scholarly journals Role of mitochondria in neuronal cell death induced by oxidative stress; neuroprotection by Coenzyme Q10

2005 ◽  
Vol 18 (3) ◽  
pp. 618-627 ◽  
Author(s):  
M. Somayajulu ◽  
S. McCarthy ◽  
M. Hung ◽  
M. Sikorska ◽  
H. Borowy-Borowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Coenzyme Q10 ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Role of oxidative stress and caspase 3 in CD47-mediated neuronal cell death

2009 ◽  
Vol 108 (2) ◽  
pp. 430-436 ◽  
Author(s):  
Changhong Xing ◽  
Sunryung Lee ◽  
Woo Jean Kim ◽  
Guang Jin ◽  
Yong-Guang Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell

Paraquat induces oxidative stress and neuronal cell death; neuroprotection by water-soluble Coenzyme Q10

2004 ◽  
Vol 201 (1) ◽  
pp. 21-31 ◽  
Author(s):  
S. McCarthy ◽  
M. Somayajulu ◽  
M. Sikorska ◽  
H. Borowy-Borowski ◽  
S. Pandey
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Coenzyme Q10 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Water Soluble

scholarly journals Anesthetic-Induced Oxidative Stress and Potential Protection

2010 ◽  
Vol 10 ◽  
pp. 1473-1482 ◽  
Author(s):  
Cheng Wang ◽  
Xuan Zhang ◽  
Fang Liu ◽  
Merle G. Paule ◽  
William Slikker, Jr.
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Superoxide Dismutase ◽  
Nmda Receptor ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Receptor Subunit ◽  
Nmda Antagonists ◽  
Nmda Receptor Subunit

Prolonged exposure of developing mammals to general anesthetics affects the N-methyl-D-aspartate (NMDA)–type glutamate or γ-aminobutyric acid (GABA) receptor systems and enhances neuronal toxicity. Stimulation of immature neurons by NMDA antagonists or GABA agonists is thought to increase overall nervous system excitability and may contribute to abnormal neuronal cell death during development. Although the precise mechanisms by which NMDA antagonists or GABA agonists cause neuronal cell death are still not completely understood, up-regulation of the NMDA receptor subunit NR1 may be an initiative factor in neuronal cell death. It is increasingly apparent that mitochondria lie at the center of the cell death regulation process. Evidence for the role of oxidative stress in anesthetic-induced neurotoxicity has been generated in studies that apply oxidative stress blockers. Prevention of neuronal death by catalase and superoxide dismutasein vitro, or by M40403 (superoxide dismutase mimetic)in vivo, supports the contention that the involvement of reactive oxygen species (ROS) and the nature of neuronal cell death in rodents is mainly apoptotic. However, more evidence is necessary to in order verify the role of the NMDA receptor subunit NR1 and ROS in anesthetic-induced neurodegeneration.

scholarly journals Comprehensive Insight of Neurodegenerative Diseases and The Role of Neurotoxin Agents — Glutamate

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Hui-Min Yap ◽  
Kwan-Liang Lye ◽  
Loh Teng-Hern Tan
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Neurodegenerative Diseases ◽  
Monosodium Glutamate ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Glutamate Excitotoxicity ◽  
Glutamate Toxicity ◽  
Extracellular Glutamate

The increased concentration of extracellular glutamate has been reported to play a key role in most of the neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease, even though its importance as an amino acid neurotransmitter in mammalian. Glutamate toxicity, which can be caused by excessive intake of monosodium glutamate (MSG), is the major contributor to pathological neuronal cell death. It causes neuronal dysfunction and degeneration in the central nervous system (CNS). Glutamate neurotoxicity can be categorized into two forms, which are receptor-mediated glutamate excitotoxicity and non-receptor mediated glutamate oxidative toxicity. The receptor-mediated glutamate excitotoxicity involved excessive stimulation of glutamate receptors (GluRs) which lead to excessive ion calcium (Ca2+) influx and activates a cell death cascade involving the accumulation of mitochondrially generated reactive oxygen species (ROS). Studies showed excessive extracellular glutamate leads to nerve cell death via the activation of N-methyl-Daspartate (NMDA) receptors in the cases of trauma or stroke. Whereas non-receptor mediated oxidative toxicity involved the breakdown of the cystine/glutamate antiporter (xc - ) mechanism, which leads to the depletion of glutathione (GSH) and causes oxidative stress and cell death. The cystine/glutamate antiporter couples the import of cystine to the export of glutamate. The increased concentration of extracellular glutamate could inhibit the uptake of cystine, which is required for the synthesis of the intracellular antioxidant GSH. GSH plays an important role in the disposal of peroxides by brain cells and in the protection against ROS. Depletion of GSH renders the cell to oxidative stress and ultimately leading to cell death. This article aims to provide a comprehensive review of neurodegenerative diseases and the role of neurotoxin agents, glutamate in these diseases.

Coenzyme Q10 protects against amyloid beta-induced neuronal cell death by inhibiting oxidative stress and activating the P13K pathway

2012 ◽  
Vol 33 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Hojin Choi ◽  
Hyun-Hee Park ◽  
Seong-Ho Koh ◽  
Na-Young Choi ◽  
Hyun-Jeung Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Amyloid Beta ◽  
Coenzyme Q10 ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Induction of the Nrf2 Pathway by Sulforaphane Is Neuroprotective in a Rat Temporal Lobe Epilepsy Model

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1702
Author(s):  
Sereen Sandouka ◽  
Tawfeeq Shekh-Ahmad
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Antioxidant Capacity ◽  
Temporal Lobe ◽  
Epileptiform Activity ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
The Brain

Epilepsy is a chronic disease of the brain that affects over 65 million people worldwide. Acquired epilepsy is initiated by neurological insults, such as status epilepticus, which can result in the generation of ROS and induction of oxidative stress. Suppressing oxidative stress by upregulation of the transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown to be an effective strategy to increase endogenous antioxidant defences, including in brain diseases, and can ameliorate neuronal damage and seizure occurrence in epilepsy. Here, we aim to test the neuroprotective potential of a naturally occurring Nrf2 activator sulforaphane, in in vitro epileptiform activity model and a temporal lobe epilepsy rat model. Sulforaphane significantly decreased ROS generation during epileptiform activity, restored glutathione levels, and prevented seizure-like activity-induced neuronal cell death. When given to rats after 2 h of kainic acid-induced status epilepticus, sulforaphane significantly increased the expression of Nrf2 and related antioxidant genes, improved oxidative stress markers, and increased the total antioxidant capacity in both the plasma and hippocampus. In addition, sulforaphane significantly decreased status epilepticus-induced neuronal cell death. Our results demonstrate that Nrf2 activation following an insult to the brain exerts a neuroprotective effect by reducing neuronal death, increasing the antioxidant capacity, and thus may also modify epilepsy development.

Sign in / Sign up

Export Citation Format

Share Document