Mitochondrial redox biology: Reactive species production and antioxidant defenses

Author(s):  
Gaetana Napolitano ◽  
Gianluca Fasciolo ◽  
Sergio Di Meo ◽  
Paola Venditti
1995 ◽  
Vol 47 (2) ◽  
pp. 510-517 ◽  
Author(s):  
Raymond Vanholder ◽  
Rita De Smet ◽  
Marie-Anne Waterloos ◽  
Nadine Van Landschoot ◽  
Pascale Vogeleere ◽  
...  

ACS Catalysis ◽  
2016 ◽  
Vol 6 (5) ◽  
pp. 3180-3192 ◽  
Author(s):  
Zan Dai ◽  
Fan Qin ◽  
Huiping Zhao ◽  
Jie Ding ◽  
Yunling Liu ◽  
...  

2021 ◽  
Vol 23 (1) ◽  
pp. 106
Author(s):  
Verena Tretter ◽  
Beatrix Hochreiter ◽  
Marie Louise Zach ◽  
Katharina Krenn ◽  
Klaus Ulrich Klein

Living organisms use a large repertoire of anabolic and catabolic reactions to maintain their physiological body functions, many of which include oxidation and reduction of substrates. The scientific field of redox biology tries to understand how redox homeostasis is regulated and maintained and which mechanisms are derailed in diverse pathological developments of diseases, where oxidative or reductive stress is an issue. The term “oxidative stress” is defined as an imbalance between the generation of oxidants and the local antioxidative defense. Key mediators of oxidative stress are reactive species derived from oxygen, nitrogen, and sulfur that are signal factors at physiological concentrations but can damage cellular macromolecules when they accumulate. However, therapeutical targeting of oxidative stress in disease has proven more difficult than previously expected. Major reasons for this are the very delicate cellular redox systems that differ in the subcellular compartments with regard to their concentrations and depending on the physiological or pathological status of cells and organelles (i.e., circadian rhythm, cell cycle, metabolic need, disease stadium). As reactive species are used as signaling molecules, non-targeted broad-spectrum antioxidants in many cases will fail their therapeutic aim. Precision medicine is called to remedy the situation.


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