Abstract
This study used a weight drop impact injury model to explore the role of iron and the reality of iron-catalyzed hydroxyl radical ((*)OH) formation in secondary spinal cord injury (SCI). The time course of total extracellular iron was measured following SCI by microcannula sampling and atomic absorption spectrophotometry analysis. Immediately following SCI, the total iron concentration increased from an undetectable level to an average of 1.32 microM. The time course of SCI-induced (*)OH-generating catalytic activity in the cord was obtained by determining the ability of tissue homogenate to convert hydrogen peroxide to (*)OH and then measuring 2,3-dihydroxybenzoic acid, a hydroxylation product of salicylate. The concentration of 2,3-DHBA quickly and significantly increased (p <.001) and returned to sham level (p = 1) by 30 min post-SCI. Desferrioxamine (80 and 800 mg/kg body weight) significantly (p <.001) reduced the catalytic activity, suggesting that iron is the major contributor of the activity. Administering FeCl(3) (100 microM)/EDTA (0.5 mM) in ACSF into the cord through a dialysis fiber significantly increased SCI-induced (*)OH production in the extracellular space, demonstrating that Fe(3+) can catalyze (*)OH production in vivo. Our results support that iron-catalyzed (*)OH formation plays a role in the early stage of secondary SCI.
Published Version
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