Quantitative Redox Biology of Exercise

2020 ◽  
Vol 41 (10) ◽  
pp. 633-645
Author(s):  
Michalis G. Nikolaidis ◽  
Nikos V. Margaritelis ◽  
Antonios Matsakas

AbstractBiology is rich in claims that reactive oxygen and nitrogen species are involved in every biological process and disease. However, many quantitative aspects of redox biology remain elusive. The important quantitative parameters you need to address the feasibility of redox reactions in vivo are: rate of formation and consumption of a reactive oxygen and nitrogen species, half-life, diffusibility and membrane permeability. In the first part, we explain the basic chemical kinetics concepts and algebraic equations required to perform “street fighting” quantitative analysis. In the second part, we provide key numbers to help thinking about sizes, concentrations, rates and other important quantities that describe the major oxidants (superoxide, hydrogen peroxide, nitric oxide) and antioxidants (vitamin C, vitamin E, glutathione). In the third part, we present the quantitative effect of exercise on superoxide, hydrogen peroxide and nitric oxide concentration in mitochondria and whole muscle and calculate how much hydrogen peroxide concentration needs to increase to transduce signalling. By taking into consideration the quantitative aspects of redox biology we can: i) refine the broad understanding of this research area, ii) design better future studies and facilitate comparisons among studies, and iii) define more efficiently the “borders” between cellular signaling and stress.

2021 ◽  
Author(s):  
Sourav Ghosh ◽  
Punarbasu Roy ◽  
Sanjay Prasad ◽  
Govindasamy Mugesh

Although reactive oxygen and nitrogen species (ROS/RNS) such as hydrogen peroxide (H2O2), nitric oxide (NO), hydroxyl radical (OH.), superoxide (O2-) etc. play crucial roles in redox biology and cellular signaling,...


2007 ◽  
Vol 102 (4) ◽  
pp. 1664-1670 ◽  
Author(s):  
Malcolm J. Jackson ◽  
Deborah Pye ◽  
Jesus Palomero

Skeletal muscle has been recognized as a potential source for generation of reactive oxygen and nitrogen species for more than 20 years. Initial investigations concentrated on the potential role of mitochondria as a major source for generation of superoxide as a “by-product” of normal oxidative metabolism, but recent studies have identified multiple subcellular sites, where superoxide or nitric oxide are generated in regulated and controlled systems in response to cellular stimuli. Full evaluation of the factors regulating these processes and the functions of the reactive oxygen species generated are important in understanding the redox biology of skeletal muscle.


2005 ◽  
Vol 289 (2) ◽  
pp. H852-H861 ◽  
Author(s):  
Jaroslaw W. Zmijewski ◽  
Douglas R. Moellering ◽  
Claire Le Goffe ◽  
Aimee Landar ◽  
Anup Ramachandran ◽  
...  

Exposure of cells to complex mixtures of oxidized lipids such as those found in oxidized low-density lipoprotein (oxLDL) induce reactive oxygen and nitrogen species (ROS/RNS) formation. The source of the ROS/RNS within cells is unknown; it is thought they may be involved in redox cell signaling. Although this possibility was initially overlooked, it is becoming clear that mitochondria, which are a source of superoxide and hydrogen peroxide, may play a critical role in the response of cells on exposure to oxidized lipids. In this study, we tested the possibility that mitochondria are a potential source of oxLDL-dependent formation of ROS/RNS in endothelial cells. Using confocal microscopy, we demonstrated that a significant proportion of oxLDL-dependent dichlorodihydrofluorescein (DCF) fluorescence is colocalized to mitochondria. In support of this concept, rho0 endothelial cells showed a substantial decrease in ROS/RNS formation stimulated by oxLDL. In contrast, mostly nonmitochondrial DCF fluorescence was detected in cells exposed to an extracellular source of hydrogen peroxide. The exposure of cells to a nitric oxide synthase inhibitor and urate resulted in a decrease in oxLDL-induced DCF fluorescence that was restored by addition of nitric oxide donors to the medium. Taken together, these results suggest that oxLDL-dependent DCF fluorescence is mitochondrially associated and may be due to the formation of peroxynitrite.


2010 ◽  
pp. 945-951 ◽  
Author(s):  
A Zembron-Lacny ◽  
M Naczk ◽  
M Gajewski ◽  
J Ostapiuk-Karolczuk ◽  
H Dziewiecka ◽  
...  

The aim of this study was to compare the levels of the plasma muscle-derived cytokines (myokines) and reactive oxygen and nitrogen species (RONS) after muscle damage triggered by different exercises, and to demonstrate the relationships between RONS, thiol redox status and myokines. Sixteen young men participated in a 90-min run at 65 % VO2max (Ex.1) or 90-min run at 65 % VO2max finished with a 15-min eccentric phase (Ex.2, downhill running). Plasma samples were collected before and at 20 min, 24 h and 48 h after exercise. The exercise trials significantly elevated the concentrations of plasma hydrogen peroxide (H2O2) and 8-isoprostane at 20 min rest. Myokines IL-6 and IL-10 increased at 20 min rest while IL-1β and TNFα increased at 24 h rest following both running. Ex.2 caused a significant increase in nitric oxide (NO), IL-6, IL-10 and oxidized glutathione (GSSG) levels. Thiol redox status (GSHtotal2GSSG/GSSG) decreased by about 30 % after Ex.2 as compared to Ex.1. H2O2 and NO directly correlated with IL-6, IL-10, IL-1β, TNFα and glutathione. These results show that eccentric work is an important factor that enhances the production of RONS and muscle-derived cytokines, and that there is a possible participation of thiol redox status in the release of myokines to blood.


2021 ◽  
Vol 22 (19) ◽  
pp. 10876
Author(s):  
Escarlata Fernández-Puente ◽  
Jesús Palomero

Reactive oxygen and nitrogen species (RONS) play an important role in the pathophysiology of skeletal muscle and are involved in the regulation of intracellular signaling pathways, which drive metabolism, regeneration, and adaptation in skeletal muscle. However, the molecular mechanisms underlying these processes are unknown or partially uncovered. We implemented a combination of methodological approaches that are funded for the use of genetically encoded biosensors associated with quantitative fluorescence microscopy imaging to study redox biology in skeletal muscle. Therefore, it was possible to detect and monitor RONS and glutathione redox potential with high specificity and spatio-temporal resolution in two models, isolated skeletal muscle fibers and C2C12 myoblasts/myotubes. Biosensors HyPer3 and roGFP2-Orp1 were examined for the detection of cytosolic hydrogen peroxide; HyPer-mito and HyPer-nuc for the detection of mitochondrial and nuclear hydrogen peroxide; Mito-Grx1-roGFP2 and cyto-Grx1-roGFP2 were used for registration of the glutathione redox potential in mitochondria and cytosol. G-geNOp was proven to detect cytosolic nitric oxide. The fluorescence emitted by the biosensors is affected by pH, and this might have masked the results; therefore, environmental CO2 must be controlled to avoid pH fluctuations. In conclusion, genetically encoded biosensors and quantitative fluorescence microscopy provide a robust methodology to investigate the pathophysiological processes associated with the redox biology of skeletal muscle.


Nanoscale ◽  
2021 ◽  
Author(s):  
Rachael Knoblauch ◽  
Chris Geddes

While the utility of reactive oxygen species in photodynamic therapies for both cancer treatments and antimicrobial applications has received much attention, the inherent potential of reactive nitrogen species (RNS) including...


Author(s):  
A. Ye. Demkovych

Introduction. Activation of lipid peroxidation is one of the trigger mechanisms of periodontium injury, which is primary caused by cellular damage. Reactive oxygen and nitrogen species (RONS) are able to cause damage to a cell as well as final products of lipid peroxidation, including unsaturated aldehydes and other metabolites. Objective. The aim of the research was to determine the role of RONS and accumulation of lipid peroxidation derivatives in initial development and formation of chronical inflammatory process in periodontium. Methods. Experimental periodontitis was modeled in animals by injection of complex mixtures of microorganisms diluted in egg protein into periodontal tissues. The results of biochemical studies of free radical processes activity in blood serum were evaluated by content of diene, triene conjugates, TBA-active products and total quantity of metabolites of nitric oxide (NO2–+NO3–), which were determined on the 7th, 14th and 30th days of the experiment. Results. Generation of active forms of oxygen is more influential, providing longevity of inflammatory process. This pays attention to typical dynamics of changes in active processes of lipid peroxidation in the development and course of experimental periodontitis. The study of inflammatory process with a bacterial-immune component in the rats’ periodontal complex proved accumulation of lipid peroxidation and nitric oxide metabolites in blood serum.Conclusions. The preservation of increased lipid peroxidation and nitric oxide metabolites in blood serum of the experimental animals with acute periodontitis conduce enhance of alteration and delayed healing that result in its sequel into chronical periodontitis.


2020 ◽  
Vol 16 (3) ◽  
pp. e1008379 ◽  
Author(s):  
Artur Santos-Miranda ◽  
Julliane Vasconcelos Joviano-Santos ◽  
Grazielle Alves Ribeiro ◽  
Ana Flávia M. Botelho ◽  
Peter Rocha ◽  
...  

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