scholarly journals Oxidative Stress, Redox Signaling, and Autophagy: Cell DeathVersusSurvival

2014 ◽  
Vol 21 (1) ◽  
pp. 66-85 ◽  
Author(s):  
Juliana Navarro-Yepes ◽  
Michaela Burns ◽  
Annadurai Anandhan ◽  
Oleh Khalimonchuk ◽  
Luz Maria del Razo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox Signaling

Oxidative stress in phenylketonuria—evidence from human studies and animal models, and possible implications for redox signaling

2021 ◽  
Vol 36 (4) ◽  
pp. 523-543
Author(s):  
Vanessa Trindade Bortoluzzi ◽  
Carlos Severo Dutra Filho ◽  
Clovis Milton Duval Wannmacher
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Redox Signaling ◽  
Human Studies

Skeletal muscle uncoupling-induced longevity in mice is linked to increased substrate metabolism and induction of the endogenous antioxidant defense system

2013 ◽  
Vol 304 (5) ◽  
pp. E495-E506 ◽  
Author(s):  
S. Keipert ◽  
M. Ost ◽  
A. Chadt ◽  
A. Voigt ◽  
V. Ayala ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Mapk Signaling ◽  
Redox Signaling ◽  
Defense System ◽  
High Fat ◽  
Substrate Metabolism ◽  
Endogenous Antioxidant

Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fat- and high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.

Oxidative Stress, Antioxidant Status, and Redox Signaling in Carcinogenesis

2014 ◽  
pp. 351-368
Author(s):  
Deepti Pande ◽  
Reena Negi ◽  
Kanchan Karki ◽  
Seema Khanna ◽  
U. S. Dwivedi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Status ◽  
Redox Signaling

scholarly journals Potential of Mitochondria-Targeted Antioxidants to Prevent Oxidative Stress in Pancreatic β-cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Lydie Plecitá-Hlavatá ◽  
Hana Engstová ◽  
Jan Ježek ◽  
Blanka Holendová ◽  
Jan Tauber ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Islets ◽  
Targeted Delivery ◽  
Complex I ◽  
Chain Complex ◽  
Redox Signaling ◽  
Complex Iii ◽  
Mitochondrial Matrix ◽  
Isolated Pancreatic Islets ◽  
Superoxide Formation

Pancreatic β-cells are vulnerable to oxidative stress due to their low content of redox buffers, such as glutathione, but possess a rich content of thioredoxin, peroxiredoxin, and other proteins capable of redox relay, transferring redox signaling. Consequently, it may be predicted that cytosolic antioxidants could interfere with the cytosolic redox signaling and should not be recommended for any potential therapy. In contrast, mitochondrial matrix-targeted antioxidants could prevent the primary oxidative stress arising from the primary superoxide sources within the mitochondrial matrix, such as at the flavin (IF) and ubiquinone (IQ) sites of superoxide formation within respiratory chain complex I and the outer ubiquinone site (IIIQ) of complex III. Therefore, using time-resolved confocal fluorescence monitoring with MitoSOX Red, we investigated various effects of mitochondria-targeted antioxidants in model pancreatic β-cells (insulinoma INS-1E cells) and pancreatic islets. Both SkQ1 (a mitochondria-targeted plastoquinone) and a suppressor of complex III site Q electron leak (S3QEL) prevented superoxide production released to the mitochondrial matrix in INS-1E cells with stimulatory glucose, where SkQ1 also exhibited an antioxidant role for UCP2-silenced cells. SkQ1 acted similarly at nonstimulatory glucose but not in UCP2-silenced cells. Thus, UCP2 can facilitate the antioxidant mechanism based on SkQ1+ fatty acid anion- pairing. The elevated superoxide formation induced by antimycin A was largely prevented by S3QEL, and that induced by rotenone was decreased by SkQ1 and S3QEL and slightly by S1QEL, acting at complex I site Q. Similar results were obtained with the MitoB probe, for the LC-MS-based assessment of the 4 hr accumulation of reactive oxygen species within the mitochondrial matrix but for isolated pancreatic islets. For 2 hr INS-1E incubations, some samples were influenced by the cell death during the experiment. Due to the frequent dependency of antioxidant effects on metabolic modes, we suggest a potential use of mitochondria-targeted antioxidants for the treatment of prediabetic states after cautious nutrition-controlled tests. Their targeted delivery might eventually attenuate the vicious spiral leading to type 2 diabetes.

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