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Absence of direct antioxidant effects from volatile anesthetics in primary mixed neuronal-glial cultures.

Publication ,  Journal Article
Kudo, M; Aono, M; Lee, Y; Massey, G; Pearlstein, RD; Warner, DS
Published in: Anesthesiology
February 2001

BACKGROUND: Volatile anesthetics decrease ischemic brain injury. Mechanisms for this protection remain under investigation. The authors hypothesized that volatile anesthetics serve as antioxidants in a neuronal-glial cell culture system. METHODS: Primary cortical neuronal-glial cultures were prepared from fetal rat brain. Cultures were exposed to iron, H2O2, or xanthine-xanthine oxidase for 30 min in serum-free media containing dissolved isoflurane (0-3.2 mm), sevoflurane (0-3.6 mm), halothane (0-4.1 mm), n-hexanol, or known antioxidants. Cell damage was assessed by release of lactate dehydrogenase (LDH) and trypan blue exclusion 24 h later. Lipid peroxidation was measured by the production of thiobarbituric acid-reactive substances in a cell-free lipid system. Iron and calcium uptake and mitochondrial depolarization were measured after exposure to iron in the presence or absence of isoflurane. RESULTS: Deferoxamine reduced LDH release caused by H2O2 or xanthine-xanthine oxidase, but the volatile anesthetics had no effect. Iron-induced LDH release was prevented by the volatile anesthetics (maximum effect for halothane = 1.2 mm, isoflurane = 1.2 mm, and sevoflurane = 2.1 mm aqueous phase). When corrected for lipid solubility, the three volatile anesthetics were equipotent against iron-induced LDH release. In the cell-free system, there was no effect of the anesthetics on thiobarbituric acid-reactive substance formation in contrast to Trolox, which provided complete inhibition. Isoflurane (1.2 mm) reduced mean iron uptake by 46% and inhibited mitochondrial depolarization but had no effect on calcium uptake. CONCLUSIONS: Volatile anesthetics reduced cell death induced by oxidative stress only in the context of iron challenge. The likely reason for protection against iron toxicity is inhibition of iron uptake and therefore indirect reduction of subsequent intracellular oxidative stress caused by this challenge. These data argue against a primary antioxidant effect of volatile anesthetics.

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Published In

Anesthesiology

DOI

ISSN

0003-3022

Publication Date

February 2001

Volume

94

Issue

2

Start / End Page

303 / 212

Location

United States

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Neuroglia
  • Malondialdehyde
  • Lipid Peroxidation
  • L-Lactate Dehydrogenase
  • Iron
  • Hydrogen Peroxide
  • Female
  • Cells, Cultured
 

Citation

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Kudo, M., Aono, M., Lee, Y., Massey, G., Pearlstein, R. D., & Warner, D. S. (2001). Absence of direct antioxidant effects from volatile anesthetics in primary mixed neuronal-glial cultures. Anesthesiology, 94(2), 303–212. https://doi.org/10.1097/00000542-200102000-00021
Kudo, M., M. Aono, Y. Lee, G. Massey, R. D. Pearlstein, and D. S. Warner. “Absence of direct antioxidant effects from volatile anesthetics in primary mixed neuronal-glial cultures.Anesthesiology 94, no. 2 (February 2001): 303–212. https://doi.org/10.1097/00000542-200102000-00021.
Kudo M, Aono M, Lee Y, Massey G, Pearlstein RD, Warner DS. Absence of direct antioxidant effects from volatile anesthetics in primary mixed neuronal-glial cultures. Anesthesiology. 2001 Feb;94(2):303–212.
Kudo, M., et al. “Absence of direct antioxidant effects from volatile anesthetics in primary mixed neuronal-glial cultures.Anesthesiology, vol. 94, no. 2, Feb. 2001, pp. 303–212. Pubmed, doi:10.1097/00000542-200102000-00021.
Kudo M, Aono M, Lee Y, Massey G, Pearlstein RD, Warner DS. Absence of direct antioxidant effects from volatile anesthetics in primary mixed neuronal-glial cultures. Anesthesiology. 2001 Feb;94(2):303–212.

Published In

Anesthesiology

DOI

ISSN

0003-3022

Publication Date

February 2001

Volume

94

Issue

2

Start / End Page

303 / 212

Location

United States

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Neuroglia
  • Malondialdehyde
  • Lipid Peroxidation
  • L-Lactate Dehydrogenase
  • Iron
  • Hydrogen Peroxide
  • Female
  • Cells, Cultured