The role of auxiliary oxidants in maintaining redox balance during phototrophic growth of Rhodobacter capsulatus on propionate or butyrate

1988 ◽  
Vol 150 (2) ◽  
pp. 131-137 ◽  
Author(s):  
David J. Richardson ◽  
Glenn F. King ◽  
David J. Kelly ◽  
Alastair G. McEwan ◽  
Stuart J. Ferguson ◽  
...  
Keyword(s):  
Rhodobacter Capsulatus ◽  
Redox Balance ◽  
Phototrophic Growth

scholarly journals The role of auxiliary oxidants in maintaining redox balance during phototrophic growth of Rhodobacter capsulatuspropionate or butyrate

1988 ◽  
Vol 150 (6) ◽  
pp. 602-602
Author(s):  
David J. Richardson ◽  
Glenn F. King ◽  
David J. Kelly ◽  
Alastair G. McEwan ◽  
Stuart J. Ferguson ◽  
...  
Keyword(s):  
Redox Balance ◽  
Phototrophic Growth

Redox State in Atrial Fibrillation Pathogenesis and Relevant Therapeutic Approaches

2019 ◽  
Vol 26 (5) ◽  
pp. 765-779 ◽  
Author(s):  
Alexios S. Antonopoulos ◽  
Athina Goliopoulou ◽  
Evangelos Oikonomou ◽  
Sotiris Tsalamandris ◽  
Georgios-Angelos Papamikroulis ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Clinical Studies ◽  
Redox State ◽  
Redox Balance ◽  
Therapeutic Approaches ◽  
Critical Determinant ◽  
Electrophysiological Properties ◽  
Antioxidant Agents ◽  
Clinical Benefits

Background: Myocardial redox state is a critical determinant of atrial biology, regulating cardiomyocyte apoptosis, ion channel function, and cardiac hypertrophy/fibrosis and function. Nevertheless, it remains unclear whether the targeting of atrial redox state is a rational therapeutic strategy for atrial fibrillation prevention. Objective: To review the role of atrial redox state and anti-oxidant therapies in atrial fibrillation. Method: Published literature in Medline was searched for experimental and clinical evidence linking myocardial redox state with atrial fibrillation pathogenesis as well as studies looking into the role of redoxtargeting therapies in the prevention of atrial fibrillation. Results: Data from animal models have shown that altered myocardial nitroso-redox balance and NADPH oxidases activity are causally involved in the pathogenesis of atrial fibrillation. Similarly experimental animal data supports that increased reactive oxygen / nitrogen species formation in the atrial tissue is associated with altered electrophysiological properties of atrial myocytes and electrical remodeling, favoring atrial fibrillation development. In humans, randomized clinical studies using redox-related therapeutic approaches (e.g. statins or antioxidant agents) have not documented any benefits in the prevention of atrial fibrillation development (mainly post-operative atrial fibrillation risk). Conclusion: Despite strong experimental and translational data supporting the role of atrial redox state in atrial fibrillation pathogenesis, such mechanistic evidence has not been translated to clinical benefits in atrial fibrillation risk in randomized clinical studies using redox-related therapies.

scholarly journals Mitochondrial Sirtuins in Reproduction

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1047
Author(s):  
Giovanna Di Emidio ◽  
Stefano Falone ◽  
Paolo Giovanni Artini ◽  
Fernanda Amicarelli ◽  
Anna Maria D’Alessandro ◽  
...  
Keyword(s):  
Stress Responses ◽  
Metabolic Pathways ◽  
Redox Balance ◽  
Antioxidant Defenses ◽  
Metabolic Abnormalities ◽  
Female Reproduction ◽  
Mitochondrial Dysfunctions ◽  
Early Embryos ◽  
The Relationship

Mitochondria act as hubs of numerous metabolic pathways. Mitochondrial dysfunctions contribute to altering the redox balance and predispose to aging and metabolic alterations. The sirtuin family is composed of seven members and three of them, SIRT3-5, are housed in mitochondria. They catalyze NAD+-dependent deacylation and the ADP-ribosylation of mitochondrial proteins, thereby modulating gene expression and activities of enzymes involved in oxidative metabolism and stress responses. In this context, mitochondrial sirtuins (mtSIRTs) act in synergistic or antagonistic manners to protect from aging and aging-related metabolic abnormalities. In this review, we focus on the role of mtSIRTs in the biological competence of reproductive cells, organs, and embryos. Most studies are focused on SIRT3 in female reproduction, providing evidence that SIRT3 improves the competence of oocytes in humans and animal models. Moreover, SIRT3 protects oocytes, early embryos, and ovaries against stress conditions. The relationship between derangement of SIRT3 signaling and the imbalance of ROS and antioxidant defenses in testes has also been demonstrated. Very little is known about SIRT4 and SIRT5 functions in the reproductive system. The final goal of this work is to understand whether sirtuin-based signaling may be taken into account as potential targets for therapeutic applications in female and male infertility.

scholarly journals Differential Expression of Peroxisomal Proteins in Distinct Types of Parotid Gland Tumors

2021 ◽  
Vol 22 (15) ◽  
pp. 7872
Author(s):  
Malin Tordis Meyer ◽  
Christoph Watermann ◽  
Thomas Dreyer ◽  
Steffen Wagner ◽  
Claus Wittekindt ◽  
...  
Keyword(s):  
Redox Balance ◽  
Matrix Proteins ◽  
Parotid Tumor ◽  
Gene Expressions ◽  
Tissue Samples ◽  
Cellular Redox ◽  
Tumor Subtypes ◽  
Parotid Tumors ◽  
Aggressive Tumors

Salivary gland cancers are rare but aggressive tumors that have poor prognosis and lack effective cure. Of those, parotid tumors constitute the majority. Functioning as metabolic machinery contributing to cellular redox balance, peroxisomes have emerged as crucial players in tumorigenesis. Studies on murine and human cells have examined the role of peroxisomes in carcinogenesis with conflicting results. These studies either examined the consequences of altered peroxisomal proliferators or compared their expression in healthy and neoplastic tissues. None, however, examined such differences exclusively in human parotid tissue or extended comparison to peroxisomal proteins and their associated gene expressions. Therefore, we examined differences in peroxisomal dynamics in parotid tumors of different morphologies. Using immunofluorescence and quantitative PCR, we compared the expression levels of key peroxisomal enzymes and proliferators in healthy and neoplastic parotid tissue samples. Three parotid tumor subtypes were examined: pleomorphic adenoma, mucoepidermoid carcinoma and acinic cell carcinoma. We observed higher expression of peroxisomal matrix proteins in neoplastic samples with exceptional down regulation of certain enzymes; however, the degree of expression varied between tumor subtypes. Our findings confirm previous experimental results on other organ tissues and suggest peroxisomes as possible therapeutic targets or markers in all or certain subtypes of parotid neoplasms.

Improving the prognosis of renal patients: the role of blood flow‐restriction resistance training on redox balance and cardiac autonomic function

2021 ◽  
Author(s):  
Lysleine Alves Deus ◽  
Rodrigo Vanerson Passos Neves ◽  
Hugo de Luca Corrêa ◽  
Andrea Lucena Reis ◽  
Fernando Sousa Honorato ◽  
...  
Keyword(s):  
Blood Flow ◽  
Resistance Training ◽  
Autonomic Function ◽  
Redox Balance ◽  
Blood Flow Restriction ◽  
Cardiac Autonomic Function ◽  
Flow Restriction

scholarly journals Novel insights on targeting ferroptosis in cancer therapy

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Sipeng Zuo ◽  
Jie Yu ◽  
Hui Pan ◽  
Linna Lu
Keyword(s):  
Cell Death ◽  
Heart Disease ◽  
Cancer Therapy ◽  
Alzheimer Disease ◽  
Cellular Structure ◽  
Redox Balance ◽  
Regulated Cell Death ◽  
Novel Theory ◽  
The Relationship

Abstract Ferroptosis belongs to a novel form of regulated cell death. It is characterized by iron dependence, destruction of intracellular redox balance and non-apoptosis. And cellular structure and molecules level changes also occur abnormally during ferroptosis. It has been proved that ferroptosis exist widespreadly in many diseases, such as heart disease, brain damage or alzheimer disease. At the same time, the role of ferroptosis in cancer cannot be underestimated. More and more indications have told that ferroptosis is becoming a powerful weapon against cancer. In addition, therapies rely on ferroptosis have been applied to the clinic. Therefore, it is necessary to understand this newly discovered form of cell death and its connection with cancer. This review summarizes the mechanism of ferroptosis, ferroptosis inducers based on different targets and inspection methods. At last, we analyzed the relationship between ferroptosis and malignancies, in order to provide a novel theory basis for cancer treatment.

scholarly journals Exploring the Use of Dimethyl Fumarate as Microglia Modulator for Neurodegenerative Diseases Treatment

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 700
Author(s):  
Maria Rosito ◽  
Claudia Testi ◽  
Giacomo Parisi ◽  
Barbara Cortese ◽  
Paola Baiocco ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Iron Homeostasis ◽  
Brain Injuries ◽  
Neuroprotective Effect ◽  
Redox Homeostasis ◽  
Dimethyl Fumarate ◽  
Redox Balance ◽  
Fumaric Acid Ester ◽  
The Central Nervous System

The maintenance of redox homeostasis in the brain is critical for the prevention of the development of neurodegenerative diseases. Drugs acting on brain redox balance can be promising for the treatment of neurodegeneration. For more than four decades, dimethyl fumarate (DMF) and other derivatives of fumaric acid ester compounds have been shown to mitigate a number of pathological mechanisms associated with psoriasis and relapsing forms of multiple sclerosis (MS). Recently, DMF has been shown to exert a neuroprotective effect on the central nervous system (CNS), possibly through the modulation of microglia detrimental actions, observed also in multiple brain injuries. In addition to the hypothesis that DMF is linked to the activation of NRF2 and NF-kB transcription factors, the neuroprotective action of DMF may be mediated by the activation of the glutathione (GSH) antioxidant pathway and the regulation of brain iron homeostasis. This review will focus on the role of DMF as an antioxidant modulator in microglia processes and on its mechanisms of action in the modulation of different pathways to attenuate neurodegenerative disease progression.

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