Cell death in primary cultures of mouse neurons and astrocytes during exposure to and ‘recovery’ from hypoxia, substrate deprivation and simulated ischemia

Sochocka, Elzbieta; Juurlink, Bernhard H.J.; Code, William E.; Hertz, Vannaphone; Peng, Liang; Hertz, Leif

doi:10.1016/0006-8993(94)90628-9

Cited by 71 publications

(39 citation statements)

References 30 publications

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“…However, this does not completely rule out the possibility that t-BuOOH metabolites penetrate the cell and act at the extracellular site. It has been reported that astrocytes are resistant to oxidative stress compared to neurones (Vibulsreth et al 1987;Yu et al 1989;Sochocka et al 1994;Desagher et al 1996). In the present study, astrocytes were relatively resistant to H202, but were as vulnerable to t-BuOOH as neurones.…”

Section: Discussionsupporting

confidence: 45%

Characterization of t‐Butyl Hydroperoxide Toxicity in Cultured Rat Cortical Neurones and Astrocytes

Abe

Saito

1998

Pharmacology & Toxicology

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The present study investigates the toxicity of 1-butyl hydroperoxide (r-BuOOH) in cultured rat cortical neurones and astrocytes. Both neurones and astrocytes were destroyed by exposure to r-BuOOH in a time-and concentrationdependent manner. Astrocytes were more resistant to destruction by hydrogen peroxide (H202) than neurones, but there was no difference in susceptibility to t-BuOOH between neurones and astrocytes. The toxic effect of t-BuOOH was significantly blocked by antioxidants, propyl gallate and trolox, but not by superoxide dismutase nor by H202-scavengers, catalase and 4-nitrophenylglyoxylic acid. These results suggest that t-BuOOH toxicity is caused by oxidative stress unrelated to superoxide and H202. In addition, the toxic effect of t-BuOOH was attenuated by the presence of iron chelators, deferoxamine and N, N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine, indicating the requirement of endogenous iron for r-BuOOH toxicity.

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Section: Discussionsupporting

confidence: 45%

Characterization of t‐Butyl Hydroperoxide Toxicity in Cultured Rat Cortical Neurones and Astrocytes

Abe

Saito

1998

Pharmacology & Toxicology

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“…Astrocytes in primary culture respond to hypoxic conditions by up regulation of glycolysis (Callahan et al, 1990;Tholey et al, 1991;Sochocka et al, 1994;Yager et al, 1994;Swanson and Benington, 1996;Niitsu et al, 1999;Marrif and Juurlink, 1999). This might aid in maintaining the intracellular ATP levels in hypoxic astrocytic cultures at levels sufficient for survival (Yager et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Effects of continuous hypoxia on energy metabolism in cultured cerebro-cortical neurons

et al. 2008

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Mechanisms underlying hypoxia-induced neuronal adaptation have not been fully elucidated. In the present study we investigated glucose metabolism and the activities of glycolytic and TCA cycle enzymes in cerebro-cortical neurons exposed to hypoxia (3 days in 1% of O 2 ) or normoxia (room air). Hypoxia led to increased activities of LDH (251%), PK (90%), and HK (24%) and decreased activities of CS (15%) and GDH (34%). Neurons were incubated with [1-13 C]glucose for 45 and 120 min under normoxic or hypoxic (120 min only) conditions and 13 C enrichment determined in the medium and cell extract using 1 H-{ 13 C}-NMR. In hypoxia-treated neurons [3-13 C]lactate release into the medium was 428% greater than in normoxia-treated controls (45-min normoxic incubation) and total flux through lactate was increased by 425%. In contrast glucose oxidation was reduced significantly in hypoxia-treated neurons, even when expressed relative to total cellular protein, which correlated with the reduced activities of the measured mitochondrial enzymes. The results suggest that surviving neurons adapt to prolonged hypoxia by up-regulation of glycolysis and downregulation of oxidative energy metabolism, similar to certain other cell types. The factors leading to adaptation and survival for some neurons but not others remains to be determined.

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“…Cell death was examined by a modification of the previously described staining method (20,22,23). PI (4.6 µg/ ml) containing 0.001% NaN 3 was added to the culture medium for 15 min before the termination of the experiment.…”

Section: Cell Viabilitymentioning

confidence: 99%

Hydrogen Peroxide-Induced Thymidine Incorporation Into Cultured Rat Astrocytes

2006

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Cell death in primary cultures of mouse neurons and astrocytes during exposure to and ‘recovery’ from hypoxia, substrate deprivation and simulated ischemia

Cited by 71 publications

References 30 publications

Characterization of t‐Butyl Hydroperoxide Toxicity in Cultured Rat Cortical Neurones and Astrocytes

Characterization of t‐Butyl Hydroperoxide Toxicity in Cultured Rat Cortical Neurones and Astrocytes

Effects of continuous hypoxia on energy metabolism in cultured cerebro-cortical neurons

Hydrogen Peroxide-Induced Thymidine Incorporation Into Cultured Rat Astrocytes

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