scholarly journals Glutamate receptor-mediated taurine release from the hippocampus during oxidative stress

2010 ◽  
Vol 17 (Suppl 1) ◽  
pp. S10 ◽  
Author(s):  
Brian Tucker ◽  
James E Olson
Keyword(s):  
Oxidative Stress ◽  
Glutamate Receptor ◽  
Taurine Release

scholarly journals Vitamin E-Mediated Modulation of Glutamate Receptor Expression in an Oxidative Stress Model of Neural Cells Derived from Embryonic Stem Cell Cultures

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Afifah Abd Jalil ◽  
Huzwah Khaza’ai ◽  
Norshariza Nordin ◽  
Nur’izzati Mansor ◽  
Amirah Salwani Zaulkffali
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Glutamate Receptor ◽  
Cell Cultures ◽  
Embryonic Stem ◽  
Receptor Expression ◽  
Neural Cells ◽  
Es Cell ◽  
Neural Lineage

Glutamate is the primary excitatory neurotransmitter in the central nervous system. Excessive concentrations of glutamate in the brain can be excitotoxic and cause oxidative stress, which is associated with Alzheimer’s disease. In the present study, the effects of vitamin E in the form of tocotrienol-rich fraction (TRF) and alpha-tocopherol (α-TCP) in modulating the glutamate receptor and neuron injury markers in an in vitro model of oxidative stress in neural-derived embryonic stem (ES) cell cultures were elucidated. A transgenic mouse ES cell line (46C) was differentiated into a neural lineage in vitro via induction with retinoic acid. These cells were then subjected to oxidative stress with a significantly high concentration of glutamate. Measurement of reactive oxygen species (ROS) was performed after inducing glutamate excitotoxicity, and recovery from this toxicity in response to vitamin E was determined. The gene expression levels of glutamate receptors and neuron-specific enolase were elucidated using real-time PCR. The results reveal that neural cells derived from 46C cells and subjected to oxidative stress exhibit downregulation of NMDA, kainate receptor, and NSE after posttreatment with different concentrations of TRF and α-TCP, a sign of neurorecovery. Treatment of either TRF or α-TCP reduced the levels of ROS in neural cells subjected to glutamate-induced oxidative stress; these results indicated that vitamin E is a potent antioxidant.

scholarly journals Transglutaminase is a Therapeutic Target for Oxidative Stress, Excitotoxicity and Stroke: A new Epigenetic Kid on the Cns Block

2013 ◽  
Vol 33 (6) ◽  
pp. 809-818 ◽  
Author(s):  
Manuela Basso ◽  
Rajiv R Ratan
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Glutamate Receptor ◽  
Therapeutic Target ◽  
Transcriptional Repression ◽  
Cell Injury ◽  
Gene Repression ◽  
Protein Substrates ◽  
Calcium Dependent ◽  
Evolving Model

Transglutaminases (TGs) are multifunctional, calcium-dependent enzymes that have been recently implicated in stroke pathophysiology. Classically, these enzymes are thought to participate in cell injury and death in chronic neurodegenerative conditions via their ability to catalyze covalent, nondegradable crosslinks between proteins or to incorporate polyamines into protein substrates. Accumulating lines of inquiry indicate that specific TG isoforms can shuttle into the nucleus when they sense pathologic changes in calcium or oxidative stress, bind to chromatin and thereby transduce these changes into transcriptional repression of genes involved in metabolic or oxidant adaptation. Here, we review the evidence that supports principally a role for one isoform of this family, TG2, in cell injury and death associated with hemorrhagic or ischemic stroke. We also outline an evolving model in which TG2 is a critical mediator between pathologic signaling and epigenetic modifications that lead to gene repression. Accordingly, the salutary effects of TG inhibitors in stroke may derive from their ability to restore homeostasis by removing inappropriate deactivation of adaptive genetic programs by oxidative stress or extrasynaptic glutamate receptor signaling.

scholarly journals Exercise Fatigue Induce the Oxidative Stress and the Expression of mGluR 4 and mGluR 5 on the Ventrolateral Thalamus in Rats

CONVERTER ◽  
2021 ◽  
pp. 220-229
Author(s):  
Meihua Su, Yong Mao, Dan Xu
Keyword(s):  
Oxidative Stress ◽  
Glutamate Receptor ◽  
Muscle Injury ◽  
Metabotropic Glutamate Receptor ◽  
Exhaustive Exercise ◽  
Control Group ◽  
Post Exercise ◽  
Metabotropic Glutamate ◽  
Ventrolateral Thalamus ◽  
Exercise Fatigue

Objective: The motor thalamus plays an important role during exercise. It aims to observe the changes of mGluR4 and mGluR5 in ventrolateral thalamus of rats induced by repeated exhaustive exercise, and to discuss the relationship of mGluR4, mGluR5 and oxidative damage occured during exhaustive exercise. Methods: There were 48 male wistar rats, which were randomly divided into four groups including CG, 0EG, 24EG and 48 EG, each group having 12 rats. Meanwhile, immunohistochemistry (IMM) technique was used to investigate the expression of positive cell and integrated optical density (IOD) of metabotropic glutamate receptor 4 (mGluR4) and metabotropic glutamate receptor 5 (mGluR5), and the impact of exhaustive exercise played on oxidative stress indexes such as malondialdehyde (MDA), glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) in ventrolateral thalamus of rats were also investigated in different groups. Results: Compared with CG, the expression of mGluR4 and mGluR5 protein of ventrolateral thalamus in 0EG and 24EG both significantly increased, and the value of mGluR4 in 48EG were still higher than control group, however the the value of mGluR5 in 48EG reduced to the rest level of control group. Meanwhile, the SOD activities of 0EG and 24EG group were significantly higher than the control group, and it was the same with GSH content in ventrolateral thalamus of rats. Meanwhile, MDA has been investigated that it increased significantly in 0EG and 24EG compared with control group, and the MDA level of 48EG was still significant higher than CG. Moreover, the indexes of muscle injury such as LD, CK and BUN all increased significantly post-exercise immediately and post-exercise 24 hours .Conclusion: Exercise fatigue could result in up-regulation of mGluR4 and mGluR5 and increace activity of SOD , GSH-PX and MDA in ventrolateral thalamus of rats, and it also induce the muscle injury by increase the level of LD, CK and BUN in serum, which suggested that ventrolateral thalamus was an important brain rigion to modulate the motor function, and mGluR4 and mGluR5 maybe two important receptors prevent from the increase of free radicals and muscle injury induced by exercise fatigue.

Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp (Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Secondary Metabolites ◽  
Human Health ◽  
Grass Carp ◽  
Aquatic Environment ◽  
Ctenopharyngodon Idellus

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.

Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov
Keyword(s):  
Oxidative Stress ◽  
Head And Neck ◽  
Transcriptional Activation ◽  
Platinum Resistance ◽  
Mrna Levels ◽  
Strong Positive Correlation ◽  
Platinum Compounds ◽  
Copper Chelation ◽  
Novel Approach ◽  
Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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