scholarly journals Effects of Endurance Training on the Coenzyme Q Redox State in Rat Heart, Liver and Brain at the Tissue and Mitochondrial Levels: Implications for Reactive Oxygen Species Formation and Respiratory Chain Remodeling

2022 ◽  
Vol 23 (2) ◽  
pp. 896
Author(s):  
Karolina Dominiak ◽  
Lukasz Galganski ◽  
Adrianna Budzinska ◽  
Andrzej Woyda-Ploszczyca ◽  
Jerzy A. Zoladz ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endurance Training ◽  
Respiratory Chain ◽  
Rat Heart ◽  
Redox State ◽  
Coenzyme Q ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Isolated Mitochondria ◽  
Ros Formation

Sixteen adult, 4-month-old male Wistar rats were randomly assigned to the training group (n = 8) or the control group (n = 8). We elucidated the effects of 8 weeks of endurance training on coenzyme Q (Q) content and the formation of reactive oxygen species (ROS) at the tissue level and in isolated mitochondria of the rat heart, liver and brain. We demonstrated that endurance training enhanced mitochondrial biogenesis in all tested organs, while a significant increase in the Q redox state was observed in the heart and brain, indicating an elevated level of QH2 as an antioxidant. Moreover, endurance training increased the mQH2 antioxidant pool in the mitochondria of the heart and liver, but not in the brain. At the tissue and isolated mitochondria level, an increase in ROS formation was only observed in the heart. ROS formation observed in the mitochondria of individual rat tissues after training may be associated with changes in the activity/amount of individual components of the oxidative phosphorylation system and its molecular organization, as well as with the size of the oxidized pool of mitochondrial Q acting as an electron carrier in the respiratory chain. Our results indicate that tissue-dependent changes induced by endurance training in the cellular and mitochondrial QH2 pool acting as an antioxidant and in the mitochondrial Q pool serving the respiratory chain may serve important roles in energy metabolism, redox homeostasis and the level of oxidative stress.

The Role of Reactive Oxygen Species in Mitochondrial Permeability Transition

1997 ◽  
Vol 17 (1) ◽  
pp. 43-52 ◽  
Author(s):  
Anibal E. Vercesi ◽  
Alicia J. Kowaltowski ◽  
Mercedes T. Grijalba ◽  
André R. Meinicke ◽  
Roger F. Castilho
Keyword(s):  
Reactive Oxygen Species ◽  
Respiratory Chain ◽  
Mitochondrial Permeability Transition ◽  
Coenzyme Q ◽  
Reactive Oxygen ◽  
Permeability Transition ◽  
Spin Labels ◽  
Oxygen Species ◽  
Binding Studies ◽  
Protein Thiols

We have provided evidence that mitochondrial membrane permeability transition induced by inorganic phosphate, uncouplers or prooxidants such as t-butyl hydroperoxide and diamide is caused by a Ca2+-stimulated production of reactive oxygen species (ROS) by the respiratory chain, at the level of the coenzyme Q. The ROS attack to membrane protein thiols produces cross-linkage reactions, that may open membrane pores upon Ca2+ binding. Studies with submitochondrial particles have demonstrated that the binding of Ca2+ to these particles (possibly to cardiolipin) induces lipid lateral phase separation detected by electron paramagnetic resonance experiments exploying stearic acids spin labels. This condition leads to a disorganization of respiratory chain components, favoring ROS production and consequent protein and lipid oxidation.

scholarly journals The mystery of reactive oxygen species derived from cell respiration.

2004 ◽  
Vol 51 (1) ◽  
pp. 223-229 ◽  
Author(s):  
Hans Nohl ◽  
Lars Gille ◽  
Katrin Staniek
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Respiration ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cell Respiration ◽  
Detection Systems ◽  
Isolated Mitochondria ◽  
Mitochondrial Ros ◽  
Ros Formation ◽  
Electron Carriers

Mitochondrial respiration is considered to provide reactive oxygen species (ROS) as byproduct of regular electron transfer. Objections were raised since results obtained with isolated mitochondria are commonly transferred to activities of mitochondria in the living cell. High electrogenic membrane potential was reported to trigger formation of mitochondrial ROS involving complex I and III. Suggested bioenergetic parameters, starting ROS formation, widely change with the isolation mode. ROS detection systems generally applied may be misleading due to possible interactions with membrane constituents or electron carriers. Avoiding these problems no conditions reported to transform mitochondrial respiration to a radical source were confirmed. However, changing the physical membrane state affected the highly susceptible interaction of the ubiquinol/bc(1) redox complex such that ROS formation became possible.

scholarly journals Role of Natural Antioxidants on Neuroprotection and Neuroinflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 608
Author(s):  
Domenico Nuzzo
Keyword(s):  
Reactive Oxygen Species ◽  
Energy Metabolism ◽  
Respiratory Chain ◽  
Reactive Oxygen ◽  
Natural Antioxidants ◽  
Oxygen Species

All cells continuously generate reactive oxygen species (ROS) through the respiratory chain during the energy metabolism process [...]

scholarly journals Pleiotropic Effects of Biguanides on Mitochondrial Reactive Oxygen Species Production

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Alena Pecinova ◽  
Zdenek Drahota ◽  
Jana Kovalcikova ◽  
Nikola Kovarova ◽  
Petr Pecina ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Respiratory Chain ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Epidemiological Studies ◽  
The Body ◽  
Oxygen Species ◽  
Brown Adipose ◽  
First Choice ◽  
Species Production

Metformin is widely prescribed as a first-choice antihyperglycemic drug for treatment of type 2 diabetes mellitus, and recent epidemiological studies showed its utility also in cancer therapy. Although it is in use since the 1970s, its molecular target, either for antihyperglycemic or antineoplastic action, remains elusive. However, the body of the research on metformin effect oscillates around mitochondrial metabolism, including the function of oxidative phosphorylation (OXPHOS) apparatus. In this study, we focused on direct inhibitory mechanism of biguanides (metformin and phenformin) on OXPHOS complexes and its functional impact, using the model of isolated brown adipose tissue mitochondria. We demonstrate that biguanides nonspecifically target the activities of all respiratory chain dehydrogenases (mitochondrial NADH, succinate, and glycerophosphate dehydrogenases), but only at very high concentrations (10−2–10−1 M) that highly exceed cellular concentrations observed during the treatment. In addition, these concentrations of biguanides also trigger burst of reactive oxygen species production which, in combination with pleiotropic OXPHOS inhibition, can be toxic for the organism. We conclude that the beneficial effect of biguanides should probably be associated with subtler mechanism, different from the generalized inhibition of the respiratory chain.

scholarly journals Intradialytic granulocyte reactive oxygen species production: a prospective, crossover trial.

1993 ◽  
Vol 4 (2) ◽  
pp. 178-186 ◽  
Author(s):  
J Himmelfarb ◽  
K A Ault ◽  
D Holbrook ◽  
D A Leeber ◽  
R M Hakim
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Ros Production ◽  
Oxygen Species ◽  
Susceptibility To Infection ◽  
Flow Cytometric ◽  
Ros Formation ◽  
Dialysis Membranes ◽  
Species Production

By the use of flow cytometric techniques, this prospective, randomized crossover study was designed to analyze intradialytic granulocyte reactive oxygen species (ROS) formation in whole blood with complement-activating and noncomplement-activating hollow fiber membranes. Dialysis with a complement-activating membrane resulted in a 6.5-fold increase in granulocyte hydrogen peroxide production 15 min after dialysis initiation and remained significantly elevated (P < 0.01) through the first 30 min with this membrane in comparison to both predialysis values and simultaneous values with a noncomplement-activating membrane. Further studies demonstrated that blood obtained at 15 min with a complement-activating membrane generated significantly less granulocyte ROS production in response to Staphylococcus aureus incubation than blood obtained either predialysis or at the same time in dialysis with a noncomplement-activating membrane. Both complement-activating and noncomplement-activating dialysis membranes caused slightly decreased granulocyte responsiveness to phorbol myristate acetate. It was concluded that hemodialysis with complement-activating membranes results in increased granulocyte ROS production and decreased responsiveness to S. aureus challenge during the dialysis procedure. These results document the potential role of ROS in hemodialysis-associated pathology and susceptibility to infection.

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