Managing the pools of cellular redox buffers and the control of oxidative stress during the ontogeny of drought-exposed mungbean (Vigna radiata L.)â€”role of sulfur nutrition

Selenium is a trace element, nutritionally classified as an essential micronutrient, involved in maintaining the correct function of several enzymes incorporating the selenocysteine residue, namely the selenoproteins. The human selenoproteome including 25 proteins is extensively described here. The most relevant selenoproteins, including glutathione peroxidases, thioredoxin reductases and iodothyronine deiodinases are required for the proper cellular redox homeostasis as well as for the correct thyroid function, thus preventing oxidative stress and related diseases. This review summarizes the main advances on oxidative stress with a focus on selenium metabolism and transport. Moreover, thyroid-related disorders are discussed, considering that the thyroid gland contains the highest selenium amount per gram of tissue, also for future possible therapeutic implication.

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Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/6842568 ◽

2016 ◽

Vol 2016 ◽

pp. 1-13 ◽

Cited By ~ 23

Author(s):

Min Hee Choi ◽

Jin Rong Ow ◽

Nai-Di Yang ◽

Reshma Taneja

Keyword(s):

Oxidative Stress ◽

Molecular Level ◽

Redox Homeostasis ◽

Redox Status ◽

Muscle Degeneration ◽

Dystrophic Muscle ◽

Telomere Shortening ◽

Cellular Redox ◽

Pathological Conditions

Oxidative stress is a loss of balance between the production of reactive oxygen species during cellular metabolism and the mechanisms that clear these species to maintain cellular redox homeostasis. Increased oxidative stress has been associated with muscular dystrophy, and many studies have proposed mechanisms that bridge these two pathological conditions at the molecular level. In this review, the evidence indicating a causal role of oxidative stress in the pathogenesis of various muscular dystrophies is revisited. In particular, the mediation of cellular redox status in dystrophic muscle by NF-κB pathway, autophagy, telomere shortening, and epigenetic regulation are discussed. Lastly, the current stance of targeting these pathways using antioxidant therapies in preclinical and clinical trials is examined.

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The Emerging Role of TXNIP in Ischemic and Cardiovascular Diseases; A Novel Marker and Therapeutic Target

International Journal of Molecular Sciences ◽

10.3390/ijms22041693 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1693

Author(s):

Alison Domingues ◽

Julia Jolibois ◽

Perrine Marquet de Rougé ◽

Valérie Nivet-Antoine

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Therapeutic Target ◽

Redox Status ◽

Interacting Protein ◽

Cellular Redox ◽

Thioredoxin Interacting Protein ◽

Potential Biomarker ◽

Ischemic Diseases

Thioredoxin interacting protein (TXNIP) is a metabolism- oxidative- and inflammation-related marker induced in cardiovascular diseases and is believed to represent a possible link between metabolism and cellular redox status. TXNIP is a potential biomarker in cardiovascular and ischemic diseases but also a novel identified target for preventive and curative medicine. The goal of this review is to focus on the novelties concerning TXNIP. After an overview in TXNIP involvement in oxidative stress, inflammation and metabolism, the remainder of this review presents the clues used to define TXNIP as a new marker at the genetic, blood, or ischemic site level in the context of cardiovascular and ischemic diseases.

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Role of Vigna Radiata extracts in modulating oxidative stress in an in vitro cell system

Proceedings of The Nutrition Society ◽

10.1017/s0029665115002153 ◽

2015 ◽

Vol 74 (OCE3) ◽

Cited By ~ 1

Author(s):

G. Kapravelou ◽

K. Brahim ◽

M Goua ◽

R. Martínez ◽

M. Lopez-Jurado ◽

...

Keyword(s):

Oxidative Stress ◽

Vigna Radiata ◽

Cell System

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Hsp104 as a key modulator of prion-mediated oxidative stress in Saccharomyces cerevisiae

Biochemical Journal ◽

10.1042/bj20121806 ◽

2013 ◽

Vol 454 (2) ◽

pp. 217-225 ◽

Cited By ~ 15

Author(s):

Kuljit Singh ◽

Aliabbas A. Saleh ◽

Ankan K. Bhadra ◽

Ipsita Roy

Keyword(s):

Oxidative Stress ◽

Saccharomyces Cerevisiae ◽

Cell Viability ◽

Protein Translation ◽

Analysis Data ◽

Cellular Redox ◽

High Level ◽

Almost All ◽

Cellular Defence

Maintenance of cellular redox homoeostasis forms an important part of the cellular defence mechanism and continued cell viability. Despite extensive studies, the role of the chaperone Hsp104 (heat-shock protein of 102 kDa) in propagation of misfolded protein aggregates in the cell and generation of oxidative stress remains poorly understood. Expression of RNQ1-RFP in Saccharomyces cerevisiae cells led to the generation of the prion form of the protein and increased oxidative stress. In the present study, we show that disruption of Hsp104 in an isogenic yeast strain led to solubilization of RNQ1-RFP. This reduced the oxidative stress generated in the cell. The higher level of oxidative stress in the Hsp104-containing (parental) strain correlated with lower activity of almost all of the intracellular antioxidant enzymes assayed. Surprisingly, this did not correspond with the gene expression analysis data. To compensate for the decrease in protein translation induced by a high level of reactive oxygen species, transcriptional up-regulation takes place. This explains the discrepancy observed between the transcription level and functional enzymatic product. Our results show that in a ΔHsp104 strain, due to lower oxidative stress, no such mismatch is observed, corresponding with higher cell viability. Thus Hsp104 is indirectly responsible for enhancing the oxidative stress in a prion-rich environment.

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