Abstract
Reactive oxygen-derived species were previously implicated in mediation of post-traumatic brain damage; however, the efficacy of traditional antioxidants in preventing/reversing the damage is sometimes limited. The present work focused on the mechanisms underlying the neuroprotective activity of cell permeable, nontoxic, anti-oxidants, namely stable nitroxide radicals in an experimental model of rat closed-head injury Brain damage was reduced by the weight-drop method and the clinical status was evaluated according to a neurological seventy score at I h and 24 h, where the difference between these scores reflects the extent of recovery. The metal chelator deferoxamine as well as three nitroxide derivatives, differing in hydrophilicity and charge, and one hydroxylamine (a reduced nitroxide) facilitated the clinical recovery and decreased the brain edema. The nitroxides, but neither the hydroxylamine nor deferoxamine, protected the integrity of the blood-brain barrier. Superoxide dismutase also improved the clinical recovery but did not affect brain edema or the blood-brain barrier. The results suggest that by switching back and forth between themselves, the nitroxide and hydroxylamine act catalytically as self-replenishing annoxidants, and protect brain tissue by terminating radical-chain reactions, oxidizing deleterious metal ions, and by removal of intracellular superoxide.
Original language | English |
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Pages (from-to) | 332-340 |
Number of pages | 9 |
Journal | Free Radical Biology and Medicine |
Volume | 24 |
Issue number | 2 |
DOIs | |
State | Published - 15 Jan 1998 |
Externally published | Yes |
Keywords
- Oxidative damage
- Spin label
- Superoxide
- Transition metals
- Traumatic brain injury
ASJC Scopus subject areas
- Biochemistry
- Physiology (medical)