scholarly journals Mitochondrial reactive oxygen species regulate the strength of inhibitory GABA-mediated synaptic transmission

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Michael V. Accardi ◽  
Bryan A. Daniels ◽  
Patricia M.G.E. Brown ◽  
Jean-Marc Fritschy ◽  
Shiva K. Tyagarajan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Synaptic Transmission ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

scholarly journals Generation of mitochondrial reactive oxygen species is controlled by ATPase inhibitory factor 1 and regulates cognition

PLoS Biology ◽  
2021 ◽  
Vol 19 (5) ◽  
pp. e3001252
Author(s):  
Pau B. Esparza-Moltó ◽  
Inés Romero-Carramiñana ◽  
Cristina Núñez de Arenas ◽  
Marta P. Pereira ◽  
Noelia Blanco ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Synaptic Transmission ◽  
Atp Synthase ◽  
Reactive Oxygen ◽  
Synaptic Function ◽  
Inhibitory Factor ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Mitochondrial Atp Synthase ◽  
Inhibitory Factor 1

The mitochondrial ATP synthase emerges as key hub of cellular functions controlling the production of ATP, cellular signaling, and fate. It is regulated by the ATPase inhibitory factor 1 (IF1), which is highly abundant in neurons. Herein, we ablated or overexpressed IF1 in mouse neurons to show that IF1 dose defines the fraction of active/inactive enzyme in vivo, thereby controlling mitochondrial function and the production of mitochondrial reactive oxygen species (mtROS). Transcriptomic, proteomic, and metabolomic analyses indicate that IF1 dose regulates mitochondrial metabolism, synaptic function, and cognition. Ablation of IF1 impairs memory, whereas synaptic transmission and learning are enhanced by IF1 overexpression. Mechanistically, quenching the IF1-mediated increase in mtROS production in mice overexpressing IF1 reduces the increased synaptic transmission and obliterates the learning advantage afforded by the higher IF1 content. Overall, IF1 plays a key role in neuronal function by regulating the fraction of ATP synthase responsible for mitohormetic mtROS signaling.

scholarly journals Astaxanthin Prevents Atrophy in Slow Muscle Fibers by Inhibiting Mitochondrial Reactive Oxygen Species via a Mitochondria-Mediated Apoptosis Pathway

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 379
Author(s):  
Luchuanyang Sun ◽  
Nobuyuki Miyaji ◽  
Min Yang ◽  
Edward M. Mills ◽  
Shigeto Taniyama ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Bilayer ◽  
Muscle Atrophy ◽  
Soleus Muscle ◽  
Reactive Oxygen ◽  
H2o2 Production ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Tail Suspension ◽  
Apoptosis Pathway

Astaxanthin (AX) is a carotenoid that exerts potent antioxidant activity and acts in the lipid bilayer. This study aimed to investigate the effects of AX on muscle-atrophy-mediated disturbance of mitochondria, which have a lipid bilayer. Tail suspension was used to establish a muscle-atrophied mouse model. AX diet fed to tail-suspension mice prevented loss of muscle weight, inhibited the decrease of myofiber size, and restrained the increase of hydrogen peroxide (H2O2) production in the soleus muscle. Additionally, AX improved downregulation of mitochondrial respiratory chain complexes I and III in the soleus muscle after tail suspension. Meanwhile, AX promoted mitochondrial biogenesis by upregulating the expressions of adenosine 5′-monophosphate–activated protein kinase (AMPK) α-1, peroxisome proliferator–activated receptor (PPAR)-γ, and creatine kinase in mitochondrial (Ckmt) 2 in the soleus muscle of tail-suspension mice. To confirm the AX phenotype in the soleus muscle, we examined its effects on mitochondria using Sol8 myotubes derived from the soleus muscle. We found that AX was preferentially detected in the mitochondrial fraction; it significantly suppressed mitochondrial reactive oxygen species (ROS) production in Sol8 myotubes. Moreover, AX inhibited the activation of caspase 3 via inhibiting the release of cytochrome c into the cytosol in antimycin A–treated Sol8 myotubes. These results suggested that AX protected the functional stability of mitochondria, alleviated mitochondrial oxidative stress and mitochondria-mediated apoptosis, and thus, prevented muscle atrophy.

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