scholarly journals Mitochondrial reactive oxygen species: which ROS signals cardioprotection?

2013 ◽  
Vol 305 (7) ◽  
pp. H960-H968 ◽  
Author(s):  
Anders O. Garlid ◽  
Martin Jaburek ◽  
Jeremy P. Jacobs ◽  
Keith D. Garlid
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Inhibitory Effects ◽  
Physiol Heart Circ ◽  
Bromoenol Lactone ◽  
Rat Heart Mitochondria ◽  
Pharmacological Preconditioning

Mitochondria are the major effectors of cardioprotection by procedures that open the mitochondrial ATP-sensitive potassium channel (mitoKATP), including ischemic and pharmacological preconditioning. MitoKATP opening leads to increased reactive oxygen species (ROS), which then activate a mitoKATP-associated PKCε, which phosphorylates mitoKATP and leaves it in a persistent open state (Costa AD, Garlid KD. Am J Physiol Heart Circ Physiol 295, H874–H882, 2008). The ROS responsible for this effect is not known. The present study focuses on superoxide (O2·−), hydrogen peroxide (H2O2), and hydroxyl radical (HO˙), each of which has been proposed as the signaling ROS. Feedback activation of mitoKATP provides an ideal setting for studying endogenous ROS signaling. Respiring rat heart mitochondria were preincubated with ATP and diazoxide, together with an agent being tested for interference with this process, either by scavenging ROS or by blocking ROS transformations. The mitochondria were then assayed to determine whether or not the persistent phosphorylated open state was achieved. Dimethylsulfoxide (DMSO), dimethylformamide (DMF), deferoxamine, Trolox, and bromoenol lactone each interfered with formation of the ROS-dependent open state. Catalase did not interfere with this step. We also found that DMF blocked cardioprotection by both ischemic preconditioning and diazoxide. The lack of a catalase effect and the inhibitory effects of agents acting downstream of HO˙ excludes H2O2 as the endogenous signaling ROS. Taken together, the results support the conclusion that the ROS message is carried by a downstream product of HO˙ and that it is probably a product of phospholipid oxidation.

Inhibitory effects of glycitein on hydrogen peroxide induced cell damage by scavenging reactive oxygen species and inhibiting c-Jun N-terminal kinase

2007 ◽  
Vol 41 (6) ◽  
pp. 720-729 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Rui Zhang ◽  
Mei Jing Piao ◽  
Kyoung Hwa Lee ◽  
Bum Joon Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Cell Damage ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Inhibitory Effects

Hydrogen peroxide-responsive AIE probe for imaging-guided organelle targeting and photodynamic cancer cell ablation

2021 ◽  
Author(s):  
Qian Wu ◽  
Youmei Li ◽  
Ying Li ◽  
Dong Wang ◽  
Ben Zhong Tang
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Cancer Cell ◽  
Reactive Oxygen ◽  
Living Cells ◽  
Oxygen Species ◽  
Cell Ablation ◽  
Selective Monitoring ◽  
Organelle Targeting

Hydrogen peroxide (H2O2), as one kind of key reactive oxygen species (ROS), is mainly produced endogenously primarily in the mitochondria. The selective monitoring of H2O2 in living cells is of...

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.

scholarly journals Upconversion-based nanosystems for fluorescence sensing of pH and H2O2

2021 ◽  
Author(s):  
Chunning Sun ◽  
Michael Gradzielski
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Excitation Energy ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Fluorescence Sensing ◽  
Living Organisms

Hydrogen peroxide (H2O2), a key reactive oxygen species, plays an important role in living organisms, industrial and environmental fields. Here, a non-contact upconversion nanosystem based on the excitation energy attenuation...

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