Suppression of oxidative stress after transient focal ischemia in interleukin-1 knock out mice

Acta Neurochir Suppl. 2003:86:191-4. doi: 10.1007/978-3-7091-0651-8_41.

Abstract

Interleukin-1 (IL-1) contributes to ischemic neurodegeneration. However, the mechanisms regulating action of IL-1 are still poorly understood. In order to clarify this central issue, mice that were gene deficient both IL-1alpha and beta (IL-1 KO) and wild-type mice were subjected to 1 hour transient middle cerebral artery occlusion (tMCAO). The concentration of 8-hydroxy deoxyguanosine (8OHdG) which is considered to be a reliable oxidative DNA damage by superoxide anion, in brain and of total nitric oxide (NO) in plasma were determined by use of HPLC. Twenty-four hours after tMCAO, the ratio of 8OHdG to dG in the ipsilateral hemisphere of wild-type mice were 2.24 x 10(-3) and 4.41 x 10(-3) in the neocortex and striatum, respectively. The concentration of 8OHdG in the ipsilateral hemisphere of the wild-type mice was higher than that of the IL-1 KO mice. The concentration of total NO in the plasma of IL-1 KO mice was also lower than that of the wild-type 24 hours after tMCAO. These results strongly suggest that IL-1 is participated in generating reactive oxygen spices and it aggravates and induces the ischemic neuronal cell death.(183 words).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 8-Hydroxy-2'-Deoxyguanosine
  • Animals
  • Brain / metabolism*
  • Cattle
  • Deoxyguanosine / analogs & derivatives*
  • Deoxyguanosine / metabolism
  • Infarction, Middle Cerebral Artery / mortality
  • Interleukin-1 / deficiency*
  • Ischemic Attack, Transient / blood
  • Ischemic Attack, Transient / metabolism*
  • Mice
  • Mice, Knockout
  • Nitrates / blood
  • Nitrites / blood
  • Oxidative Stress*

Substances

  • Interleukin-1
  • Nitrates
  • Nitrites
  • 8-Hydroxy-2'-Deoxyguanosine
  • Deoxyguanosine