The time course of hydroxyl radical formation following spinal cord injury: The possible role of the iron-catalyzed Haber-Weiss reaction

Danxia Liu, Jing Liu, Dachuan Sun, Jing Wen

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

This study explores whether the hydroxyl radical (.OH)-one of the most destructive reactive oxygen species-plays a role in secondary spinal cord injury (SCI). First, we measured the time course of .OH formation in rat spinal tissue after impact SCI by administering salicylate as a trapping agent into the intrathecal space of the cord and measuring the hydroxylation products of salicylate, 2,3- and 2,5-dihydroxybenzoic acid (2,3- and 2,5-DHBA) by HPLC. The 2,3-DHBA concentration was significantly higher in injured spinal tissue than in sham controls at 5 min, 1 and 3 h, but not at 5 h post-injury. Second, we generated ·OH by administering H 2O2 and FeCl2/EDTA (Fenton's reagents) at the concentrations produced by SCI into the gray matter of the cord for 4 h and found that it induced significant cell loss at 24 h post-.OH exposure. Mn (III) tetrakis (4-benzoic acid) porphyrin(MnTBAP)-a broad spectrum reactive species scavenger-significantly reduced .OH-induced cell death. Finally, we generated superoxide and administered FeCl3/EDTA in the intrathecal space of the cord at the concentration produced by SCI and measured extracellular .OH formation in the gray matter of the cord by microdialysis sampling. We found that the levels of .OH significantly increased compared to the pre-administration level, indicating that .OH can be produced in vivo by the iron-catalyzed Haber-Weiss reaction. All together, we demonstrated that .OH is an endogenous secondary damaging agent following SCI and the metal-catalyzed Haber-Weiss reaction may contribute to early .OH formation after SCI.

Original languageEnglish (US)
Pages (from-to)805-816
Number of pages12
JournalJournal of Neurotrauma
Volume21
Issue number6
DOIs
StatePublished - Jun 2004

Fingerprint

Spinal Cord Injuries
Hydroxyl Radical
Iron
Salicylates
Edetic Acid
Microdialysis
Hydroxylation
Superoxides
Reactive Oxygen Species
Cell Death
Metals
High Pressure Liquid Chromatography
Wounds and Injuries

Keywords

  • Hydrogen peroxide
  • Hydroxyl radical
  • Iron-catalyzed Haber-Weiss/Fenton reaction
  • Microdialysis sampling and administration
  • Reactive oxygen species
  • Secondary spinal cord injury
  • Superoxide anion

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

The time course of hydroxyl radical formation following spinal cord injury : The possible role of the iron-catalyzed Haber-Weiss reaction. / Liu, Danxia; Liu, Jing; Sun, Dachuan; Wen, Jing.

In: Journal of Neurotrauma, Vol. 21, No. 6, 06.2004, p. 805-816.

Research output: Contribution to journalArticle

@article{f152f8094d794d8a95f9bc3b9146df61,
title = "The time course of hydroxyl radical formation following spinal cord injury: The possible role of the iron-catalyzed Haber-Weiss reaction",
abstract = "This study explores whether the hydroxyl radical (.OH)-one of the most destructive reactive oxygen species-plays a role in secondary spinal cord injury (SCI). First, we measured the time course of .OH formation in rat spinal tissue after impact SCI by administering salicylate as a trapping agent into the intrathecal space of the cord and measuring the hydroxylation products of salicylate, 2,3- and 2,5-dihydroxybenzoic acid (2,3- and 2,5-DHBA) by HPLC. The 2,3-DHBA concentration was significantly higher in injured spinal tissue than in sham controls at 5 min, 1 and 3 h, but not at 5 h post-injury. Second, we generated ·OH by administering H 2O2 and FeCl2/EDTA (Fenton's reagents) at the concentrations produced by SCI into the gray matter of the cord for 4 h and found that it induced significant cell loss at 24 h post-.OH exposure. Mn (III) tetrakis (4-benzoic acid) porphyrin(MnTBAP)-a broad spectrum reactive species scavenger-significantly reduced .OH-induced cell death. Finally, we generated superoxide and administered FeCl3/EDTA in the intrathecal space of the cord at the concentration produced by SCI and measured extracellular .OH formation in the gray matter of the cord by microdialysis sampling. We found that the levels of .OH significantly increased compared to the pre-administration level, indicating that .OH can be produced in vivo by the iron-catalyzed Haber-Weiss reaction. All together, we demonstrated that .OH is an endogenous secondary damaging agent following SCI and the metal-catalyzed Haber-Weiss reaction may contribute to early .OH formation after SCI.",
keywords = "Hydrogen peroxide, Hydroxyl radical, Iron-catalyzed Haber-Weiss/Fenton reaction, Microdialysis sampling and administration, Reactive oxygen species, Secondary spinal cord injury, Superoxide anion",
author = "Danxia Liu and Jing Liu and Dachuan Sun and Jing Wen",
year = "2004",
month = "6",
doi = "10.1089/0897715041269650",
language = "English (US)",
volume = "21",
pages = "805--816",
journal = "Journal of Neurotrauma",
issn = "0897-7151",
publisher = "Mary Ann Liebert Inc.",
number = "6",

}

TY - JOUR

T1 - The time course of hydroxyl radical formation following spinal cord injury

T2 - The possible role of the iron-catalyzed Haber-Weiss reaction

AU - Liu, Danxia

AU - Liu, Jing

AU - Sun, Dachuan

AU - Wen, Jing

PY - 2004/6

Y1 - 2004/6

N2 - This study explores whether the hydroxyl radical (.OH)-one of the most destructive reactive oxygen species-plays a role in secondary spinal cord injury (SCI). First, we measured the time course of .OH formation in rat spinal tissue after impact SCI by administering salicylate as a trapping agent into the intrathecal space of the cord and measuring the hydroxylation products of salicylate, 2,3- and 2,5-dihydroxybenzoic acid (2,3- and 2,5-DHBA) by HPLC. The 2,3-DHBA concentration was significantly higher in injured spinal tissue than in sham controls at 5 min, 1 and 3 h, but not at 5 h post-injury. Second, we generated ·OH by administering H 2O2 and FeCl2/EDTA (Fenton's reagents) at the concentrations produced by SCI into the gray matter of the cord for 4 h and found that it induced significant cell loss at 24 h post-.OH exposure. Mn (III) tetrakis (4-benzoic acid) porphyrin(MnTBAP)-a broad spectrum reactive species scavenger-significantly reduced .OH-induced cell death. Finally, we generated superoxide and administered FeCl3/EDTA in the intrathecal space of the cord at the concentration produced by SCI and measured extracellular .OH formation in the gray matter of the cord by microdialysis sampling. We found that the levels of .OH significantly increased compared to the pre-administration level, indicating that .OH can be produced in vivo by the iron-catalyzed Haber-Weiss reaction. All together, we demonstrated that .OH is an endogenous secondary damaging agent following SCI and the metal-catalyzed Haber-Weiss reaction may contribute to early .OH formation after SCI.

AB - This study explores whether the hydroxyl radical (.OH)-one of the most destructive reactive oxygen species-plays a role in secondary spinal cord injury (SCI). First, we measured the time course of .OH formation in rat spinal tissue after impact SCI by administering salicylate as a trapping agent into the intrathecal space of the cord and measuring the hydroxylation products of salicylate, 2,3- and 2,5-dihydroxybenzoic acid (2,3- and 2,5-DHBA) by HPLC. The 2,3-DHBA concentration was significantly higher in injured spinal tissue than in sham controls at 5 min, 1 and 3 h, but not at 5 h post-injury. Second, we generated ·OH by administering H 2O2 and FeCl2/EDTA (Fenton's reagents) at the concentrations produced by SCI into the gray matter of the cord for 4 h and found that it induced significant cell loss at 24 h post-.OH exposure. Mn (III) tetrakis (4-benzoic acid) porphyrin(MnTBAP)-a broad spectrum reactive species scavenger-significantly reduced .OH-induced cell death. Finally, we generated superoxide and administered FeCl3/EDTA in the intrathecal space of the cord at the concentration produced by SCI and measured extracellular .OH formation in the gray matter of the cord by microdialysis sampling. We found that the levels of .OH significantly increased compared to the pre-administration level, indicating that .OH can be produced in vivo by the iron-catalyzed Haber-Weiss reaction. All together, we demonstrated that .OH is an endogenous secondary damaging agent following SCI and the metal-catalyzed Haber-Weiss reaction may contribute to early .OH formation after SCI.

KW - Hydrogen peroxide

KW - Hydroxyl radical

KW - Iron-catalyzed Haber-Weiss/Fenton reaction

KW - Microdialysis sampling and administration

KW - Reactive oxygen species

KW - Secondary spinal cord injury

KW - Superoxide anion

UR - http://www.scopus.com/inward/record.url?scp=2942695288&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2942695288&partnerID=8YFLogxK

U2 - 10.1089/0897715041269650

DO - 10.1089/0897715041269650

M3 - Article

C2 - 15253806

AN - SCOPUS:2942695288

VL - 21

SP - 805

EP - 816

JO - Journal of Neurotrauma

JF - Journal of Neurotrauma

SN - 0897-7151

IS - 6

ER -