Fructose-1,6-bisphosphate preserves glucose metabolism integrity and reduces reactive oxygen species in the brain during experimental sepsis

2018 ◽  
Vol 1698 ◽  
pp. 54-61 ◽  
Author(s):  
Anderson V. Catarina ◽  
Carolina Luft ◽  
Samuel Greggio ◽  
Gianina T. Venturin ◽  
Fernanda Ferreira ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Glucose Metabolism ◽  
Reactive Oxygen ◽  
Experimental Sepsis ◽  
Oxygen Species ◽  
Fructose 1,6 Bisphosphate ◽  
The Brain

scholarly journals Reactive Oxygen Species: Beyond Their Reactive Behavior

2021 ◽  
Vol 46 (1) ◽  
pp. 77-87
Author(s):  
Arnaud Tauffenberger ◽  
Pierre J. Magistretti
Keyword(s):  
Reactive Oxygen Species ◽  
Second Messengers ◽  
Critical Role ◽  
Complex Function ◽  
Reactive Oxygen ◽  
High Reactivity ◽  
Oxygen Species ◽  
Health And Disease ◽  
Cellular Dysfunction ◽  
The Brain

AbstractCellular homeostasis plays a critical role in how an organism will develop and age. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. More recent research suggests more complex function of ROS, reaching far beyond the cellular dysfunction. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease.

Real-time monitoring of peroxynitrite (ONOO−) in the rat brain by developing a ratiometric electrochemical biosensor

The Analyst ◽  
2019 ◽  
Vol 144 (6) ◽  
pp. 2150-2157 ◽  
Author(s):  
Feiyue Liu ◽  
Hui Dong ◽  
Yang Tian
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Rat Brain ◽  
Real Time ◽  
Superoxide Anion ◽  
Electrochemical Biosensor ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Real Time Monitoring ◽  
The Brain

As a reactive oxygen species (ROS), peroxynitrite (ONOO−) generated by nitric oxide (NO) and superoxide anion (O2˙−) plays important roles in physiological and pathological processes in the brain.

scholarly journals Hypothalamic Apelin/Reactive Oxygen Species Signaling Controls Hepatic Glucose Metabolism in the Onset of Diabetes

2014 ◽  
Vol 20 (4) ◽  
pp. 557-573 ◽  
Author(s):  
Anne Drougard ◽  
Thibaut Duparc ◽  
Xavier Brenachot ◽  
Lionel Carneiro ◽  
Alexandra Gouazé ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Glucose Metabolism ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Onset Of Diabetes ◽  
Reactive Oxygen Species Signaling

Imbalance of central nitric oxide and reactive oxygen species in the regulation of sympathetic activity and neural mechanisms of hypertension

2011 ◽  
Vol 300 (4) ◽  
pp. R818-R826 ◽  
Author(s):  
Yoshitaka Hirooka ◽  
Takuya Kishi ◽  
Koji Sakai ◽  
Akira Takeshita ◽  
Kenji Sunagawa
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Brain Stem ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sympathetic Nervous ◽  
The Brain

Nitric oxide (NO) and reactive oxygen species (ROS) play important roles in blood pressure regulation via the modulation of the autonomic nervous system, particularly in the central nervous system (CNS). In general, accumulating evidence suggests that NO inhibits, but ROS activates, the sympathetic nervous system. NO and ROS, however, interact with each other. Our consecutive studies and those of others strongly indicate that an imbalance between NO bioavailability and ROS generation in the CNS, including the brain stem, activates the sympathetic nervous system, and this mechanism is involved in the pathogenesis of neurogenic aspects of hypertension. In this review, we focus on the role of NO and ROS in the regulation of the sympathetic nervous system within the brain stem and subsequent cardiovascular control. Multiple mechanisms are proposed, including modulation of neurotransmitter release, inhibition of receptors, and alterations of intracellular signaling pathways. Together, the evidence indicates that an imbalance of NO and ROS in the CNS plays a pivotal role in the pathogenesis of hypertension.

Polymorphism, Heteroplasmy, Mitochondrial Fusion and Diabetes

2003 ◽  
Vol 23 (5-6) ◽  
pp. 313-337 ◽  
Author(s):  
Aya Sato ◽  
Hitoshi Endo ◽  
Kazuo Umetsu ◽  
Hideyuki Sone ◽  
Yoshiko Yanagisawa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Dna ◽  
Membrane Fusion ◽  
Coiled Coil ◽  
Reactive Oxygen ◽  
Mitochondrial Fusion ◽  
Vicious Circle ◽  
Oxygen Species ◽  
The Brain

Mitochondrial DNA (mtDNA) is highly susceptible to mutations that result in polymorphisms and diseases including diabetes. We analyzed heteroplasmy, polymorphisms related to diabetes, and complementation by fusogenic proteins. Cytoplast fusion and microinjection allow, defects in mutated mtDNA inside a heteroplasmic cell to be complemented by fusing two mitochondria via human fusogenic proteins. We characterized three hfzos as well as two OPA1s that prevent apoptosis. Two coiled coil domains and GTPase domains in these fusogenic proteins regulate membrane fusion. The hfzo genes were expressed mainly in the brain and in muscle that are postmitotic, but not in the pancreas. Under the in.uence of polymorphisms of mtDNA and nDNA, the vicious circle of reactive oxygen species and mutations in cell can be alleviated by mitochondrial fusion.

scholarly journals BAM15 treats mouse sepsis and sepsis-AKI, linking circulating mitochondrial DNA and tubule reactive oxygen species

2021 ◽  
Author(s):  
Naoko Tsuji ◽  
Takayuki Tsuji ◽  
Tetsushi Yamashita ◽  
Xuzhen Hu ◽  
Peter S.T. Yuen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Dna ◽  
Precision Medicine ◽  
Cecal Ligation ◽  
Reactive Oxygen ◽  
Kidney Injury ◽  
Experimental Sepsis ◽  
Oxygen Species ◽  
Clinical Sepsis

The pathogenesis of sepsis is complex and heterogeneous; hence, a precision medicine strategy may be required. Acute kidney injury (AKI) following sepsis portends higher mortality. Overproduction of mitochondrial reactive oxygen species (mtROS) is a potential mediator of sepsis and sepsis-induced AKI. BAM15 is a chemical uncoupler that dissipates the mitochondrial proton gradient without generating mtROS, and improves experimental renal ischemic injury. We injected BAM15 into mice at 0 or 6 hours after cecal ligation and puncture (CLP) treated with fluids and antibiotics. BAM15 reduced mortality, even when started at 6 hours, when mice were ill, and reduced kidney damage but did not affect other organs. Serial plasma and urinary levels of mitochondrial DNA (mtDNA) were increased following CLP, and decreased after BAM15 (at 0 and at 6 hours). In vitro BAM15 prevented mtROS overproduction and mtDNA release from septic kidney tubule cells; mtROS generation correlated with mtDNA release. BAM15 also promotes mitochondrial biogenesis signaling. We conclude that BAM15 is an effective preventive and therapeutic candidate in experimental sepsis, and that BAM15 and mtDNA are mechanistically linked via mtROS, which may form a drug-companion diagnostic pair to improve precision medicine approaches to diagnosing and treating clinical sepsis.

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