Prostaglandin F rises in response to hydroxyl radical generated in vivo

Danxia Liu, Liping Li

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Free radicals and some free fatty acids, such as arachidonic acid metabolites, have been hypothesized to be contributors to secondary damage to the spinal cord upon injury. These two types of species may form a feedback loop in which generation of one type leads to formation of the other. In this study, to determine whether hydroxyl radical causes generation of arachidonic acid metabolites in vivo, we generated hydroxyl radical, a most reactive oxygen radical, in the rat spinal cord and measured resulting changes in levels of prostaglandin F, an arachidonic acid metabolite that rises following traumatic injury. The hydroxyl radical was generated in the rat spinal cord by administering H2O2 through one microdialysis fiber and FeC12/EDTA through a parallel fiber. The prostaglandin F in the collected microdialysates was measured by HPLC as its 3-bromomethyl-6,7-dimethoxy-l-methyl-2-(1H)-quinoxalinone derivative. Prostaglandin F dramatically increased in response to hydroxyl radical generation, but declined substantially after 3 h of exposure. Prostaglandin F was undetectable when either H2O2 or FeC12/EDTA was administered alone in control experiments, demonstrating that its formation was caused by generated hydroxyl radical.

Original languageEnglish (US)
Pages (from-to)571-576
Number of pages6
JournalFree Radical Biology and Medicine
Issue number3
StatePublished - Mar 1995


  • Arachidonic acid metabolites
  • Fenton's reagents
  • Free radicals
  • HPLC analysis
  • Hydroxyl radical generation
  • Microdialysis
  • Prostaglandin F Secondary spinal cord injury

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)


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