerve cells in the substantia nigra pars compacta (SN-PC). The etiology and pathogenesis underlying the emergence of PD is still obscure. However, expanding corroboration encourages the involvement of genetic and environmental factors in the etiology of PD. The destruction of numerous cellular components, namely oxidative stress, ubiquitin-proteasome system (UPS) dysfunction, autophagy-lysosome system dysfunction, neuroinflammation and programmed cell death, and mitochondrial dysfunction partake in the pathogenesis of PD. Present-day pharmacotherapy can alleviate the manifestations, but no therapy has been demonstrated to cease disease progression. Peroxisome proliferator-activated receptors (PPARs) are ligand-directed transcription factors pertaining to the class of nuclear hormone receptors (NHR), and are implicated in the modulation of mitochondrial operation, inflammation, wound healing, redox equilibrium, and metabolism of blood sugar and lipids. Numerous PPAR agonists have been recognized to safeguard nerve cells from oxidative destruction, inflammation, and programmed cell death in PD and other neurodegenerative diseases. Additionally, various investigations suggest that regular administration of PPAR-activating non-steroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, indomethacin), and leukotriene receptor antagonists (montelukast) were related to the de-escalated evolution of neurodegenerative diseases. The present review elucidates the emerging evidence enlightening the neuroprotective outcomes of PPAR agonists in in vivo and in vitro models experiencing PD. Existing articles up to the present were procured through PubMed, MEDLINE, etc., utilizing specific keywords spotlighted in this review. Furthermore, the authors aim to provide insight into the neuroprotective actions of PPAR agonists by outlining the pharmacological mechanism. As a conclusion, PPAR agonists exhibit neuroprotection through modulating the expression of a group of genes implicated in cellular survival pathways, and may be a propitious target in the therapy of incapacitating neurodegenerative diseases like PD.

scholarly journals Targeting the disturbed redox equilibrium in chronic lymphocytic leukemia by novel reactive oxygen species-catalytic ‘sensor/effector’ compounds

2011 ◽  
Vol 52 (7) ◽  
pp. 1407-1411 ◽  
Author(s):  
Nils Lilienthal ◽  
Christian Prinz ◽  
Abdul A. Peer-Zada ◽  
Mandy Doering ◽  
Lalla A. Ba ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Lymphocytic Leukemia ◽  
Reactive Oxygen ◽  
Lymphocytic Leukemia ◽  
Oxygen Species ◽  
Redox Equilibrium

scholarly journals Visualization of the Redox Status of Cytosolic Glutathione Using the Organelle- and Cytoskeleton-Targeted Redox Sensors

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 129
Author(s):  
Yuta Hatori ◽  
Takanori Kubo ◽  
Yuichiro Sato ◽  
Sachiye Inouye ◽  
Reiko Akagi ◽  
...  
Keyword(s):  
Fluorescent Protein ◽  
Biological Membrane ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Redox Status ◽  
Golgi Body ◽  
Redox Equilibrium ◽  
Cytosolic Glutathione ◽  
Redox Sensors ◽  
Subcellular Resolution

Glutathione is a small thiol-containing peptide that plays a central role in maintaining cellular redox homeostasis. Glutathione serves as a physiologic redox buffer by providing thiol electrons for catabolizing harmful oxidants and reversing oxidative effects on biomolecules. Recent evidence suggests that the balance of reduced and oxidized glutathione (GSH/GSSG) defines the redox states of Cys residues in proteins and fine-tunes their stabilities and functions. To elucidate the redox balance of cellular glutathione at subcellular resolution, a number of redox-sensitive green fluorescent protein (roGFP) variants have been developed. In this study, we constructed and functionally validated organelle- and cytoskeleton-targeted roGFP and elucidated the redox status of the cytosolic glutathione at a subcellular resolution. These new redox sensors firmly established a highly reduced redox equilibrium of cytosolic glutathione, wherein significant deviation was observed among cells. By targeting the sensor to the cytosolic and lumen sides of the Golgi membrane, we identified a prominent redox gradient across the biological membrane at the Golgi body. The results demonstrated that organelle- and cytoskeleton-targeted sensors enable the assessment of glutathione oxidation near the cytosolic surfaces of different organelle membranes.

scholarly journals Chlororespiration Serves as Photoprotection for the Photo-Inactivated Oxygen-Evolving Complex in Zostera marina, a Marine Angiosperm

2020 ◽  
Vol 61 (8) ◽  
pp. 1517-1529
Author(s):  
Ying Tan ◽  
Quan Sheng Zhang ◽  
Wei Zhao ◽  
Zhe Liu ◽  
Ming Yu Ma ◽  
...  
Keyword(s):  
Zostera Marina ◽  
Thylakoid Membrane ◽  
Physiological Role ◽  
Reducing Power ◽  
Pentose Phosphate ◽  
Oxygen Evolving Complex ◽  
Redox Equilibrium ◽  
Strong Connectivity ◽  
Oxygen Evolving ◽  
Marine Angiosperm

Abstract As an alternative electron sink, chlororespiration, comprising the NAD(P)H dehydrogenase complex and plastid terminal plastoquinone oxidase, may play a significant role in sustaining the redox equilibrium between stroma and thylakoid membrane. This study identified a distinct role for chlororespiration in the marine angiosperm Zostera marina, whose oxygen-evolving complex (OEC) is prone to photo-inactivation as a result of its inherent susceptibility to excess irradiation. The strong connectivity between OEC peripheral proteins and key chlororespiratory enzymes, as demonstrated in the interaction network of differentially expressed genes, suggested that the recovery of photo-inactivated OEC was connected with chlororespiration. Chlorophyll fluorescence, transcriptome and Western blot data verified a new physiological role for chlororespiration to function as photoprotection and generate a proton gradient across the thylakoid membrane for the recovery of photo-inactivated OEC. Chlororespiration was only activated in darkness following excess irradiation exposure, which might be related to electron deficiency in the electron transport chain because of the continuous impairment of the OEC. The activation of chlororespiration in Z. marina was prone to proactivity, which was also supported by the further activation of the oxidative pentose-phosphate pathway synthesizing NADPH to meet the demand of chlororespiration during darkness. This phenomenon is distinct from the common assumption that chlororespiration is prone to consuming redundant reducing power during the short transition phase from light to dark.

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