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Sepsis Inhibits Reduction of Dehydroascorbic Acid and Accumulation of Ascorbate in Astroglial Cultures: Intracellular Ascorbate Depletion Increases Nitric Oxide Synthase Induction and Glutamate Uptake Inhibition by Jasminka Korcok; Feng Wu; Karel Tyml; Robert R. Hammond; John X. Wilson is a Neuroscience article available to read on EtoBox.

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## Abstract Sepsis is associated with oxidative stress and impaired glutamatergic transmission in brain. We investigated whether sepsis impairs accumulation of the antioxidant, ascorbate, and uptake of glutamate by astrocytes. Bacterial endotoxin (__Escherichia coli__ lipopolysaccharide, LPS) and the inflammatory cytokine, interferon‐γ (IFNγ), were applied to primary astrocyte cultures to model sepsis. In the absence of ascorbate, the combination of LPS and IFNγ (LPS + IFNγ) up‐regulated inducible nitric oxide synthase (iNOS) and decreased the initial rate of glutamate uptake by 50% within 24 h. Cell viability and facilitated glucose transport activity were not affected at 24 h. Pre‐treatment with ascorbate‐2‐__O__‐phosphate increased intracellular ascorbate concentration and attenuated the induction of iNOS and inhibition of glutamate uptake caused by LPS + IFNγ. Subsequent experiments examined the mechanisms by which cells accumulate ascorbate. LPS + IFNγ decreased slightly the initial rate of uptake of ascorbate and inhibited markedly the rate with which intracellular dehydroascorbic acid (DHAA) was reduced to ascorbate. We conclude that septic insult impairs astrocytic clearanc

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Author

Jasminka Korcok; Feng Wu; Karel Tyml; Robert R. Hammond; John X. Wilson

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)

Published

2002

Language

EN

Field

Neuroscience (Life Sciences)