Effect of Exposure to the Edge Signal on Oxidative Stress in Brain Cell Models

2011 ◽  
Vol 175 (2) ◽  
pp. 225-230 ◽  
Author(s):  
F. Poulletier de Gannes ◽  
E. Haro ◽  
A. Hurtier ◽  
M. Taxile ◽  
G. Ruffié ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Cell ◽  
Cell Models

scholarly journals Neuroprotective Effects of Mitochondria-Targeted Plastoquinone in a Rat Model of Neonatal Hypoxic–Ischemic Brain Injury

Molecules ◽  
2018 ◽  
Vol 23 (8) ◽  
pp. 1871 ◽  
Author(s):  
Denis Silachev ◽  
Egor Plotnikov ◽  
Irina Pevzner ◽  
Ljubava Zorova ◽  
Anastasia Balakireva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Targeted Delivery ◽  
Cell Damage ◽  
Brain Cell ◽  
Neuroprotective Effects ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia ◽  
Causes Of Mortality ◽  
High Production ◽  
The Brain

Neonatal hypoxia–ischemia is one of the main causes of mortality and disability of newborns. To study the mechanisms of neonatal brain cell damage, we used a model of neonatal hypoxia–ischemia in seven-day-old rats, by annealing of the common carotid artery with subsequent hypoxia of 8% oxygen. We demonstrate that neonatal hypoxia–ischemia causes mitochondrial dysfunction associated with high production of reactive oxygen species, which leads to oxidative stress. Targeted delivery of antioxidants to the mitochondria can be an effective therapeutic approach to treat the deleterious effects of brain hypoxia–ischemia. We explored the neuroprotective properties of the mitochondria-targeted antioxidant SkQR1, which is the conjugate of a plant plastoquinone and a penetrating cation, rhodamine 19. Being introduced before or immediately after hypoxia–ischemia, SkQR1 affords neuroprotection as judged by the diminished brain damage and recovery of long-term neurological functions. Using vital sections of the brain, SkQR1 has been shown to reduce the development of oxidative stress. Thus, the mitochondrial-targeted antioxidant derived from plant plastoquinone can effectively protect the brain of newborns both in pre-ischemic and post-stroke conditions, making it a promising candidate for further clinical studies.

scholarly journals Isomeric O-methyl cannabidiolquinones with dual BACH1/NRF2 activity

2020 ◽  
Author(s):  
Laura Casares ◽  
Juan Diego Unciti ◽  
Maria Eugenia Prados ◽  
Diego Caprioglio ◽  
Maureen Higgins ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Neurodegenerative Diseases ◽  
Cell Models ◽  
Therapeutic Approaches ◽  
Neuroprotective Effects ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
The Brain

ABSTRACTOxidative stress and inflammation in the brain are two key hallmarks of neurodegenerative diseases (NDs) such as Alzheimer’s, Parkinson’s, Huntington’s and multiple sclerosis. The axis NRF2-BACH1 has anti-inflammatory and anti-oxidant properties that could be exploited pharmacologically to obtain neuroprotective effects. Activation of NRF2 or inhibition of BACH1 are, individually, promising therapeutic approaches for NDs. Compounds with dual activity as NRF2 activators and BACH1 inhibitors, could therefore potentially provide a more robust antioxidant and anti-inflammatory effects, with an overall better neuroprotective outcome. The phytocannabinoid cannabidiol (CBD) inhibits BACH1 but lacks significant NRF2 activating properties. Based on this scaffold, we have developed a novel CBD derivative that is highly effective at both inhibiting BACH1 and activating NRF2. This new CBD derivative provides neuroprotection in cell models of relevance to Huntington’s disease, setting the basis for further developments in vivo.

scholarly journals Sense and sensibility: ATM oxygen stress signaling manages brain cell energetics

2019 ◽  
Vol 218 (3) ◽  
pp. 732-734 ◽  
Author(s):  
Katharina Schlacher
Keyword(s):  
Oxidative Stress ◽  
High Energy ◽  
Brain Cell ◽  
Oxidative Stress Response ◽  
Stress Signaling ◽  
Response Functions ◽  
Ataxia Telangiectasia Mutated ◽  
Oxygen Stress ◽  
Damage Repair ◽  
Atm Gene

The ataxia-telangiectasia mutated (ATM) gene regulates DNA damage repair, oxidative stress, and mitochondrial processes. In this issue, Chow et al. (2019. J. Cell Biol. https://doi.org/10.1083/jcb.201806197) connects ATM’s oxidative stress response functions to the sensing of metabolic ATP energetics distinctively important in high energy–demanding Purkinje brain cells, which could explain the most distinct A-T patient feature, cerebellar ataxia.

γ-Oryzanol mitigates oxidative stress and prevents mutant SOD1-Related neurotoxicity in Drosophila and cell models of amyotrophic lateral sclerosis

2019 ◽  
Vol 160 ◽  
pp. 107777 ◽  
Author(s):  
Chunting Zhang ◽  
Weiwei Liang ◽  
Hongyong Wang ◽  
Yueqing Yang ◽  
Tianhang Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyotrophic Lateral Sclerosis ◽  
Cell Models ◽  
Mutant Sod1 ◽  
Lateral Sclerosis

FABP4 inhibitors suppress inflammation and oxidative stress in murine and cell models of acute lung injury

2018 ◽  
Vol 496 (4) ◽  
pp. 1115-1121 ◽  
Author(s):  
Yuanqi Gong ◽  
Zhihong Yu ◽  
Yi Gao ◽  
Linlin Deng ◽  
Meng Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Models ◽  
And Oxidative Stress

scholarly journals Resistance of nerve cells to oxidative injury

2011 ◽  
Vol 64 (7-8) ◽  
pp. 386-391 ◽  
Author(s):  
Zorica Jovanovic ◽  
Svetlana Jovanovic
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Neuronal Damage ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Brain Cell ◽  
Nerve Cells ◽  
Oxygen Species ◽  
The Brain

Introduction. Reactive oxygen species are particularly active in the brain and neuronal tissue, and they are involved in numerous cellular functions, including cell death and survival. Brain and oxidative stress. A high metabolic rate and an abundant supply of the transition metals make the brain an ideal target for a free radical attack. In addition, the brain has a high susceptibility to oxidative stress due to the high lipid content and relatively lower regenerative capacity in comparison with other tissues. Vulnerability of nerve cells to oxidative stress. The neurons are more vulnerable to oxidative stress than other brain cell types. In addition to the two conventional enzymes, catalase and glutathione peroxidase, peroxiredoxins remove intracellular hydrogen peroxide by reducing it to water. The recent work increasingly supports the hypothesis that peroxiredoxins are not only antioxidant proteins, but they also play a role in cell signaling by controlling hydrogen peroxide and alkyl hydroperoxide levels. The accumulating evidence demonstrates that microglia can become deleterious and damage neurons. The overactivated microglia release reactive oxygen species that cause neuronal damage in neurodegenerative diseases. Conclusion. The defense of nerve cells against reactive oxygen species - mediated oxidative damage is essential for maintaining the functionality of nerve cells. The ongoing studies show that neuron-glial compartmentalization of antioxidants is critical for the neuronal signaling by hydrogen peroxide as well as the neuronal protection.

Sign in / Sign up

Export Citation Format

Share Document