Effect of Barbiturates on Hydroxyl Radicals, Lipid Peroxidation, and Hypoxic Cell Death in Human NT2-N Neurons

Almaas, Runar; Saugstad, Ola Didrik; Pleasure, David E; Rootwelt, Terje

doi:10.1097/00000542-200003000-00020

Cited by 69 publications

(57 citation statements)

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“…Ntera2/clone D1 is a human teratocarcinoma-derived cell line which differentiates into post-mitotic neuron-like cells (NT2-N cells) upon treatment with retinoic acid [222][223][224] .…”

Section: Nt2-n Cellsmentioning

confidence: 99%

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Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

et al. 2009

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“…Ntera2/clone D1 is a human teratocarcinoma-derived cell line which differentiates into post-mitotic neuron-like cells (NT2-N cells) upon treatment with retinoic acid [222][223][224] .…”

Section: Nt2-n Cellsmentioning

confidence: 99%

“…Accumulation of hypoxanthine is an indicator of energy failure 80,222 and correlates with LDH release 223 . Hypoxanthine release (ȝmol/L) to supernatant was used as a marker of cellular energy failure in the NT2-N model (paper I).…”

Section: Hypoxanthine Releasementioning

confidence: 99%

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

et al. 2009

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“…The combination of five HRE with a cytomegalovirus (CMV) minimal promoter exhibited excellent hypoxia responsiveness with over 500-fold induction in some cell types. 10 Ntera2c1.D2 (NT2), a human embryonic carcinoma cell line, terminally differentiates into postmitotic neurons (NT2N) by treatment with retinoic acid, [11][12][13] and may be used as a cell culture model for human neurons. Nondifferentiated NT2 cells ( Figure 1A) are rapidly dividing and may be conveniently expanded before treatment with retinoic acid, which then induces typical morphological changes with differentiation to postmitotic neurons (NT2N) ( Figure 1B).…”

mentioning

confidence: 99%

Hypoxia-inducible transgene expression in differentiated human NT2N neurons – a cell culture model for gene therapy of postischemic neuronal loss

Cao

Shibata

2001

Gene Ther

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Expression of anti-apoptotic or neurotrophic transgene proteins in hypoxic neurons may provide a novel therapeutic strategy for neuroprotection and alleviation of damage to ischemic brain areas. NT2, a human neoplastic cell line which terminally differentiates into postmitotic neuronsIschemia of the brain due to major vessel thrombosis causes hypoxia in the respective vascular territory and subsequently induces neuronal death which is at least in part caused by apoptosis, especially in the penumbra of the lesion. 1,2 Hypoxia-inducible expression of anti-apoptotic or neurotrophic transgenes in hypoxic neurons may provide a novel therapeutic strategy for neuroprotection and alleviation of damage to ischemic brain areas.Hypoxia has been known as a potent inducer of a large number of genes including those encoding erythropoietin, vascular endothelial growth factor (VEGF), and some glycolytic enzymes, eg phosphoglycerate kinase. These genes have specific regulatory sequences in their promoter regions, known as hypoxia responsive elements (HRE). 3 Under hypoxic conditions, the upregulated hypoxia-inducible transcription factor 1 (HIF-1) binds to the HRE and initiates transcription of 3Ј sequences. This physiological mechanism has been utilized for develop- ment of hypoxia-responsive gene transfer vectors with HRE-based promoters. Hypoxia-inducible expression of transgenes has been reported in tumor cells and in cardiac myocytes. [4][5][6][7][8][9] Recently, new hypoxia-responsive vectors for tumor-specific gene therapy were developed. 10

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“…Propofol (2, 6-diisopropylphenol) and thiopental are highly lipid-soluble anaesthetics and have antioxidant activities, protecting against lipid peroxidation (35). Both are often used to reduce cerebral edema during liver transplantation in fulminant hepatic failure patients (36)(37) the antioxidant activities of propofol and thiopental were able to protect the liver from oxidative stress in the setting of biliary obstruction had not been asked.…”

Section: Discussionmentioning

confidence: 99%

“…Thiopental is a highly lipid soluble anaesthetic which has demonstrated antioxidant properties by inhibiting lipid peroxidation (51,52) and to a lesser degree, antihemolytic activity by inhibiting free-radical-mediated hemolysis of red blood cell in vitro (53,54). In one study, at clinically relevant concentrations, thiopental signifi cantly reduced reactive oxygen species production of neutrophils (54).…”

Section: Discussionmentioning

confidence: 99%

The protective effects of ketamine and propofol in obstructive jaundice: an experimental study

Yıldız¹,

Çoşkuner²,

Bülbüloğlu³

et al. 2012

BLL

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Abstract:Objective: In this study, we investigated the protective effects of frequently used intravenous anesthetics (ketamine, propofol, thiopental, and fentanyl) in oxidative stress in a rat liver model of obstructive jaundice. Materials and methods: Thirty-two Wistar albino rats were divided into four groups in a randomized fashion. All rats were subjected to laparotomy, common bile duct ligation and severance on day 0. Following 7 days, laparotomy was again performed using ketamine, propofol, pentobarbital, or fentanyl anesthesia. After 2 hours, the animals were sacrifi ced and tissue specimens were acquired for histopathological scoring and determination of malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activities. Results: All rats demonstrated enlargement in the bile duct, obstructive jaundice, and histopathologic ductal proliferation. MDA and SOD levels were signifi cantly lower in the ketamine group compared with the thiopental and fentanyl groups. CAT was signifi cantly increased in the ketamine group compared with the other groups. The best portal polymorphonuclear leukocyte and necrosis scores were in the ketamine group, but this difference was not statistically signifi cant ( p=0.07) Conclusion: Ketamine and propofol were observed to cause the least amount of oxidative stress in this rat model of induced oxidative stress generated by ligation of the common bile duct. This experiment is the fi rst study on this subject in the literature (Tab. 3, Ref. 65). Full Text in PDF www.elis.sk.

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Effect of Barbiturates on Hydroxyl Radicals, Lipid Peroxidation, and Hypoxic Cell Death in Human NT2-N Neurons

Abstract: Barbiturates differ markedly in their neuroprotective effects against combined oxygen and glucose deprivation in human NT2-N neurons. The variation in neuroprotective effects could only partly be explained by differences in antioxidant action.

Cited by 69 publications

References 0 publications

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

Hypoxia-inducible transgene expression in differentiated human NT2N neurons – a cell culture model for gene therapy of postischemic neuronal loss

The protective effects of ketamine and propofol in obstructive jaundice: an experimental study

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