scholarly journals Protection of Hippocampal Neuronal Cells from Buthionine Sulfoximine‐induced Oxidative Stress by Food‐derived Phase 2 Detoxifying Enzyme Inducers

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Jong-Sang Kim ◽  
Ji Sun Lim ◽  
Jiyeon Seo ◽  
Chaelim Jung ◽  
Jung-Hwa Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuronal Cells ◽  
Buthionine Sulfoximine ◽  
Phase 2 ◽  
Detoxifying Enzyme ◽  
Enzyme Inducers

Therapeutic potential of dietary phase 2 enzyme inducers in ameliorating diseases that have an underlying inflammatory component

2001 ◽  
Vol 79 (3) ◽  
pp. 266-282 ◽  
Author(s):  
Bernhard HJ Juurlink
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Therapeutic Effects ◽  
Phase 2 ◽  
Phase 2 Enzymes ◽  
Anti Oxidant ◽  
Inflammatory Component ◽  
Enzyme Inducers

Many diseases associated with ageing have an underlying oxidative stress and accompanying inflammatory component, for example, Alzheimer's disease or atherosclerosis. Reviewed in this manuscript are: the role of oxidative stress in activating the transcription factor nuclear factor kappa B (NFκB), the role of NFκB in activating pro-inflammatory gene transcription, strong oxidants produced by cells, anti-oxidant defense systems, the central role of phase 2 enzymes in the anti-oxidant defense, dietary phase 2 enzyme inducers and evidence that dietary phase 2 enzymes decrease oxidative stress. It is likely that a diet containing phase 2 enzyme inducers may ameliorate or even prevent diseases that have a prominent inflammatory component to them. Research should be directed into the potential therapeutic effects of dietary phase 2 enzyme inducers in ameliorating diseases with an underlying oxidative stress and inflammatory component to them.Key words: Alzheimer's disease, atherosclerosis, diet, glutathione, inflammation, stroke.

scholarly journals Upregulation of Nrf2 expression by human cytomegalovirus infection protects host cells from oxidative stress

2013 ◽  
Vol 94 (7) ◽  
pp. 1658-1668 ◽  
Author(s):  
Junsub Lee ◽  
Kyungmi Koh ◽  
Young-Eui Kim ◽  
Jin-Hyun Ahn ◽  
Sunyoung Kim
Keyword(s):  
Oxidative Stress ◽  
Human Cytomegalovirus ◽  
Survival Rates ◽  
Buthionine Sulfoximine ◽  
Host Cells ◽  
Related Factor ◽  
Downstream Target ◽  
Human Foreskin Fibroblasts ◽  
Cellular Defence ◽  
Nrf2 Expression

NF-E2 related factor 2 (Nrf2) is a transcription factor that plays a key role(s) in cellular defence against oxidative stress. In this study, we showed that the expression of Nrf2 was upregulated in primary human foreskin fibroblasts (HFFs), following human cytomegalovirus (HCMV/HHV-5) infection. The expression of haem oxygenase-1, a downstream target of Nrf2, was also increased by HCMV infection, and this induction was suppressed in HFFs expressing a small hairpin RNA (shRNA) against Nrf2. The HCMV-mediated increase in Nrf2 expression was abolished when UV-irradiated virus was used or when the activity of casein kinase 2 was inhibited. Host cells infected by HCMV had higher survival rates following oxidative stress induced by buthionine sulfoximine compared with uninfected control cells, but this cell-protective effect was abolished by the use of Nrf2 shRNA. Our results suggest that HCMV-mediated activation of Nrf2 might be beneficial to the virus by increasing the host cell’s ability to cope with oxidative stress resulting from viral infection and/or inflammation.

scholarly journals Effects of Cimicifuga racemosa extract Ze450 on mitochondria in models of oxidative stress in neuronal cells

Data in Brief ◽  
2018 ◽  
Vol 21 ◽  
pp. 1872-1879 ◽  
Author(s):  
Malena Rabenau ◽  
Matthias Unger ◽  
Jürgen Drewe ◽  
Carsten Culmsee
Keyword(s):  
Oxidative Stress ◽  
Neuronal Cells ◽  
Cimicifuga Racemosa

scholarly journals Novel mechanism of increased Ca2+ release following oxidative stress in neuronal cells involves type 2 inositol-1,4,5-trisphosphate receptors

Neuroscience ◽  
2011 ◽  
Vol 175 ◽  
pp. 281-291 ◽  
Author(s):  
S. Kaja ◽  
R.S. Duncan ◽  
S. Longoria ◽  
J.D. Hilgenberg ◽  
A.J. Payne ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuronal Cells ◽  
Inositol 1,4,5 Trisphosphate

scholarly journals Neuronal-specific function of hTim8a in Complex IV assembly provides insight into the molecular mechanism underlying Mohr-Tranebjærg syndrome

2019 ◽  
Author(s):  
Yilin Kang ◽  
Alexander J. Anderson ◽  
David P. De Souza ◽  
Catherine S. Palmer ◽  
Kenji M. Fujihara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disease ◽  
Neuronal Cells ◽  
Underlying Mechanism ◽  
Copper Chaperone ◽  
Intermembrane Space ◽  
Specific Function ◽  
Hydrophobic Membrane ◽  
Complex Iv ◽  
Enhanced Sensitivity

AbstractHuman Tim8a is a member of an intermembrane space chaperone network, known as the small TIM family, which transport hydrophobic membrane proteins through this compartment. Mutations in TIMM8A cause a neurodegenerative disease, Mohr-Tranebjærg syndrome (MTS), which is characterised by sensorineural hearing loss, dystonia and blindness. Nothing is known about the function of hTim8a in neuronal cells and consequently how lack of hTim8a leads to a neurodegenerative disease. We identified a novel cell-specific function of hTim8a in the assembly of Complex IV, which is mediated through a transient interaction with the copper chaperone COX17. Complex IV assembly defects in cells lacking hTim8a leads to oxidative stress and changes to key apoptotic regulators, including cytochrome c and Bax, which primes cells for cell death. Alleviation of oxidative stress using Vitamin E rescues cells from apoptotic vulnerability. We hypothesis that enhanced sensitivity of neuronal cells to apoptosis is the underlying mechanism of MTS.

scholarly journals 7,8-Dihydroxyflavone Protects High Glucose-Damaged Neuronal Cells against Oxidative Stress

2019 ◽  
Vol 27 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Suk Ju Cho ◽  
Kyoung Ah Kang ◽  
Mei Jing Piao ◽  
Yea Seong Ryu ◽  
Pincha Devage Sameera Madushan Fernando ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Neuronal Cells

scholarly journals Inhibition of Glutathione and Thioredoxin Metabolism Enhances Sensitivity to Perifosine in Head and Neck Cancer Cells

2009 ◽  
Vol 2009 ◽  
pp. 1-10 ◽  
Author(s):  
Andrean L. Simons ◽  
Arlene D. Parsons ◽  
Katherine A. Foster ◽  
Kevin P. Orcutt ◽  
Melissa A. Fath ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Neck Cancer ◽  
Reductase Activity ◽  
Thioredoxin Reductase ◽  
Buthionine Sulfoximine ◽  
Human Head ◽  
Akt Inhibitor ◽  
Simultaneous Treatment

The hypothesis that the Akt inhibitor, perifosine (PER), combined with inhibitors of glutathione (GSH) and thioredoxin (Trx) metabolism will induce cytotoxicity via metabolic oxidative stress in human head and neck cancer (HNSCC) cells was tested. PER induced increases in glutathione disulfide (%GSSG) in FaDu, Cal-27, and SCC-25 HNSCCs as well as causing significant clonogenic cell killing in FaDu and Cal-27, which was suppressed by simultaneous treatment with N-acetylcysteine (NAC). An inhibitor of GSH synthesis, buthionine sulfoximine (BSO), sensitized Cal-27 and SCC-25 cells to PER-induced clonogenic killing as well as decreased total GSH and increased %GSSG. Additionally, inhibition of thioredoxin reductase activity (TrxRed) with auranofin (AUR) was able to induce PER sensitization in SCC-25 cells that were initially refractory to PER. These results support the conclusion that PER induces oxidative stress and clonogenic killing in HNSCC cells that is enhanced with inhibitors of GSH and Trx metabolism.

Angiotensin II-mediated biphasic regulation of proximal tubular Na+/H+ exchanger 3 is impaired during oxidative stress

2011 ◽  
Vol 301 (2) ◽  
pp. F364-F370 ◽  
Author(s):  
Anees Ahmad Banday ◽  
Mustafa F. Lokhandwala
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
Tap Water ◽  
Buthionine Sulfoximine ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Sprague Dawley ◽  
High Concentration ◽  
Nitric Oxide Signaling ◽  
Proximal Tubular

Angiotensin (ANG) II via AT1 receptors (AT1Rs) maintains sodium homeostasis by regulating renal sodium transporters including Na+/H+ exchanger 3 (NHE3) in a biphasic manner. Low-ANG II concentration stimulates whereas high concentrations inhibit NHE3 activity. Oxidative stress has been shown to upregulate AT1R function that could modulate the ANG II-mediated NHE3 regulation. This study was designed to identify the signaling pathways responsible for ANG II-mediated biphasic regulation of proximal tubular NHE3 and the effect of oxidative stress on this phenomenon. Male Sprague-Dawley rats were chronically treated with a pro-oxidant l-buthionine sulfoximine (BSO) with and without an antioxidant tempol in tap water for 3 wk. BSO-treated rats exhibited oxidative stress and high blood pressure. At low concentration (1 pM) ANG II increased NHE3 activity in proximal tubules from all animals. However, in BSO-treated rats, the stimulation was more robust and was normalized by tempol treatment. ANG II (1 pM)-mediated NHE3 activation was abolished by AT1R blocker, intracellular Ca2+ chelator, and inhibitors of phospholipase C (PLC) and Ca2+-dependent calmodulin (CaM) but it was insensitive to Giα and protein kinase C inhibitors or AT2R antagonist. A high concentration of ANG II (1 μM) inhibited NHE3 activity in control and tempol-treated rats. However, in BSO-treated rats, ANG II (1 μM) continued to induce NHE3 stimulation. Tempol restored the inhibitory effect of ANG II (1 μM) in BSO-treated rats. The inhibitory effect of ANG II (1 μM) involved AT1R-dependent, cGMP-dependent protein kinase (PKG) activation and was independent of AT2 receptor and nitric oxide signaling. We conclude that ANG II stimulates NHE3 via AT1R-PLC-CaM pathway and inhibits NHE3 by AT1R-PKG activation. Oxidative stress impaired ANG II-mediated NHE3 biphasic response in that stimulation was observed at both high- and low-ANG II concentration.

Degeneration of neuronal cells due to oxidative stress—microglial contribution

2002 ◽  
Vol 8 (6) ◽  
pp. 401-406 ◽  
Author(s):  
E. Koutsilieri ◽  
C. Scheller ◽  
F. Tribl ◽  
P. Riederer
Keyword(s):  
Oxidative Stress ◽  
Neuronal Cells
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