Mitochondria and Neuronal Survival

2000 ◽  
Vol 80 (1) ◽  
pp. 315-360 ◽  
Author(s):  
David G. Nicholls ◽  
Samantha L. Budd
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Neuronal Survival ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Oxygen Species ◽  
Inner Membrane ◽  
Isolated Mitochondria ◽  
Integral Role

Mitochondria play a central role in the survival and death of neurons. The detailed bioenergetic mechanisms by which isolated mitochondria generate ATP, sequester Ca2+, generate reactive oxygen species, and undergo Ca2+-dependent permeabilization of their inner membrane are currently being applied to the function of mitochondria in situ within neurons under physiological and pathophysiological conditions. Here we review the functional bioenergetics of isolated mitochondria, with emphasis on the chemiosmotic proton circuit and the application (and occasional misapplication) of these principles to intact neurons. Mitochondria play an integral role in both necrotic and apoptotic neuronal cell death, and the bioenergetic principles underlying current studies are reviewed.

scholarly journals Cadmium induction of reactive oxygen species activates the mTOR pathway, leading to neuronal cell death

2011 ◽  
Vol 50 (5) ◽  
pp. 624-632 ◽  
Author(s):  
Long Chen ◽  
Baoshan Xu ◽  
Lei Liu ◽  
Yan Luo ◽  
Hongyu Zhou ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Mtor Pathway ◽  
Oxygen Species

scholarly journals Low-DoseAronia melanocarpaConcentrate Attenuates Paraquat-Induced Neurotoxicity

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
A. J. Case ◽  
D. Agraz ◽  
I. M. Ahmad ◽  
M. C. Zimmerman
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
High Dose ◽  
Low Doses ◽  
Oxygen Species ◽  
High Doses

Herbicides containing paraquat may contribute to the pathogenesis of neurodegenerative disorders such as Parkinson’s disease. Paraquat induces reactive oxygen species-mediated apoptosis in neurons, which is a primary mechanism behind its toxicity. We sought to test the effectiveness of a commercially available polyphenol-richAronia melanocarpa(aronia berry) concentrate in the amelioration of paraquat-induced neurotoxicity. Considering the abundance of antioxidants in aronia berries, we hypothesized that aronia berry concentrate attenuates the paraquat-induced increase in reactive oxygen species and protects against paraquat-mediated neuronal cell death. Using a neuronal cell culture model, we observed that low doses of aronia berry concentrate protected against paraquat-mediated neurotoxicity. Additionally, low doses of the concentrate attenuated the paraquat-induced increase in superoxide, hydrogen peroxide, and oxidized glutathione levels. Interestingly, high doses of aronia berry concentrate increased neuronal superoxide levels independent of paraquat, while at the same time decreasing hydrogen peroxide. Moreover, high-dose aronia berry concentrate potentiated paraquat-induced superoxide production and neuronal cell death. In summary, aronia berry concentrate at low doses restores the homeostatic redox environment of neurons treated with paraquat, while high doses exacerbate the imbalance leading to further cell death. Our findings support that moderate levels of aronia berry concentrate may prevent reactive oxygen species-mediated neurotoxicity.

Heat-induced inhibition of superoxide dismutase and accumulation of reactive oxygen species leads to HT-22 neuronal cell death

2011 ◽  
Vol 36 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Naglaa F. El-Orabi ◽  
Colin B. Rogers ◽  
Heather Gray Edwards ◽  
Dean D. Schwartz
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Superoxide Dismutase ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Cadmium induces neuronal cell death through reactive oxygen species activated by GADD153

2013 ◽  
Vol 14 (1) ◽  
Author(s):  
Seungwoo Kim ◽  
Hyo-Soon Cheon ◽  
So-Young Kim ◽  
Yong-Sung Juhnn ◽  
Young-Youl Kim
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Oxygen Species

Sirtuin 5-Mediated Lysine Desuccinylation Protects Mitochondrial Metabolism Following Subarachnoid Hemorrhage in Mice

Stroke ◽  
2021 ◽  
Vol 52 (12) ◽  
pp. 4043-4053
Author(s):  
Zhi-Peng Xiao ◽  
Tao Lv ◽  
Pin-Pin Hou ◽  
Anatol Manaenko ◽  
Yuandong Liu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Atp Synthase ◽  
Citrate Synthase ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Oxygen Species ◽  
Lysine Succinylation ◽  
Brain Ph ◽  
The Brain

Background and Purpose: Sirt5 (Sirtuin 5) desuccinylates multiple metabolic enzymes and plays an important role in maintaining energy homeostasis. The goal of this study was to determine whether Sirt5-mediated desuccinylation restores the energy metabolism and protects brain against subarachnoid hemorrhage (SAH). Methods: Male C57BL/6 or Sirt5 −/− mice were used. The endovascular perforation SAH model was applied. Protein lysine succinylation in the brain cortex was examined using liquid chromatography-tandem mass spectrometry analysis. The brain metabolism was evaluated by measurement of brain pH as well as ATP and reactive oxygen species level. Neuronal cell death and neurobehavioral deficits were assessed 24 hours after SAH. The expression and desuccinylation activity of Sirt5, lysine succinylation of citrate synthase and ATP synthase subunits were investigated by Western blot, immunohistochemistry, and ELISA in SAH mice and patients. Furthermore, the benefits of resveratrol-mediated Sirt5 activation were investigated. Results: A total of 211 lysine succinylation sites were differentially expressed on 170 proteins in mice brain after SAH. Thirty-nine percent of these succinylated proteins were localized in mitochondria and they are related to energy metabolism. SAH caused a decrease of Sirt5 expression and succinylated citrate synthase as well as the subunits of ATP synthase, subsequently lowered brain pH, reduced ATP and increased reactive oxygen species production, leading to neuronal cell death, and neurological deficits. Knockdown of Sirt5 aggravated SAH-induced effects, mentioned above. Administration of resveratrol resulted in activation of Sirt5. The activation was accompanied both with restoration of the mitochondrial metabolism and alleviation of early brain injury as well as with desuccinylating citrate synthase and ATP synthase. Conclusions: Protein lysine succinylation is a biochemical hallmark of metabolic crisis after SAH, and disruption of lysine succinylation through activation of Sirt5 might be a promising therapeutic strategy for the treatment of SAH.

scholarly journals Apoptotic Neuronal Cell Death Induced by the Non-fibrillar Amyloid-β Peptide Proceeds through an Early Reactive Oxygen Species-dependent Cytoskeleton Perturbation

2002 ◽  
Vol 278 (5) ◽  
pp. 3437-3445 ◽  
Author(s):  
Isabelle Sponne ◽  
Alexandre Fifre ◽  
Béatrice Drouet ◽  
Christophe Klein ◽  
Violette Koziel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Amyloid Β Peptide ◽  
Oxygen Species

scholarly journals Methylmercury induces neuronal cell death by inducing TNF-α expression through the ASK1/p38 signaling pathway in microglia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Toyama ◽  
Takayuki Hoshi ◽  
Takuya Noguchi ◽  
Yoshiro Saito ◽  
Atsushi Matsuzawa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Mouse Brain ◽  
Neuronal Cell Death ◽  
Brain Slices ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Bv2 Cells ◽  
Tnf Α

AbstractWe recently found that tumor necrosis factor-α (TNF-α) may be involved in neuronal cell death induced by methylmercury in the mouse brain. Here, we examined the cells involved in the induction of TNF-α expression by methylmercury in the mouse brain by in situ hybridization. TNF-α-expressing cells were found throughout the brain and were identified as microglia by immunostaining for ionized calcium binding adaptor molecule 1 (Iba1). Methylmercury induced TNF-α expression in mouse primary microglia and mouse microglial cell line BV2. Knockdown of apoptosis signal-regulating kinase 1 (ASK1), an inflammatory cytokine up-regulator that is responsible for reactive oxygen species (ROS), decreased methylmercury-induced TNF-α expression through decreased phosphorylation of p38 MAP kinase in BV2 cells. Suppression of methylmercury-induced reactive oxygen species (ROS) by antioxidant treatment largely abolished the induction of TNF-α expression and phosphorylation of p38 by methylmercury in BV2 cells. Finally, in mouse brain slices, the TNF-α antagonist (WP9QY) inhibited neuronal cell death induced by methylmercury, as did the p38 inhibitor SB203580 and liposomal clodronate (a microglia-depleting agent). These results indicate that methylmercury induces mitochondrial ROS that are involved in activation of the ASK1/p38 pathway in microglia and that this is associated with induction of TNF-α expression and neuronal cell death.

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